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Gastroenterology > Tumors of the Bowel > Flashcards

Tumors of the Bowel Flashcards

1
Q

Familial adenomatous polyposis treatment options

A

Removal organ at risk:
- proctocolectomy with ileostomy –> best option
Other options with equivalent results in patients with milder sparing of rectum:
- colectomy with ileo-rectal anastomosis (spare rectum)
- restorative proctocolectomy with ileo-anal pouch (IPAA)

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2
Q

What is MYH polyposis

A

Autosomal recessive polyposis…..
APC gene - susceptible to oxidative injuries that the mutY gene is supposed to repair.

Similar clinical presentation, risk of extra-colonic tumors, surgical options FAP.
Difference: Not quite as extensive disease as FAP. Risk of cancer is at a later age than FAP –> Proximal Colon.

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3
Q

Hereditary Non-Polyposis Colon Canacer

A

Most common inherited

Do no recommend prophylactic surgery

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4
Q

Two groups of HNPCC

A
  1. colorectal cancers only

2. colorectal and other cancers (endometrial…..

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5
Q

Clinical features of HNPCC

A

accelerated polyp-cancer sequence

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6
Q

Amsterdam Criteria for HNPCC 3-2-1 rule for considering HNPCC

A

3 or more relatives with an HNPCC associated cancer (colorectal cancer, or cancer of the endometrium, small intestine, ureter or renal pelvis)

2 or more successive generations (1 should be a first-degree relative of the other two)

1 or more relatives diagnosed before the age of 50 years

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7
Q

Bethseda guidelines for HNPCC

A
  • more involved way of screening for this disorder

Increase in sensitivity but decrease in specificity )nolonger just based on FMH)

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8
Q

immunohistochemistry screeing for mismatch repair genes in resected crc

A

MLH1, MSH2, MSH6, PmS2, –> positive is good. When proteins are not present, we worry about

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9
Q

Types of non-neoplastic polyps

A
  1. Hyperplastic, 2. Juvenile or Retention, 3. Peutz Jeghers
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10
Q

morphologic features of adenoma

A

mucin depletion
nuclei enlarged and different
–> low grade dysplasia

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11
Q

adenocarcinoma on histology

A

haphazard growth of glands

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12
Q

tubular adenoma

A

cells are crowded
have a high number of glandular/tubular compartments on low grade picture
Many nuclei –> look blue on H&E
mucin depleted

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13
Q

Villous adenoma

A

long villi which rise from the fibrovascular cores
they can carpet the mucosa in broad areas
- can lead to electrolyte disorders

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14
Q

Villous adenoma gross

A

carpeting of the villous adenoma - seen on endoscopy

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15
Q

tubullovillous adenoma

A

both glandular and villous components
- crowding, elongation and stratification of nuclei
loss of maturation seen as loss of mucin
low grade dysplasia

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16
Q

Treatment

A

excision of adenoma

- easier with pedunculated

17
Q

Hyplastic polyp

A

hypermucinous lookk,
starfish appearance -
serration
—- appearance due to continued prolferation of cells - mature but do not slough so they need to accommodate themselves

18
Q

juvenile

A

outline
inflamed lamina propia
difficult to distinguish from inflammatory polyps

19
Q

Peutz-jeghers polyp

A

Non-neoplastic
Hamartomatous
Branching smooth muscle and glands lined by goblet cells
Slight malignant potential (LOH at LKB1 locus)
PJS pts at increased risk of developing CA of pancreas, breast, lung, ovary, and uterus.

20
Q

colorectal adenocarcinoma

A
  1. Left-sided tumors (distal) tend to grow as annular, circumferential, ulcerated masses. So-called “napkin ring lesions”. Obstruction (change in bowel pattern) is common.
  2. Right-sided tumors (proximal colon) tend to grow as polypoid, exophytic masses. May still be deeply infiltrating. Obstruction is uncommon. Occult bleeding (anemia) or melena.
21
Q

STaging of CRC

A

no lymphoid vessels in mucosa –> so no lymph node metastases
those connected to lymph vessels = distant metastases

22
Q

Forms of inherited Colorectal Cancer

A 
Adenomatous Polyposis Syndromes:
- FAP (Gardner’s; Turcot’s); MUTYH Polyposis
Hamartomatous Polyposis Syndromes:
- Peutz-Jeghers; Juvenile Polyposis
Non-Polyposis Syndromes:
- HNPCC  (Lynch I & II)
23
Q

FAP

A

Autosomal dominant genetic disorder
Germline mutation in the APC gene 5q21
Diagnosis: >100 polyps in the colon and rectum
25% of probands have no family history

24
Q

Clinical Features of FAP

A

intestinal disease= by polyps present not only in the colon, but in the stomach and small intestine (duodenum).
extra-intestinal manifestations = desmoid tumors, osteomas, brain tumors, congenital hypertrophy of the retinal pigmented epithelium, hepatobiliary tumors, thyroid tumors, and adrenal tumors. Epidermoid cysts.
? Most common cause of death in FAP

25
Q

Ileo-anal puch advantages and disadvantages

A 
Advantages= No permanent stoma
Removes all mucosa?
Preserves anal defecation
Disadvantages= Multiple stages
Higher morbidity
Risk of pouch failure Requires good sphincter
26
Q

MutHY Polyposis

A

Autosomal recessive polyposis syndrome caused by
bi-allelic germ line mutations in mutY homolog gene (base excision repair gene). Repairs oxidative DNA injuries. APC gene particularly prone to these injuries = may lead to somatic mutations in APC gene.
Mono-allelic carriers -> no increased Ca risk.
May have identical clinical presentation to FAP but generally pt’s have 15-100 adenomas.
Mean age at cancer dx = 45 yrs.
Not always accompanied by polyposis and may account for a proportion of patients with familial CRC.

27
Q

Epidemiology of MutHY Polyposis

A

66% of cancers occur in the ascending colon.
Similar range of extracolonic tumors to those seen in FAP with addition of breast Ca. No established screening guidelines. Similar surgical options to those for FAP
Consider MUTYH gene analysis in pts with FAP or AFAP w/ no APC gene abnormality.

28
Q

HNPCC

A

Most common inherited colon cancer syndrome.
Autosomal dominant inheritance pattern.
Germline mutation in mismatch repair genes (MMR): MSH2, MLH1, MSH6, PMS2.
Lifetime risk of colorectal cancer = 60-80%.
Originally, dx based on personal and family hx; clinically indistinguishable from sporadic CRC

29
Q

The precursor lesion is an adenomatous polyp, just as in sporadic CRC and clinical features may be indistinguishable from pts with sporadic CRC.
Penetrance 40-60% therefore currently do not recommend prophylactic Rx

A

HNPCC

30
Q

Types of Lynch

A

Lynch Syndrome 1 = Colorectal cancers only
Lynch Syndrome 2= Colorectal cancers; Other cancers (Endometrial, ovarian, pancreatic, gastric, small bowel, transitional cell of kidney/ureter)

31
Q

Bethseda Guidelines for HNPCC

A
  • Colorectal carcinoma <50 years old
  • Synchronous or metachronous CRC or other Lynch syndrome-associated tumors, regardless of age
  • CRC with high microsatellite instability histology diagnosed in a patient less than 60 years old
  • CRC diagnosed in one or more first-degree relatives with a Lynch syndrome-associated tumor, with one of the cancers being diagnosed at less than 50 years of age
  • CRC diagnosed in two or more first-degree or second-degree relatives with Lynch syndrome-associated tumors, regardless of age
32
Q

Diagnosis of Bethseda

A

Amsterdam I= 61% sensitivity
Amsterdam II = 72% sensitivity
Bethesda criteria = 94% sensitivity
Decreasing Specificity with increasing specifity

33
Q

Juvenile or Retention Polyp

A

Hamartomatous malformations
Most frequent in the rectum
Most often in children (<5yoa)
Usually large (1 to 3 cm), round, smooth lesions with stalks
Inflamed lamina propria with cystically dilated glands
No malignant potential

34
Q

Pathologic Staging of Colon Adenocarcinoma

A

Carcinoma in situ (pTis)
- Intraepithelial carcinoma (Severe dysplasia): No risk of metastasis
- Intramucosal carcinoma = Limited to lamina propria: Very low risk of metastasis.
Invasion into submucosa (pT1)
Into muscularis propria (pT2)
Through muscularis propria (pT3)
Penetration of serosa or invasion of adjacent viscera (pT4)
***Increasing Risk of Mets as you Go Down.

35
Q

Hyperplastic Polyp

A

Small (usually <5 mm) sessile polyps
Most common in the rectum/sigmoid
Elongated and serrated, stellate crypts lined by “hypermature” goblet cells
Do not have malignant potential

36
Q

Carcinoid Tumors malignant potential

A

All carcinoids are potentially malignant tumors.
More likely benign depending on:
(1) Site of origin = Appendiceal and rectal carcinoids usually benign
(2) Depth of local penetration <2 cm)
Intervention: Monitor Chromogranin A levels, urinary 5HIAA, Octreotide scans

37
Q

Carcinoid Syndrome

A

Occurs in Pulmonic & tricuspid valve stenosis/regurge

Gastroenterology (11 decks)

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