BAP39 - Polyps and neoplasms of small and large bowels Flashcards
Which of the following are non-neoplastic polyps? A. Hamartomatous polyps B. Hyperplastic polyps C. Inflammatory polyps D. Adenoma (tubular) E. Sessile serrated adenoma F. Traditional serrated adenoma
A,B,C
Which 3 types of polyps can also be classified as serrated polyps?
Which type is the MC polyp in adults
- Hyperplastic polyps (MC, 75% of serrated polyp)
- Sessile serrated adenoma
- Traditional serrated adenoma
All neoplasitc polyps (adenoma, sessile serrated adenoma..) are pre-malignant lesions that may develop into malignant polyps such as?
Carcinoma/ Lymphoma/ Sarcoma
What are harmatomatous polyps?
They are mostly sporadic, sometimes syndrome - with extraintestinal manesfistations
Disorganized overgrowth of tissue indigenous to the site (= normal tissue, abnormal configuration)
____________ is the MC site of diverticular, GI polyps and carcinoma.
Sigmoid colon
Haramatomatous polyps can be further divided into ____________ and ____________ polyps.
Juvenile polyps and Peutz-Jeghers polyps
Which of the following about Juvenile polyps are correct?
A. MC in children less than 5 y/o
B. Mostly located in the jejunum
C. with 3-100 polyps
D. with increased risk of adenocarcinoma
E. there is cystic dilation of glandular structures in inflamed stroma
All except B
B: most common in the rectum, with rectal bleed, prolapse through anal sphincter
Which of the following about Peutz-Jeghers polyps are correct?
A. Most common in jejunum > ileum > colon > stomach
B. Patients may present with mucosal pigmentation of the buccal mucosa
C. Polyps are localized rather than all over in the GI tract
D. There is a small malignant potential per se, but increased risk of CA colon, pancreas, breast and ovary
E. In histology, pedunculated polyp with arborizing smooth muscle cores can be seen with Christmas tree appearance
All except C
Polyps are all over the entire GI tract
Inflammatory polyps are _____________overgrowth secondary to chronic recurrent mucosal injury and regeneration.
muscosal
What is the clinical triad for inflammatory polyps?
Rectal bleed, mucus discharge, inflammatory lesion of anterior rectal wall
Inflammatory bowels is associated with _____________, solitary rectal ulcer and other chronic colitis.
IBD
Colorectal neoplasms can be classified into epithelial, mesenchymal tumors and lymphoma.
Name the 3 epithelial tumors and the 2 mesenchymal tumors.
Epithelial tumors
- Adenoma
- Adenocarcinoma
- Neuroendocrine neoplasm
Mesenchymal tumor
- Gastrointestinal stromal tumor (GIST)
- Leiomyoma
Colorectal adenoma are A. Benign B. Glandular C. Precursor of colorectal CA but must does not develop D. With villous type as majority E. With epithelial dysplasia
All except D
Tubular type is MC, >75% tubular glands;
MC in sigmoid colon;
Tubulovillous > villious is least common (with protein and K-rich mucous
Differences between LG and HG dysplasia? (grade)
- Architecture
- LG: simple
- HG: complex, fused glands - Cytological atypia
LG: mild: cigar-shaped nuclei, preserved nuclear polarity
HG: marked: loss of nuclear polatiry, distinct nucleoi
Compare the malignancy of hyperplastic polyp, sessile serrated polyp and traditional serrated polyp.
Hyperplasitc polyp is non-malignant;
others are pre-malignant
Compare the MC sites of hyperplastic polyp, sessile serrated polyp and traditional serrated polyp.
Hyperplasitc polyp: left colon (sigmoid)
Sessile serrated polyp: right colon
Traditional serrated polyp: left colon
This type of polyp has star-shaped lumina, <5mm and it is non-malignant. It is the MC form of serrated adenoma.
Hyperplasitic polyp
Both sessile and traditional serrated ademona are larger/smaller than hyperplastic polyps.
Which one of them have an anbnormal crypt base?
larger;
Sessile serrated adenoma
Familial syndrome like _____________- and __________ accounts for 10% of CRC.
- FAP - Familial adenomatous polypopsis
2. Lynch syndrome (= HNPCC hereditary non-poplyposis colorectal cancer)
____________ has chromosomal instability in which there is autosomal dominant mutation in APC.
There are over 100 adenomas prsent, with 100% risk of CRC.
Familial adenomatous poplyposis (FAP)
In FAP, there is increased risk of CA A. Thyroid B. Gallbladder C. endometrium D. adrenal glands E. stomach (multiple gastric fundic polyps)
All except C
How can FAP and Lynch syndrome be diagnosed respectively?
FAP: colonoscopy > 100 adenomatous polyps
Lynch: genetic analysis of DNA MMR genes
______________ shows microsatellite instability (MSI) with autosomal dominant mutation in the mismatch repair genes such as MLH1,MSH2 that matches wtih PMS2 adn MSH6.
Lynch syndrome// HNPCC
Which of the following about Lynch syndrome is incorrect?
A. It is predominantly left sided
B. there are multiple polyps
C. there is increased risk of CA endometrium and ovary
D. genetic counselling is given to patient
D. prophylactic colectomy and hysterectomy is considered
A
Should be right-sided
FAP is treated by prophylactic colectomy and ___________ inhibitors ro reduce polyp burden.
COX2/ NSAID
Amsterdam criteria is used in screening Lynch clinically.
Pathologically, Lynch can be screened by immunohistochemistry of ____________ or detection of microsatellite instability by PCR.
Mismatch repair proteins
e.g. Loss of MSH2/MSH6 > detect > geentic test to see which gene is affected
Microsatellite are ___________ repeats and _________ repeats, which are repetitive, non-coding, short DNA sequences
short tandem repeat
simple sequence repeat
____________syndrome is when there is FAP + extra-intestinal manifestation (sebaceous cysts, osteomas, desmoid tumor…)
Gardner syndrome
Turcot syndyrome = FAP + ___________?
CNS tumors (glioblastoma/medulloblastoma)
Desribe, architectually and cytologically, what you would except to see in a malignant glandular neoplasm (Adenocarcinoma)
**EXAM
Architectually, it is composed of proliferation of tumor cells with glandular differentiation in desmoplastic stroma.
Cytologically, tumor cells show malignant cytology with nuclear enlargement, pleomorphism and hyperchromasia, increased N:C ratio, and frequent mitosis.
Other than genetics risk factors like Polyposis syndrome, Lynch syndrome, give examples of risk factors of colorectal carcinoma.
Lifestyle:
- diet with high fat and refined carbs, low fibres and vitamins A/C/E
- smoking
- alcohol
- obesity
IBD: Ulcerative colitis > Chron’s disease
__________ is a protective factor of Colorectal carcinoma.
Prolonged aspirin/NSAID use
Sequence from MC to Least common, the location of colorectal cancer.
Rectosgimoid > asecending colon and caecum > transverse colon > desceding colon
What are the differences in morphology in right-sided and left-sided CRC?
Right-sided: tends to bleed, larger calibre, polypoid
Left-sided: tends to obstruct, smaller calibre, annular lesion
Difference in patient presentations in right-sided and left-sided CRC?
Right-sided: IDA due to bleeding > fatigue…
Left-sided: Altered bowel habits: constipation, diarrhea
Difference between grading and staging?
Grading: by histology
- well-differentited G1; moderately differentiated G2; poorly differentiated G3
Staging: TNM
What is TNM staging?
T: tumor growth
N: lymph nodes, nodal metastasis
M: distant metastasis
One of the biomakers of CRC is _________, which is overexpressed in 80% of metastatic patients, therefore ________ is given as treatment in stage 4 patients.
EGFR (Epidermal growth factor receptor);
Anti-EGFR monoclonal Ab
_________ and _______ are signalling downstream of EGFR, and they have to be tested before prescribing anti-EGFR treatment, why?
NRAS, KRAS
RAS/RAF mutation tested because if present, no respone to anti-EGFR treatment
_____________ is the commonest GI mesenchymal tumor.
GIST
Gastrointestinl stromal tumor
GIST is characterized by the expression of ______________, a _______ receptor which is the target of Gleevec (Imatinib) for treating metastatic or unresectable GIST.
c-kit/ CD117;
tyrosine kinase
Staging of GIST depends on?
Tumor, mitotic count, location
Other than KIT gene mutation, _______ mutation is also a cause of GIST.
PDGFRA gene
