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GI 3 > GI neoplasms 1 > Flashcards

GI neoplasms 1 Flashcards

1
Q

SB is ____% of GI with only ___% of tumors

most common is the ____

A

75%

3-6%

Adenoma near ampula

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2
Q

Risk factors for SI adenocarcinoma

A

Crohns/ Adenomas/ Celiac/ Familial polyposis Syndrome

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3
Q

most common non-epi tumor of GI, from Cajal cells (mesenchymal)

A

GIST

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4
Q

GIST is seen in which syndromes:

A

Seen in: Carney triad/ Neurofibromatosis/ Carney-Stratakis syndrome

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5
Q

Treatement for GIST tumors

A

Tx: Gleevac (bc of c-kit mutation seen in 85% = tyrosine kinase and is a driver mutation. PDGFRA same)

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6
Q

Location of GIST tumors

A

Location:

60% stomach/

30% sm.intestine

4% colon:

with a glossy grayish color

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7
Q

Key histological markers in GIST

Histology: test + for ckit = CD117 in almost 100% cases

DOG1

CD34 (90% time)—> shows up dark stain

Also has different muscle markers: actin, desmin, S-100

A
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8
Q

Pt comes in with tumors in the small intestine and your Preceptor states it is ammendable to Gleevac for tx. What type of markers would you expect it to have?

A

This is a GIST tumor; c-kit positive (tyr/kinase), DOG1 and CD34 +

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9
Q

Tumor that secreates bioactives = vasomotor/flushing/hepatomegaly and increase serotonin 5-HT

A

carcinoid tumor

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10
Q

Where are carcinoid tumors commonly located in the intetinal tract?

A

located in WALL of intestine; presents as submucosal nodule. Mass of neuroendocrine cells pushing upward

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11
Q

What levels will be elevated in a pt with carcinoid tumor?

A

Seratonin: 5-HT

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12
Q

epithelium derived tumor mass, protrudes through lumen: either pedunculate or sessile

A

Intestinal Polyp

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13
Q

d/t abnormal mucosal maturation, inflammation, fucked arch. NO MALIG potential

A

Non-neoplastic =

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14
Q

d/t proliferation+dysplasia (adenomas) and is precursor to carcinoma

A

Neoplastic

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15
Q

benign, focal mass with mature, histologically normal elements in disorganized manner

A

Hamartoma: non neoplastic polyp

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16
Q

What are my 3 non-neoplastic polyps?

A

Hamartomatous

Inflammatory

Lymphoid

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17
Q

seen in kids

A

Juvenile polyps

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18
Q

Describe what a juvenile polyp looks like histologically

A
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19
Q

What is Juvenile polyposis syndrome?

Where is it located?

What gene mutation?

A

multple polyps >5: in stomach/sm.intest/colon/rectum

        **Auto. Dominant** of **SMAD4, BMPR1A**, r*isk of adenomas,* 10-50% lifetime risk colon,  gastric, small intestine and pancreas cancer
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20
Q

multple polyps >5: in stomach/sm.intest/colon/rectum

        Auto. Dominant of SMAD4, BMPR1A, risk of adenomas, 10-50% lifetime risk colon,  gastric, small intestine and pancreas cancer
A

Juvenile polyposis Syndrome

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21
Q

Peutz-Jeghers Polyps:____ malignant potential

A

no

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22
Q

Pt has hyperpigmented mouth and fingers and multple GI polyps. Dx and inheritance pattern?

A

Peutyz-Jegher Syndrome = STK11; auto-Dominant

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23
Q

What are risks associated with Peutz-Jeghers Syndrome?

A

Risk intussusseption.

Risk of cancer of: pancrease/breast/ovary/uterus/lung of 50% lifetime risk

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24
Q

Describe what you see on histology and what disease this is assoicated with

A
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25
Q

hamartomous GI polpys with facial trichilemmomas, oral papillomas, acral keratoses.

A

Cowden syndrome

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26
Q

Pt has Cowden syndrome. What is the inheritance pattern?

What are associated risks?

What is the maligant potential?

A

Cowden = hamartomatous polyps, Autosomal Dominant

Assoicated with thyroid and breast cancer

polyps have no maligant potential

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27
Q

non-hereditary, GI hamartomas, Ectodermal shit: nail atrophy + alopecia

  1. Inflammatory polyps: pseudopolyps—regenarating mucosa next to ulceration (seen in bad IBD)
  2. Lymphoid polyps: mucosal bumps, d/t intramucosal lymphoid follicles; NORMAL
A

Cronkite-Canada

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28
Q

pseudopolyps—regenarating mucosa next to ulceration (seen in bad IBD)

A

Inflammatory polyps

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29
Q

mucosal bumps, d/t intramucosal lymphoid follicles; NORMAL

A

Lymphoid polyps

30
Q

Two types of serrated polyps

A

Hyperplastic and Sessile serrated

31
Q
A
32
Q

Describe location, histology and maligant potential of Hyperplastic Serrated polyps

A

Distally located

no maligant potential

make up 60-90% of serrated polyps and grow upward so deep, narrow stalk

33
Q

Describe location, maligant potential and histology of Sessile Serrated polyps

A

more proximally located

HIGH malignant potetial: BRAF V600 mutation; methlyation

–+/- microsatalite instability

Look like flasks on histology bc grow horizontal and verticle

34
Q

epithelial proliferative dysplasia + precursor to adenocarcinoma

A

Adenomatous Polpys; adenomas

35
Q

Three types of adenoma polpys

A
36
Q

Epidemiology for Adenomatous polyps

A

seen in 40-60% population >60. Familial pattern; 4x risk of devo adenoma if 1st degree relative had one

Adenoma has 4x increase risk of devoing carcinoma with M=F

37
Q

What do Tubular adenoma’s look like and where are they found?

A

small, pedunculate w/ 90% in colon. Can be mult or single

IG

38
Q

Describe the histology of tubular adenomas

A

-dysplastic epithelium: elongated, pseudostratified, HYPERchromatic nuclei, loss of mucin production

39
Q

lots of projections, large and sessile, no stalk, seen in OLDER peep in RECTOsigmoid

A

Villious Adenoma:

40
Q

Describe histology of villous adenoma

why is there such high maligant potential?

A

-no stalk to act as buffer in case of invasive carcinoma—> invasion directly into colon wall

—up to 10cm diameter; see fungating and slightly raised for gross

41
Q

Tubular adenoma; rare to get cancer if _____

Risk approaches ____ in sessile, villous adnomas >4cm;

high grade dysplasia if present IG in_____ areas but also found in any polyp

A

<1cm

40%

villious

42
Q

Intramucosal carcinoma = invades LP but

A

NO malignant potential

43
Q

Invasive carcionoma IN a pedunuclated adenoma that has gone through muscularis: endoscopic removal is enough IF what 3 critera are met

A

resection margins are negative

no lymph or vascular invasion

carcinoma not poorly different

44
Q

Invasive carcinoma in Sessile polyp: polypectomy_____, need partial colectomy

A

inadequte

***regardless of carcinoma presence, only tx for adenoma is complete resection!

45
Q

Colorectal Cancer epidemiology

A

98% adnocarcinoma

9% of all cancer deaths in US

Peak incidicend is 90% over age 50

99% occur singly

1-3% familila or IBD

most in rectosigmoid, followed by cecum and ascending

46
Q

Colorectal cancers causes fatige, weak, Fe anemia.

More common in cecum, slow bleed causing progressive weakness.

D/t polypoid or exophytic lesions

A

Right Sided (non-obstructive) colorectal cancer

47
Q

What type of lesions commonly seen with right sided CRC?

A

polypoid or exophytic

48
Q

Colorectal cancer that is obstructive, get occult bleed, change in bowel habits, ab discomfort and Annular ‘napkin’ obstruction. More infiltrative

A

Left sided: (obstructive) CRC

49
Q

Male comes in that is in his 60s and has been tiring easily and feels weak. His labs show Fe deficinecy anemia. What do we need to rule out?

A

Dx as colon cancer till proven otherwise; often has aysmptomatic and insidious onset

50
Q
A
51
Q

Population w/ high prevelance of adenomas = high chance of____ cancer

distribution of polyps and cancer in colorectal is simular

Peak age for adenomas anteda___tes peak age for cancer; if you find cancer early, often see adenomatous tissue surrounding it

Cancer risk is_____ related to # adenomas; will get cancer with FAP; thus remove polyps!

A

colorectal

colorectal

DIRECTLY

52
Q

Explain pathogenesis of CRC

A

Multi-hit hypothesis; accumulation of mutations (more important than order) with the last to accumlate is p53

53
Q

>80% colon cancer has inactivated____ and 50% w/out ACP have ____ mutations (10%)

A

ACP

B-catenin

54
Q

—dysfnx of APC seen in colorectal cancer leads to

A

increased WNT signaling, decreased cell adhesions, increase cell proliferate

55
Q

Not frequent, but hard to identify grossly, associated with Ulcerative colitis, aggressive, spread early

A

Infiltrative colorectal cancer

56
Q

Staging based on depth of invasion;

T1 =

T2=

T3=

Stage = T+N+M

A

1 = Submucosa

2= muscularis propria

3= Serosa

57
Q

Stage 0 =

Stage I:

Stage II:

Stage III:

A

Stage 0 = in situ carcinoma

Stage I: T1, T2, N0, M0

Stage II: T2 or T4, NO, MO

Stage III: any T, positive Nodes StageIV-mets

I and II can be cured by excision

III need adjuvant therapy

IV is palliative care

58
Q

Single most important prognostic indicator of colorectal carcinoma is

A

extent or STAGE at time of dx

59
Q

Survival rates for Colorectal Carcinoma

A

I and II = 93 and 85% 5 yr surival

Stage II = 70%

stage IV= 8%

60
Q

Where do CRC mets genrally go to?

A

Direct extension to adjacent structures. Mets via LN then to liver, lungs, bones

25-30% pts have METS when they present

61
Q

Options for targeted therapy in mCRC

A

Targeted Therapy: to the tumor cell w/ Bevacizumab, Cetuximab, Pantiumamb

62
Q

______ gives info about pt overall outcome, regardless of therapy

______: info about effects of particular therapeutic intervention

A

Prognostic:

Predictive:

63
Q

activation stims key processes in tumor growth & progression; key for proliferation, angiogenesis, invasion, metastasis

A

EGFR

64
Q

What 3 major pathways are activated in EGFR?

A

RAS-RAF-MAP kinase

PI3K-AKT

PLC-gamma

that are overexposed in range of solid tumors: there is a transmembrane domain and intracellular domain

65
Q

What are our key EGFRs involved in colon and breast cancer?

A

ErbB1/EGFR/Her1 in colon

B2/Her2/Neu in breast

66
Q

What happens in EGFR signal transduction?

A

turn on STAT or RAS/RAF/MAPK path to induce gene transcription = anti-apoptosis, metastasis, angiogenesis and proliferation and maturation

67
Q

Monoclonal anti-EGFR tx:_____ and______ used in treatement but no correlation with EGFR expression and response: Doesn’t work for pts with____ mutation bc that’s downstream

A

Cetuximab

pantumumab

KRAS

68
Q

There is a lack of correlation btween anti-EGFR therapy and

A

EGFR expression

69
Q

If a patient has ______ then giving them anti-EGFR mAB won’t help their cancer

A

KRAS

70
Q

this mutant tumor is associated with lower progression free surival and overall survival compated to WT tumor

A

BRAF mutant

71
Q

how don’t does the anti-EGFR therapy work?

A

only for 12-18 months and only in tumors that don’t have downstream effector molecule mutations

72
Q

_____mutaiton is major NEGATIVE predictor for efficacy in EFGR therapy and____ correlates w/ poor prognosis

A

KRAS

BRAF

GI 3 (15 decks)

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