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GI/Nutrition > Neoplasms of the Small & Large Bowel > Flashcards

Neoplasms of the Small & Large Bowel Flashcards

1
Q

What is the most common small intestine neoplasm?

A

Adenoma

75% length of GI

3-6% of GI tumors

Mesenchymal tumors are more rare: lipoma, GIST, lymphoma

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2
Q

What are the risk factors for small intestine Adenocarcinoma?

A
  • Crohn’s disease
  • Adenomas
  • Celiac disease
  • Familial Polyposis Syndrome
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3
Q

What is the most common non-epithelial (soft tissue) tumor in the GI tract?

A

GIST

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4
Q

GIST

  • Origin
  • May be seen in
  • Treatment
A
  • Mesenchymal origin (intestinal cells of Cajal - pacemaker cells)
  • May be seen in:
    • Carney triad
    • Neurofibromatosis
    • Carney-Stratakis syndrome
  • Gleevec (Imatinib)
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5
Q

GIST

  • IHC Markers
  • Muscle Markers
A
  • CD117 (c-KIT), DOG1, CD34
  • Actin, Desmin, S-100
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6
Q

GIST Mutations

A
  • c-KIT (80%), PDGFRA (5-10%)
  • Tyrosine kinase receptors
  • Ligand –> receptor dimerizes –> intracellular domains autophosphorylate –> constitutive activation of kinase in presence/absence of ligand
  • Gain-of-function mutation
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7
Q

What are the symptoms of carcinoid syndrome?

What becomes elevated?

A
  • Neuroendocrine tumor
  • Symptoms
    • Vasomotor disturbances
    • Intestinal hypermotility
    • Wheezing
    • Hepatomegaly
    • Cardiac involvement
  • Serotonin (5-HT) elevated
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8
Q

What is an intestinal polyp?

A

Epithelium-derived tumor mass

Protrudes into gut lumen

Pedunculated = stalk w/ polyp

Sessile = flat polyps that grow upward (no stalk)

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9
Q

What is the difference between a non-neoplastic polyp & neoplastic polyp?

A
  • Non-neoplastic polyp
    • Abnormal mucosal maturation
    • Inflammation
    • Distorted architecture
    • No malignant potential
  • **Neoplastic polyp **
    • Proliferation & dysplasia (adenomas)
    • Precursor of carcinoma
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10
Q

What are some examples of non-neoplastic polyps?

A
  • Hamartoma
  • Juvenile polyp
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11
Q

What is a hamartoma?

A
  • Benign tumor
  • Mature, histologically normal elements from that site growing in a disorganized manner
  • Developmental error
  • Occurs at many sites
  • Contrast w/ choristomas (haphazard tissue in wrong place)
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12
Q

What is a juvenile polyp?

What age group does it most commonly present?

Where in the GI tract does it present?

A
  • Kids <5 YO
  • 80% rectum
  • Pedunculated (1-3 cm)
  • Expanded LP w/ variable inflammation
  • Abundant cystically dialted, tortuous glands
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13
Q

What is the inheritance of Juvenile Polyposis Syndrome?

A

Autosomal dominant

Gain-of-function mutations

SMAD4 (20%)

BMPR1A (20%)

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14
Q

What is Juvenile Polyposis Syndrome?

A
  • Multiple juvenile polyps
    • >5
    • 5-100
  • Stomach, small intestine, colon, rectum
  • 10-15% lifetime incidence of colon cancer
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15
Q

Peutz-Jeghers polyps (do/don’t) have malignant potential

A

**Don’t **

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16
Q

A patient presents to you with multiple GI polyps and hyperpigmentation around their mouth & on their fingers? What do they likely have?

A

**Peutz-Jeghers Syndrome **

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17
Q

What does a Peutz-Jeghers Polyp look like on histology?

A
  • Large & pedunculated
  • Connective tissue & smooth muscle extends into the polyp
  • Abundant glands rich in goblet cells
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18
Q

Inheritance & Risk of Peutz-Jeghers Syndrome

A
  • Autosomal dominant (STK11)
  • Increased risk of intussusception
  • Increased risk of cancer
    • Pancreas, breast, lung, ovary, uterus
  • 50% cumulative lifetime risk of cancer
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19
Q

What are some clinical features of Cowden Syndrome?

A
  • Facial trichilemmomas
  • Oral papillomas
  • Acral keratoses
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20
Q

Inheritance & Risk of Cowden Syndrome

A
  • Autosomal dominant
  • Hamartomatous GI polyps
  • Risk of thyroid & breast cancer
  • Polyps themselves have _no malignant potential _
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21
Q

What is Cronkite-Canada?

How do these patients present?

A
  • Non-hereditary
  • GI Hamartomatous polyps
  • Ectodermal abnormalities
    • Nail atrophy
    • **Alopecia **
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22
Q

What is the difference between Inflammatory Polyps & Lymphoid Polyps?

A
  • Inflammatory Polyps
    • Pseudopolyps
    • Regenerating mucosa adjacent to ulceration
    • Severe IBD
  • Lymphoid Polyps
    • Mucosal bumps caused by intramucosal lymphoid follicles
    • Normal
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23
Q

What are Serrated Polyps? What do they look like?

A
  • Smooth protrusions of mucosa at tops of mucosal folds
  • Rectosigmoid colon (>50%)
  • “Serrated” lumina
  • Increased # of goblet cells
  • Small (<5 mm diameter)
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24
Q

What is the difference between Hyperplastic & Sessile Serrated polyps?

A
  • Hyperplastic
    • 60-90%
    • Distal
    • No malignant potential
  • Sessile Serrated
    • 10-30%
    • Proximal
    • High malignant potential
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25
Q

What are the genetics of Sessile Serrated Polyps?

A
  • BRAF V600E mutations
  • Methylation
  • Microsatellite instability
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26
Q

What is the difference between Hyperplastic & Sessile Serrated Polyps with regards to growth?

A
  • Hyperplastic Polyps
    • Grows from bottom to top
    • Growth rate faster than death rate of normal colonic cells
    • Serrations at tips of crypts
  • Sessile Serrated Polyps
    • Grows up & down
    • Cystically dilated glands
    • Bottom growing faster than cells dying
    • Horizontal growth along BM
27
Q

What is this?

A
  • HIGH GRADE DYSPLASIA
  • Large “salt & pepper” nuclei
  • Elongated, crowded, stretched out
  • Mitotic figures present in mucosa
  • Carcinoma in situ
28
Q

What are Adenomatous Polyps?

What are the 3 architectural types?

Demographics?

A

Arise from epithelial proliferative dysplasia

Precursor lesions for adenocarcinoma

**Tubular, villous, tubulovillous **

>60 YO, M = F

29
Q

What is a Tubular Adenoma?

A
  • Tubular glands
  • Small, pedunculated
  • Colon (90%)
  • Single or multiple
  • Rarely >2.5 cm
30
Q

What does a Tubular Adenoma look like histologically?

A
  • Dysplastic epithelium
    • Elongated, pseudostratified
    • Hyperchromatic nuclei
    • Loss of mucin production
31
Q

What is a Villous Adenoma?

A
  • Villous projections
  • Large, sessile
  • Older people
  • Rectosigmoid colon
  • Invasive carcinoma
    • No stalk for buffer zone
    • Cancer invasion direct into colon wall
  • _<_10 cm diameter
32
Q

What does a Villous Adenoma look like histologically?

A

flat, polypoid

fungating, irregular

33
Q

What is the relative cancer risk with polyps?

A

<1cm = rare

sessile, villous adenomas >4cm (40%)

high grade dysplasia in villous areas

high grade dysplasia/carcinoma can be in any polyp

34
Q

What is the clinical significance of an Intramucosal Carcinoma vs. Invasive Carcinoma?

A
  • Asymptomatic vs. rectal bleeding/anemia
  • Intramucosal carcinoma
    • Invades LP
    • No metastatic potential
  • **Invasive carcinoma **
    • Pedunculated adenoma (endoscopy)
    • Sessile polyp (partial colectomy)
35
Q

Regardless of whether carcinoma is present, the only adequate treatment for adenoma is __________.

A

**Complete Resection **

36
Q

Colorectal Cancer

  • Stats
  • Distribution
  • Risk
A
  • Stats
    • 98% adenocarcinoma
    • 90% diagnosed >50 YO
  • Distribution
    • Rectosigmoid colon (55%)
    • Cecum & ascending colon (22%)
  • Risk factors
    • Excess dietary caloric intake
    • Low fiber
    • High refined carbs
    • Red meat
    • Micronutrients
    • Obesity, physical inactivity
37
Q

Right-sided vs. Left-sided Colon Cancer

A
  • Right-Sided
    • Non-obstructive
    • Fatigue, weakness, iron deficiency anemia
    • Polypoid, exophytic lesions
  • Left-Sided
    • May be obstructive
    • Occult bleeding, changes in bowel habit, abdominal discomfort
    • Annular “napkin ring” constrictions
    • Infiltrative
38
Q

You have a patient who is an older adult male w/ iron deficiency anemia. What is your primary concern?

A

**Colon Cancer **

*suspicion until proven otherwise*

39
Q

What is the Adenocarcinoma Sequence?

A
  • Development of carcinoma from adenomatous lesions
  • High prevalence of adenomas ~ high prevalence of colon cancer
  • Cancer risk directly related to # of adenomas
  • Colorectal carcinogenesis
    • Accumulation of mutations more important than specific order
40
Q

What is the Adenocarcinoma Pathway? (genes, etc.)

A

Inactivated APC (>80%)

50% of cancers w/APC mutations: ß-catenin mutations

Dysfunction of APC –> increased WNT signaling –> decreased cell adhesion –> increased cellular proliferation

Loss of p53 late in colon carcinogenesis

41
Q

What are some characteristics of Infiltrative Colorectal Cancer?

A
  • Infrequent, infiltrative & difficult to identify
  • Pattern associated with Ulcerative Colitis
  • Exceedingly aggressive
  • Spread at early stage in evolution
42
Q

The most important prognostic indicator of colorectal carcinoma is the ______________ at the time of diagnosis.

A

Extent of tumor (stage)

Stage = T + N + M

43
Q

What are the 4 types of tumor classification?

A
  • TIS = mucosa
  • T1 = submucosa
  • T2 = muscularis propria
  • T3 = serosa
44
Q

What is the T, N & M for:

  • Stage 0
  • Stage I
  • Stage II
  • Stage III
  • Stage IV
45
Q

What is the 5 year survival for the Colorectal Cancer Staging?

A
  • Stage I (93.2%)
  • Stage II (85%)
  • Stage III (70%)
  • Stage IV (8.1%)
46
Q

How does colon cancer normally metastasize?

A
  • Direct extension into adjacent structures
  • Metastases through lymph nodes & vessels
  • Regional lymph nodes, liver, lungs, bones
  • Metastatic spread at presentation (25-30%)
47
Q

What are the targeted therapeutic options for treating Colorectal Carcinoma?

A

Bevacizumab

Cetuximab

Panitumumab

48
Q

What are the prognostic & predictive biomarkers for adjuvant therapy of colorectal cancer?

A
  • Prognostic
    • Provide information about patient’s overall outcome
    • Regardless of therapy
  • Predictive
    • Give information about the effects of a particular therapeutic intervention
49
Q

How and why is EGFR a key target in cancer?

A
  • Activation stimulates key processes involved in tumor growth & progression
    • Proliferation
    • Angiogenesis
    • Invasion
    • Metastasis
  • Overexpressed in a range of solid tumors
50
Q

What 3 major pathways are activated by EGFR?

A

RAS-RAF-MAP kinase

P13K-AKT

PLC-gamma

51
Q

What is the structure of EGFR?

What are the two most important members of the EGFR family involved in cancer?

A
  • Transmembrane domain + intracellular domain
  • ErbB1/EGFR/Her1
  • ErbB2/Her2/Neu
    • **Breast cancer **
52
Q

In what circumstance would a patient be responsive to moAB therapy vs. resistant to moAB therapy?

A
  • Sensitive to moAB therapy
    • Transient response
    • 12-18 mo
  • moAB therapy resistant
    • Mutation in downstream effector
    • TUMOR GROWTH
    • Shouldn’t give the drug
53
Q

______ is the major negative predictor of efficacy in EGFR moAB therapy.

A

KRAS mutation

54
Q

______ correlates w/ poor diagnosis & lack of response to EGFR moAB therapy.

A

BRAF mutation

55
Q

What are some hereditary diseases involving the GI tract?

A
  • Peutz-Jeghers Syndrome, Cowden Disease, Juvenile Polyposis Syndrome
  • Familial Adenomatous Polyposis
    • Gardner’s Syndrome
    • Turcot’s Syndrome
  • MYH Associated Polyposis
  • Lynch Syndrome/HNPCC
56
Q

What is the inheritance of Familial Adenomatous Polyposis?

A
  • **Autosomal dominant **
  • Germline mutations in APC gene
  • ~25% FAP patients have no FaHx
  • 2nd normal allele mutated
    • **Loss of heterozygosity **
    • Tumor formation
57
Q

Familiar Adenomatous Polyposis

  • Characteristics
  • Prevalence
  • Age
A
  • 500-2,000 colonic adenomas
    • 100 minimum
  • Colon adenocarcinoma (100%)
    • Prophylactic colectomy required
    • Adenomas elsewhere in GI tract
  • Median age: 16 YO
  • Age range: 5-38 YO
  • Age of onset of colorectal cancer
    • Late 30s, early 40s
58
Q

What are the variants of FAP?

A

Attentuated FAP (<100)

Gardner’s syndrome

Turcot syndrome

59
Q

What is Gardner’s Syndrome?

A
  • Adenomatous polyposis PLUS:
    • Osteomas
    • Epidermoid cysts
    • Desmoid tumors
60
Q

What is Turcot Syndrome?

A

Adenomatous polyposis + medulloblastoma

61
Q

FAP mutations

  • Classical
  • Attenuated
  • Desmoid
A
  • Classical FAP: N-terminus
  • Attenuated FAP: C-terminus
  • Desmoid: middle
62
Q

What is MYH Associated Polyposis?

What makes it different from FAP?

A
  • Hereditary colorectal cancer syndrome
  • Phenotype overlap w/ FAT
  • 20-100 adenomatous polyps
  • Autosomal recessive
  • Age at presentation > FAP
63
Q

What are the mutations for MYH Associated Polyposis?

A
  • 1p34.3-p32.1
  • MYH protein = DNA repair protein
    • Base excision repair
    • Removes oxidation-induced DNA damage
    • Removes A mis-paired w/ G
  • Two common mutations (85-90%)
    • 494A –> G
    • 1145G –> A

GI/Nutrition (36 decks)

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