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My DEMS I > Neoplasms of Lower GI Tract (use ppt for pics, chart @ end) > Flashcards

Neoplasms of Lower GI Tract (use ppt for pics, chart @ end) Flashcards

1
Q

Right sided mass

A

stool semi-liquid, so might not detect mass

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2
Q

left sided mass

A

stool progressively well formed/solid, so more likely to get stuck/be detected if mass present

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3
Q

Where are epithelial stem cells?

A

base of crypts

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4
Q

Polyp

A
  • sessile vs. pedunculated, neoplastic vs non-neoplastic
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5
Q

adeoma

A

precurtsor to malignancy

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6
Q

adenocarcinoma

A

invasive

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7
Q

Pedunculated vs sessil

A

pedunculated has stalk

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8
Q

Inflammatory polyps

A

Often present with bleeding
Often due to mucosal prolapse (very common in the rectum)
Cycles of injury and healing result in “polyp” formation = inflamed colonic mucosa with ulceration/erosion, epithelial hyperplasia

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9
Q

Hamartomatous polyps

A

Most occurring in childhood (pre-pubertal)
Hamartoma: “tumor-like” over-growth / mature tissue / developing where it is normally present (e.g. colonic tissue developing in the colon)
Juvenile (sporadic and syndromic) and Peutz-Jeghers (syndromic)

Key Points
Polyps: Variable locations in lower GI system

Benign features histologically but syndromic juvenile polyps often have foci of dysplasia

May portend:

Risk of future GI carcinoma (increase frequency of screening)

Both Peutz-Jeghers and Juvenile polyposis = 40% cumulative risk for CA

Extra-GI manifestations

Need to consider familial screening (genetic counseling) in some cases

Types
Juvenile
Peutz-Jeghers
Others: Cowden, Cronkhite-Canada

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10
Q

Extra-GI manifestations of Peutz Jeghers

A

Mucocutaneous pigmented lesions; increased risk of thyroid, breast, lung, pancreas, gonadal, and bladder cancers

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11
Q

Extra-GI Manifestations of juvenile polyposis

A

Pulmonary arteriovenous malformations, digital clubbing

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12
Q

Hyperplastic Polyps

A

Location: left colon including rectum (90%)

increases w/ age

small (

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13
Q

Hyperplastic polyp histology

A 
Smooth, nodular lesion with flat base
	 sessile 
Need microscopic evaluation to definitively distinguish 
Hyperplastic polyp
Adenomatous polyp

composed of mixed absorptive and goblet cells; cells are crowded, possibly due to delayed shedding of epithelium  “hyperplastic.” A serrated architecture results. This is a benign, usually non-neoplastic lesion to be distinguished from SSPs

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14
Q

Serrated polyps

A

Not pre-malignant: hyperplastic (left sided)
Crypts with “star-shaped” / “serrated” appearance- Cytology: Not dysplastic
- Have been considered for decades “non- neoplastic

Premalignant:
Sessile Serrated Polyps/Adenoma (tend to be right sided) –> alternate pathways to carcinoma than the usual adenomatous polyp
Microsatellite Instability pathway
DNA hypermethylation pathway (CpG island methylation)

Architecture: looks like “serrated” knife
- Cytology: Dysplastic epithelium may or may not be present
Pre-neoplastic = DEFINITELY can progress to adenocarcinoma

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15
Q

Adenomas

A

Size is variable – range from a few mm to several cm (10 cm or more)
In nearly 50% of Western adults by age 50

Present throughout the colon

Have epithelial cytologic dysplasia ranging from low grade to high grade (carcinoma in situ)

Villous adenomas contain foci of invasion more frequently than tubular adenomas but SIZE MATTERS (correlates with risk of malignancy )
Presence of high grade dysplasia increases risk of malignant transformation in that polyp but not in the rest of the colon

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16
Q

Adenomatous changes on histology

A
  1. Cells
    • Piling up on each other (no respect!)
  2. Nuclei
    • Darker
      (hyperchromasia)
    • Progressive loss of basal-orientation
  3. Cytoplasm - Reduced compared to nucleus
    (increased N:C ratio)
    • Reduced mucin production
  4. Mitotic Figures - Increased mitotic activity
17
Q

Villous adenoma

A

Lesion is sessile – No stalk
Architecture: multiple, slender villi (finger-like projections)

Adenomatous(dysplastic)
histologic features

18
Q

Colorectal cancer

A

3rd most common in men and women

19
Q

Common mutation in Adenoma

A

APC @ 5q21

Later events: Beta catenin, K-RAS, loss of p53/SMAD2 and 4 tumor suppressor genes

20
Q

RFs/ PRotective factors for colorectal cancer

A

age
country of birth
FAP/HNPCC
longstanding UC

moderate:
high red meat diet
previous adenoma or cancer
pelvic irradiation

modest
high fat diet
smoking/alc
obesity 
cholecystectomy

Protective
phys activity
aspirin/NSAIDs

fruit/veg/fiber/folate methionine
Ca
Postmenopausal hormone therapy

21
Q

Main molecular pathways

A

WNT/APC/beta-catenin – classical adenoma-carcinoma sequence
K-Ras/MAP kinase/PI3 kinase signaling pathways—activating mutations
Microsatellite Instability – defects in mismatch repair proteins

methylation induced gene silencing enhances progression along pathway

22
Q

most CR cancers are

A

sporadic (followed by familial)

23
Q

WNT signaling altered in what % of CRC pts?

A

92%

24
Q

WNT pathway

A

Wnt protein ligands are critical for development

Animals lacking Wnt homologs fail to develop entire organs. (fly wnt-1 mut =wingless)

Wnt ligands drive proliferation of their target tissues/organs

The Wnt pathway regulates the levels of cytoplasmic beta-catenin

***WNT pathwayd involves APC and Beta-catenin (made often, degraded fast) Need all components in “destruction complex”: APC, Beta catenin, axin, etc. (Dishevelled activated and allows Beta catenin to escape destruction and act on genes)

25
Q

Where is beta-catenin turned off

A

@ top of crypt (if stays on, accumulation of cells @ site of future polyp formation)

Polyps represent 
An increase in the 
size of the 
proliferating crypt 
compartment
26
Q

FAP

A

Familial Adenometous Polyposis (Aut dom)

APC mutations can run in families, producing Familial Adenomatous Polyposis (FAP)
FAP patients have increased risk of colon cancer, but these account for a small fraction of the total cases of colon cancer (~5%)
Most people who acquire colon cancer without FAP acquire spontaneous somatic mutations in APC

In FAP: 100% will develop invasive adenocarcinoma, often before age 30

27
Q

Cetuximab

A

EGFR inhibitor (monoclonal antibody)

28
Q

Hereditary Non-Polyposis Colorectal Cancer aka Lynch Syndrome

A

Develop colon cancer at an earlier age than sporadic forms
Tend to be right-sided
Inherit mutation of mismatch repair gene allele, acquire the second allele mutation over time leading to microsatellite instability

29
Q

Advancing vs early colon carcinoma

A 
Change in bowel habits and indicators
Constipation
Urgency
Narrowing of stool
Cramping / pain
Blood Loss
Blood in stool or bleeding from rectum (BBBPR)
Anemia (iron-deficiency)
Unexplained weight loss
Early Colon Carcinoma
No symptoms most often
Nonspecific findings
Fatigue
Weight loss 
Anemia
30
Q

Detection of neoplasms

A

Visualization +/- Biopsy
= Colonoscopy
= Barium enema
= Other options

Blood Detection in Stool
- Hemorrhage of ulcerated lesion

DNA / Mutation Detection in Stool
- Shed neoplastic cells vs. normal colonic epithelial cells

31
Q

Carcinoma

A

Invasion of dysplastic epithelial cells into and beyond the lamina propria
Adenomas at risk:
4 cm: high risk (~40% in one study) of identification of invasive component within lesion

32
Q

typical adenocarcinoma histology

A

gland formation
mucin production

Neoplastic glands (adenocarcinoma) invading into muscularis propria, inciting a “desmoplastic” (fibrotic) response. There is “dirty necrosis” in the lumen of some of the glands (arrow), a fairly common finding in colon carcinoma.

33
Q

Prognosis

A

Most important prognostic factors:
Depth of invasion
Presence or absence of lymph node metastasis
Distant metastasis

34
Q

Where does colon cancer most commonly metastasize to?

A

LIVER

35
Q

Therapy for colon cancer

A

Surgery
Local excision – e.g. polypectomy
Colonic resection

Radiofrequency ablation

Cryosurgery

Chemotherapy
-Only treatment = palliative
-Adjunctive treatment
Pre or Post-Operative

Radiation therapy

Targeted Therapy

  • Monoclonal antibodies
  • Angiogenesis inhibitors

My DEMS I (26 decks)

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