27 Mar 2009

MRCS: Pathology MCQs 1

1. Concerning small intestinal fistulae, all the following are true EXCEPT:

a) A fistula may have a high output or a low output depending on its site.
b) High output fistulae occur in the upper small bowel.
c) Low output fistulae occur in the ileum.
d) Isotonic saline should be used to replace intravascular and interstitial volume in high output fistulae.
e) The lower the fistula the higher the fluid and nutrient loss.



2. Concerning colonic polyps:

a) Polyposis means the presence of hundreds of polyps, usually in the small intestine.
b) Pedunculated polyps are more likely to become malignant than sessile ones.
c) Villous adenomas are associated with hyperkalaemia.
d) Metaplastic polyps commonly become malignant.
e) Most adenocarcinomas arise within pre-existing adenomas.




3. Concerning adenomatous polyps, all the following are true EXCEPT:

a) They may cause anaemia
b) They may cause diarrhoea
c) They occur mainly in the ileum
d) They may initiate an intussusception
e) They have a malignant potential

4. Familial polyposis coli

a) is inherited as autosomal recessive
b) is more common in males
c) cancer develops after the age of 50 in untreated patients
d) polyps develop throughout the colon and rectum early in the second decade of life
e) the responsible gene is on the long arm of chromosome 6

5. Gardner's syndrome is associated with all the following EXCEPT:

a) multiple colorectal adenomas
b) sebaceous and dermoid cysts
c) adenomas of the mandible or skull
d) desmoid tumours of the abdominal wall
e) no malignant potential



6. All the following may predispose to colorectal cancer EXCEPT

a) Familial adenomatous polyposis
b) High fibre, high fat diets
c) Ulcerative colitis
d) Schistosomal colitis
e) Exposure to irradiation

7. Genes implicated in the pathogenesis of colorectal cancer include all the following EXCEPT:

a) c-Ki-ras gene
b) c-myc gene
c) APC gene
d) BRCA1 gene
e) p53 gene





Answers and explanations

1. e. Fluid loss is lower in low fistulae because there is still a large proximal surface area to deal with fluid absorption. Also, loss of nutrients is less because most have already been absorbed in the proximal small bowel.

2. e. Polyposis means the presence of hundreds of polyps in the large intestine. Sessile lesions are more likely to become malignant than pedunculated ones. Villous adenomas may secrete copious amounts of potassium rich mucus, resulting in hypokalaemia. Metaplastic polyps are not neoplastic and, therefore, do not become malignant. Their origin is unknown. The vast majority of adenocarcinomas arise within pre-existing adenomas.
3. c. Adenomatous polyps occur mainly in the rectum and sigmoid colon. They are often asymptomatic but may produce anaemia from chronic occult bleeding. Rarely they may initiate an intussusception. If a lot of mucus is secreted, spurious diarrhoea may occur, although this is more common with villous papillomas. Adenomatous polyps may give rise to adenocarcinoma.
4. d. Familial polyposis coli (familial adenomatous polyposis – FAP) is a rare condition inherited as autosomal dominant, with equal sex incidence. Hundreds of adenomas develop throughout the colon and rectum early in the second decade of life. Cancer develops before the age of 40 in almost all untreated patients. The gene responsible for FAP is on the long arm of chromosome 5.
5. e. The patient with Gardner's syndrome develops multiple colorectal adenomas (similar to those of FAP) in association with sebaceous and dermoid cysts, osteomas of the mandible and skull and desmoid tumours of the abdominal wall. The risk of cancer is similar to that in FAP.
6. b. Low fibre, high fat diets may predispose to colorectal cancer. High fat leads to an increase in bile acid production, and bile acids are promoters of carcinogenesis. Dietary fibre contains lignans which may protect against cancer. Low fibre diets also prolong intestinal transit time and, therefore, allow for a prolonged contact between any carcinogens and the bowel mucosa.
7. d. The c-Ki-ras and the c-myc genes are the oncogenes most frequently altered in colorectal cancer. Antigen presenting cells (APC) gene, a tumour suppressor gene located on chromosome 5q, is a inactivated by a point mutation in FAP. The p53 gene is also implicated in colorectal cancer. It checks the integrity of the genome prior to mitosis. Defective cells are switched to apoptosis. BRCA1 gene is associated with familial breast cancer.