Path GI tract Flashcards
1.5cm long distal oesophageal mass is biopsied yielding diagnosis of adenocarcinoma. Origin of lesion most likely ? Rob p553
1.Barrett’s oesophagus
2.Extension from adjacent Ca lung
3.Extension from fundal Ca stomach
1.Barrett’s oesophagus
1.Barrett’s oesophagus Adenocarcinoma : 30 - 40X increased risk with > 2cm of Barrett mucosa. UTD: most if not all oesophageal adenocarcinoma arises from Barrett’s metaplasia.
2.Tracheo-oesophageal fistula, MOST COMMON ? Rob p549
1.Proximal fistula, distal blind pouch
2.“H” type
3.Distal fistula, proximal pouch
4.Misnomer because no atresia
5.Misnomer because no fistula
3.Distal fistula, proximal pouch
2.Tracheo-oesophageal fistula, MOST COMMON ? Rob p (TW)
1.Proximal fistula, distal blind pouch
2.“H” type
3.Distal fistula, proximal pouch - T - oesophageal atresia and tracheo oesophageal fistula not in communication with proximal oesophagus (82%)
4.Misnomer because no atresia
5.Misnomer because no fistula
3.Classic appearance of Malloy Weiss tear is ? Rob p550
1.Linear at gastro-oesphageal junction
2.Linear with hiatus hernia
3.Undermined proximal mucosa
4.Circular at GOJ
5.Circular with
1.Linear at gastro-oesphageal junction
3.Classic appearance of Malloy Weiss tear is ? Rob p768 (–)
1.Linear at gastro-oesphageal junction (linear lacerations in axis of oesophagus lumen, at or below the G-E junction)
2.Linear with hiatus hernia
3.Undermined proximal mucosa
4.Circular at GOJ
5.Circular with
Note : Boerhaave syndrome = oesophageal rupture (rare)
4.What are risk factors for malignancy in a stomach ulcer ?
1.pernicious anaemia
2.Crohn’s disease
3.coeliac disease
4.H. Pylori
Answer: H.pylori. Probably old questions (see below)
ROBBINS
Malignant transformation of peptic ulcers occurs rarely, if ever, and reports of transformation probably represetn cases in which a lesion thought to be a chronic peptic ulcer was actually an ulcerated carcinoma from the start.
STATDX
2 major risk factors for gastric ulcer (malignant or benign): Helicobacter pylori, NSAID use.
5.Malignant gastric ulcer. What would be the indicator of malignancy? Rob p561
1.> 4cm diameter
2.single ulcer of greater curvature
3.heaped edges
3.heaped edges
5.Malignant gastric ulcer. What would be the most concerning for malignancy? Rob p780 (TW)
1.> 4cm diameter - size does not diffentiate a benign from malignant ulcer, usually less than 2cm)
2.single ulcer of greater curvature – Robbins p780 – size & location do not differentiate benign & malignant ulcers. location of gastric carcinoma within stomach is: pylorus and antrum 50-60%; cardia 25%; remainder in body an fundus. The lesser curvature is involved in about 40% and the greater curvature in 12%. Thus, a favored location is the lesser curvature of the antropyloric region. Although less frequent, an ulcerative lesion on the greater curvature is more likely to be malignant.
3.heaped edges - heaping up of the margins is rare in the benign ulcer but is characteristic of the malignant lesion.
6.Stomach cancer, which is NOT TRUE? Rob p561
1.Benign ulcers on lesser curvature at antrum
2.Alcohol is not a risk factor
3.Most common is adeno-carcinoma/ then lymphoma/ then carcinoid/then GIST
4.Early gastric cancer is confined to the mucosa/submucosa with negative perigastric nodes
5.Macro – excavated, exophytic,flat
4.Early gastric cancer is confined to the mucosa/submucosa with negative perigastric nodes
6.Stomach cancer, which is NOT TRUE? Rob p784 (TW)
1.Benign ulcers on lesser curvature at antrum - T - gastric ulcers are predominantly located along the lesser curvature, in or around the border zone between the corpus and the antral mucosa.
2.Alcohol is not a risk factor - T
3.Most common is adenocarcinoma/ then lymphoma/ then carcinoid/then GIST - T - Adeono 90-95%, Lymphoma 4%, Carcinoids 3%, malignant stromal cell tumours (2%).
4.Early gastric cancer is confined to the mucosa/submucosa with negative perigastric nodes - F - regardless (ie not influenced by) of presence of perigastric nodes (Robbins).
5.Morphological types – excavated, exophytic or flat (true)
Note : Ulcerated carcinomas usually have nodular raised margins with “dirty” necrotic bases, and lack surrounding radiating folds
Early gastric carcinoma: lesion confined to mucosa and submucosa, regardless of presence or absence of perigastric lymph node metastases.
Advanced gastric carcinoma: neoplasm that has extendd below the submucos into the muscular wall.
**LJS - Depth of invasion and extent of nodal spread/mets at dx most imp indicator of prognosis
If found early and surgical resection still possible, 5YS 90% even if nodal mets present
7.Which of the following statements concerning GIT diseases IS INCORRECT:
1.Most gut lymphomas are T-cell type
2.Villous adenomas are most common in the rectum
3.In Hirshsprung’s Disease, the rectum is always involved
4.Angiodysplasia is most common in the proximal colon
5.Necrotising enterocolitis is most common in neonates
1.Most gut lymphomas are T-cell type
7.Which of the following statements concerning GIT diseases IS INCORRECT: (JS)
1.Most gut lymphomas are T-cell type - F - most are B cell lymphomas (90%)
2.Villous adenomas are most common in the rectum - T - only 1% of adenomatous polyps, more common in rectum and rectosigmoid but can occur anywhere.
3.In Hirshsprung’s Disease, the rectum is always involved - T
4.Angiodysplasia is most common in the proximal colon - T - most common in caecum and right colon
5.Necrotising enterocolitis is most common in neonates - T
8.Coeliac disease. What is the least likely?
1.anti-gliadin antibodies
2.treatment prevents development of lymphoma
2.treatment prevents development of lymphoma
8.Coeliac diseasease What is the least likely? (JS)
1.anti-gliadin antibodies - T - due to a sensitivity to gluten (gliadin)
2.treatment prevents development of lymphoma - F - there is a long term risk of malignant disease at 2 times the usual rate - intestinal lymphomas (including disproportionately high number of T-cell lymphomas) and GIT and breast cancers.
SK – UTD 2011 – “Whether the degree of compliance with a gluten-free diet influences the rates of these cancers is uncertain. In one study, the increased risk of non-Hodgkin lymphoma persisted for five years after diagnosis despite adherence to a gluten-free diet”
9.Celiac disease associated with?
1.Less than 2x risk of malignancy
2.Bowel wall thinning
*LW:
- Option stated LESS than 2x risk of cancer, most of the large research studies quote risks > 2, so this answer is favored to be FALSE.
- Bowel wall thinning, seems a non specific term, but given villi are part of the bowel wall, and there is villous atrophy, I would favour this to be correct.
1.Less than 2x risk of malignancy
9.Coeliac disease associated with? Rob p571 (JS)
1.2x risk of malignancy - T - there is a long term risk of malignant disease at 2 times the usual rate - intestinal lymphomas (including disproportionately high number of T-cell lymphomas) and GIT and breast cancers.
SK – studies give variable numbers for increased risk of malignancy, would be safe with at least double risk (more like 5 x’s for lymphoma)
2.Bowel wall thinning - F - crypts are elongated, hypoplastic and tortuous but the overall mucosal thickness remains the same
**LJS - Rob just says incr lymphoma/adenoca, no indictation of how much.
Loss of mucosal and brush border surface area = malabsorption
10.Coeliac disease, most correct statement is
1.definitive diagnosis is shown by showing histological total villous atrophy
2.10-20% have anti-gliadin Ab’s without having the disease
Answer: Unsure, probable old question, incomplete recall. See below
FROM ROBBINS
Histopathology characterized by increased numbers of intraepithelial CD8+ T lymphoctyes, crypt hyperplasia, and villous atrophy.
With increased serologic screening and early detection of disease-associated antibodies, it is now appreciated that increased numbers of intraepithelial lymphocytes, particularly within the villus, is a sensitive marker of celiac disease, even in the absence of epithelial damage and villous atrophy. However, intraepithelial lymphocytosis and villous atrophy are not specific for celiac disease and can be present in other diseases, including viral enteritis.
With increased serologic screening and early detection of disease-associated antibodies, it is now appreciated that increased numbers of intraepithelial lymphocytes, particularly within the villus, is a sensitive marker of celiac disease, even in the absence of epithelial damage and villous atrophy. However, intraepithelial lymphocytosis and villous atrophy are not specific for celiac disease and can be present in other diseases, including viral enteritis.
PATH OUTLINES
Gold standard for diagnosis is serology with confirmation of histology on duodenal biopsy
TGA has the highest sensitivity for celiac disease (98%); specificity is 90%.
Positive even in individuals on gluten free diet
11.Which of the following statements concerning gastrointestinal diseases is most correct?
1.The colon is the most common site for GIT lymphoma
2.Pseudomembranous colitis is due to toxins of clostridium difficile
3.Inflammatory pseudo-polyps are a characteristic feature of Crohn’s colitis
4.Apthous ulcers are a characteristic feature of ulcerative colitis
5.Juvenile polyps typically occur in the ascending colon.
2.Pseudomembranous colitis is due to toxins of clostridium difficile
11.Which of the following statements concerning gastrointestinal diseases is most correct? (JS)
1.The colon is the most common site for GIT lymphoma - F - Stomach (55-60%), small intestine (25-30%), proximal colon (10-15%) and distal colon (10%) with appendix and oesophagus rarely involved.
2.Pseudomembranous colitis is due to toxins of clostridium difficile - T - Caused by exotoxins A and B of C. difficle after antibiotic therapy
3.Inflammatory pseudo-polyps are a characteristic feature of Crohn’s colitis - F - associated with UC but can occur in Crohns
4.Apthous ulcers are a characteristic feature of ulcerative colitis - F - associated with Crohns
5.Juvenile polyps typically occur in the ascending colon. - F - hamartomatous malformations of mucosa, typically in the rectum
12.In which one of the following are granulomas NOT a characteristic feature?
1.Crohn’s disease
2.Sarcoidosis
3.Foreign body response
4.Ulcerative colitis
5.Tuberculosis
4.Ulcerative colitis
12.In which one of the following are granulomas NOT a characteristic feature? (JS/SK)
1.Crohn’s disease – found in 50-60% (characteristic??), non-caseating
2.Sarcoidosis T non-caseating
3.Foreign body response T
4.Ulcerative colitis F
5.Tuberculosis T caseating
13.Which of the following IS NOT a recognised feature of diverticular disease of the colon:
1.Hypertrophy of the circular muscle layer of the bowel
2.Dissection into the appendices epiploicae
3.Crypt abscesses
4.Fistulae
5.Haemorrhage
3.Crypt abscesses
13.Which of the following IS NOT a recognised feature of diverticular disease of the colon: (JS)
1.Hypertrophy of the circular muscle layer of the bowel - T
2.Dissection into the appendices epiploicae - T
3.Crypt abscesses - F - Typical lesion of Crohn - collections of neutrophils within crypt lumens
4.Fistulae - T
5.Haemorrhage - T
**EDWH. Disagree. Diverticular disease causes focal colitis of which crypt abscesses are a feature (not specific of chron’s).
Perferred answer 2. Dissection into the appendices epiploicae. Diverticulae herniate at sites of vasavasoum penetration, between taeniae coli layers. Appendices epiploicae are small fat lobules hanging off the coli - of no significance in diverticular disease.
14.Concerning carcinoid tumours of the gastro-intestinal tract, which of the following statements IS LEAST correct:
1.The appendix is the most common site
2.They have a characteristic desmopiostic reaction
3.They are benign tumours
4.A characteristic feature is a solid, yellow-tan appearance on transections
5.They are a more common small bowel neoplasm than primary adenocarcinomas
Answer: The appendix is the most common site < they are benign tumors.
Probable incorrect recall given 2 wrong answers.
ROBBINS: GI NEUROENDOCRINE
- intramural or submucosal masses that create polypoid lesions
- Yellow or tan in colour, and very firm as a consequence of intense desmoplasia
- can be subdivided into neuroendocrin tumours and neuroendocrine carcinomas on the basis of histology and immunohistochemistry for Ki-67
- Small intestine tumours tend to be most aggressive, while those of the appendix are typically benign.
15.Amebiasis which is TRUE ? Rob p314,569 Dan p791
1.Organsism is Ngareri foweri
2.Invasion through mucosa into Peyers patches
3.10% of infected people have dysentry
4.cysts release trophozoites secondary to pancreatic enzymes (? Pancreatic ?)
5.release exotoxin and denude epithelium
- 10% of infected people have dysentry
15.Amebiasis which is TRUE ? Rob p806 (JS)
1.Organism is Ngareri Fowleri - F - Entamoeba histolytica
2.Invasion through mucosa and into peyers patches - F - invade the crypts of the colonic glands and burrow through the lamina propria and are halted by the muscularis mucosae.
3.10% of infected people have dysentery - T
4.Cysts release trophozoites secondary to pancreatic enzymes. - F - release trophozoites under anaerobic conditions in colon (cysts resistant to gastric acid)
5.Release exotoxin and denude epithelium - F - This is referring to C difficle in pseudomembranous colitis. Amoebae produce proteins involved in tissue invasion including proteinases, lectin and amebapore, resulting in ulcers and sloughing of the mucosa
16.Crohn’s disease in counselling a sibling of risk
1.1% risk
2.No increased risk
3. 10% risk.
- 10% risk.
16.Crohn’s disease in counselling a sibling of risk (JS)
1.1% risk
2.No increased risk
3.10% risk - T - lifetime risk if either a parent or sibling is affected is 9% (Robbins): PathOutlines 15% have affected first degree relatives
17.Crohns disease is NOT ASSOCIATED with ?
1.Hydronephrosis
2.Carcinoma
3.Hip arthopathy
4.Sclersoing cholangitis
5.Sclerosing peritonits
Answer: Sclerosing peritonitis
18.Patient with ulcerative colitis with elevated CEA (Carcinoembryonic antigen)? Rob p574, 208,585
1.Likely colon cancer
2.May be colon cancer but also raised in UC active inflammation
3.Active ulcerative Colitis
2.May be colon cancer but also raised in UC active inflammation
18.Patient with ulcerative colitis with elevated CEA (Carcinoembryonic antigen)? Rob p574, 208,585 (JS)
1.Likely colon cancer
2.May be colon cancer but also raised in UC active inflammation - T - produced in embryonic tissue of the gut, pancreas and liver. Elevated in 60-90% of colorectal, 50-80% of pancreatic and 25-50% of gastric and breast cancer. Also elevated in cirrhosis, hepatitis, UC, Crohns and in smokers. Lacks specificity and sensitivity for early cancer detection but can be used in prognosis and detection of recurrence.
3.Active ulcerative Colitis
19.Which does not cause bowel obstruction? Rob p578
1.Tuberous Sclerosis
2.GVHD
3.Collagen vascular disorders
4.Viral infections
5.Ingested toxins
3.Collagen vascular disorders (scleroderma, dermatomyositis – muscle dysfunction – marked dilatation of small bowel simulating small bowel obstruction)
19.Which does not cause bowel obstruction? mRob (–)
1.Tuberous Sclerosis ?? by leiomyoma ??
2.GVHD
3.Collagen vascular disorders (scleroderma, dermatomyositis – muscle dysfunction – marked dilatation of small bowel simulating small bowel obstruction)
20.In colonic polyps which is TRUE ? Rob p579
1.Peutz Jeger is sporadic hamartomatous polyps
2.HNPCC (Hereditary Nonpolyposis Colorectal Cancer) not associated with adenoma
3.Most common type in adults is villous
4.Juvenille polyps occur in ileum
2.HNPCC (Hereditary Nonpolyposis Colorectal Cancer) not associated with adenoma
*LW: probably most true out of options listed:
Robbins states: HNPCC…adenomas occur in low numbers and considerably earlier than in genral population, however colonic malignancies that develop are multiple and not usually associated with pre exisiting adenomas. Hallmark is mutations in DNA repair genes.
20.In colonic polyps which is TRUE ? Rob p815 (JS)
1.Peutz Jeger is sporadic hamartomatous polyps - F - Autosomal dominant syndrome (not sporadic) characterised by multiple hamartomatous polyps
2.HNPCC (Hereditary Nonpolyposis Colorectal Cancer) not associated with adenoma – T/F -
JS: HNPCC is characterised by familial carcinoma of the colon, affecting predominantly caecum and proximal colon, which DON’T arise within adenomatous polyps.
SK: Robbins & Mayo both mention adenomatous polyps occurring in HNPCC. Other reference (SemSurgOnc 1995) “It appears that HNPCC patients form adenomas at about the same rate as the general population and there is circumstantial evidence that adenoma is the precursor to colorectal carcinoma in the syndrome. It is hypothesized that HNPCC features accelerated progression from colonic adenoma to carcinoma”
3.Most common type in adults is villous - F - Tubular adenomas are the most common (90%) followed by tubulovillous (5-10%) then villous (1%)
4.Juvenille polyps occur in ileum F - Focal hamartomatous polyps found most frequently in the rectum in children younger than 5y
21.Adenomatous polyps are NOT a feature of ? Rob p820
1.Gardners Syndrome
2.Familial Polyposis
3.Turcot’s Syndrome
4.Peutz-Jeghers Syndrome
5.Sessile Villous lesions
4.Peutz-Jeghers Syndrome
21.Adenomatous polyps are NOT a feature of ? (JS) Rob p815
1.Gardners Syndrome - F - AD variant of FAP with intestinal polyps, osteomas and soft tissue tumours
2.Familial Polyposis - F - AD disorder with innumerable adenomatous polyps with progression to adenocarcinoma in 100%
3.Turcot’s Syndrome - F - rare variant of Gardners syndrome with colonic polyposis and tumours of the CNS
4.Peutz-Jeghers Syndrome - T - hamartomatous lesions which don’t have malignant potential themselves, but patients have an increased risk of colon & other cancers (pancreas, breast, lung, ovary and uterus)
5.Sessile Villous lesions - F - type of adenomatous polyps
22.Following associated with increased risk of bowel malignancy EXCEPT? Rob p579
1.Obesity
2.Diabetes
3.Crohns
4.Meat/low fibre diet
2.Diabetes
22.Following associated with increased risk of bowel malignancy EXCEPT? Rob p579 (JS)
1.Obesity
2.Diabetes - T
3.Crohns
4.Meat/low fibre diet
Risk factors for colorectal cancer include diet (low fibre, high intake of refined carbs, intake of red meat, reduced intake of protective micronutrients such as vitamins A, C and E), obesity, physical inactivity, family history, IBD, previous XRT, FAP, HNPCC.
23.A 60 year old male has colonic carcinoma which involves muscularis mucosa. No regional lymph nodes, no distant metastasis. What is prognosis? Rob p582
1.100% 5 year survival
2.95% 5 year survival
3.60% 5 year survival
4.40% 5 year survival
5.10% 5 year survival
3.60% 5 year survival
23.A 60 year old male has colonic carcinoma which involves muscularis mucosa. No regional lymph nodes, no distant metastasis. What is prognosis? Rob p582 (–) (GC & TW)
1.100% 5 year survival
2.95% 5 year survival
3.67% 5 year survival B1 = 67% (path notes); TNM staging is 90%
4.40% 5 year survival
5.10% 5 year survival
*LW:
RP Dukes staging prognosis:
Overall 5-year survival rate is 40-50%, with the stage at operation the single most important factor affecting prognosis.
Duke A: 80-90%
Duke B: 70%
Duke C: 33%
Duke D: 5%
This tumour is T1 or Duke B1
WILD: Muscularis mucosa is confined to the mucosal layer ie has not penetrated basement membrane- TIS, 100% 5YS. Misinterpreted above as muscularis propria.
25.Histologically appendicitis characterised by ? Rob p588
1.Neutrophils in the mucosa
2.Neutrophils in the the muscularis propria
3.Plasma cells/lymphocytes in muscularis
4.Serosal hyperaemia
2.Neutrophils in the the muscularis propria
25.Histologically appendicitis characterised by ? Rob p588 (JS)
1.Neutrophils in the mucosa
2.Neutrophils in the the muscularis propria - T - Histologic criterion is neutrophilic infiltration of muscularis. Usually neutrophils and ulceration is also present within the mucosa but other conditions can cause mucosal infiltrate (ie spread from GIT infection elsewhere)
3.Plasma cells/lymphocytes in muscularis
4.Serosal hyperaemia - F - is present but not specific
26.A fifty year old female develops a colovaginal fistula. Ten years earlier she had treatment for choriocarcinoma and colonoscopy six months ago was normal. Most likely cause is ? Dan p857
1.Radiotherapy change
2.Colon Cancer
3.Crohns
4.Diverticular abscess
5.Bladder Cancer
4.Diverticular abscess
26.A fifty year old female develops a colovaginal fistula. Ten years earlier she had treatment for choriocarcinoma and colonoscopy six months ago was normal. Most likely cause is ? (TW)
1.Radiotherapy change - choriocarcinoma treated with surgery and chemotherapy. Dysgerminoma however can get XRT.
2.Colon Cancer - normal scope 6/12 ago.
3.Crohns - normal scope 6/12 ago. Most cases of CD and UC have onset between ages of 15 and 40yo. Many suggest a second peak between 50 and 80yo. Approx 80% pts have small bowel involvement, 50% iliocolitis, 20% limited to colon.
4.Diverticular abscess - prevalence of diverticular disease of colon: 5% at age 40yo, 30% age 60, 65% age 85yo.
*LW: only thing that makes me uneasy about this is a normal scope 6months prior, as one would expect background vierticular disease to be present before development of a diverticular abscess and resulting fistula. However, probability states this would be most likely.
*AJL: I also feel uneasy about this. Why have they mentioned cholangiocarcinoma? I wonder if it is to see if you can get the connectiong back to crohns (cholangio - PSC - IBD - Crohns (even though UC is more commonly associated). Though I agree statistically diverticular disease is more common, both crohns and diverticular disease leading to fistula would presumably have a slightly abnormal colonoscopy 6 months earlier?
**LJS - agree (although Q mentions choriocarcinoma rather than cholangio)
5.Bladder Cancer - more frequent in men than women. 80% Dx after age of 60yo.
Note : Manifestation of radiation colitis can occur up to 15 years following radiation
Common causes of fistulas iatrogenic,diverticula,Crohns; less common – amoebiasis,
27.Risk of Caecal carcinoma :
- 1% synchronous
- 0.1% synchronous
- 1% synchronous & metachronous
- 39% in the caecum and ascending colon
- 10% synchronous
27.Risk of Caecal carcinoma : (TW)
- 1% synchronous - rate of synchronous CRC is about 5%.
- 0.1% synchronous
- 1% synchronous & metachronous - metachronous carcinoma occured in 2% of total, so metachronous and synchronous would be about 0.1%
- 39% in the caecum and ascending colon - (true for BR) *LW Robbins states 22%
- 10% synchronous
Info from Japanese Journal of Clinical Oncology 2003
28.HNPCC – barium enema is performed to look for
1.colonic carcinoma
2.polyps
3.detect colonic hamartoma
28.HNPCC – barium enema is performed to look for (TW)
1.Colonic carcinoma - T - HNPCC (Lynch syndrome) an AD condition, characterised by familial carcinomas of the colon, predominantly affecting the caecum and proximal colon.
2.polyps - N = nonpolyposis
3.detect colonic hamartoma - Peutz Jeghers
HNPCC / Lynch sydrome is the most common of the inherited colon susceptibility syndromes. Significantly increase risk of colon cancer and endometrial cancer as well as small risk of sever other associated cancers (ovariian, upper GUT, gastric, small bowel, biliary/pancreatic, skin, brain).
Lifetime risk of developing CRC in Lynch = 70%. Like most sporadic CRCs, Lynch cancers appear to evolve from adenomas, but when detected the adenomas tend to be larger, flatter, and are oftenmore proximal.
Accelerated adenoma-carcinoma sequence, dysplasia in flat mucosa of colon.
There are several types of DNA damage, and, correspondingly, there are many forms of DNA repair.
HNPCC results from defects in genes involved in DNA mismatch repair.
DNA repair genes themselves are not oncogenic, but they allow mutations in other genes during the process of normal cell division
29.Patient with suspected mononucleosis, which would be atypical?
1.Abnormal LFT
2.Proteinuria with viral inclusions in epithelial cells in urine
3.Groin lymphadenopathy
4.Mononuclear meningitis
5.Atypical lymphocytes on FNA
2.Proteinuria with viral inclusions in epithelial cells in urine
29.Patient with suspected mononucleosis, which would be atypical? (JS)
1.Abnormal LFT - F - commonly causes hepatic dysfunction
2.Proteinuria with viral inclusions in epithelial cells in urine - T - this occurs in CMV infection
3.Groin lymphadenopathy - F - presents with fever, sore throat and lymphadenopathy
4.Mononuclear meningitis - F - can occur - not sure if it is “typical”
5.Atypical lymphocytes on FNA - F - lymph nodes contain abnormal lymphocytes which may resemble Reed-Sternberg cells
30.Amoebiasis which is true
1.Organism is Ngareri Fowleri
2.Invasion through mucosa and into peyers patches
3.20% of infected people have dysentery
4.Cysts release trophozoites secondary to pancreatic enzymes.
5.Release exotoxin and denude epithelium
Answer: 20% of infected people have dysentery. ?unsure where the number comes from, but probably true as more commonly asymptomatic
ROBBINS
Entamoeba histolytica.
Cysts are resistant to gastric acid, allowing them to pass through the stomach without harm, and colonize the epithelial surface of the colon and release trophozoites, ameboid forms that reproduced under anaerobic conditions.
Amebiasis affects the cecum and ascending colon most often.
Dysentery develops when the ameba attach to colonic epithelium, induced apoptosis, invade crypts, and burrow laterally into lamina propria.
Can penetrate splanchnic vessels and embolize to the liver to produce abscesses in 40% of patients with amebic dysentery.
If it persists, and can reach the lung and heart by direct extension.
Treatment with metronidazole.
31.Echinococcus Granulosus, which is true?
1.20% infected have liver lesions
2.Myocardial involvement is by antigen cross reaction rather than direct invasion
3.Entry is by breach in skin and mucosal membranes
4.Initially cysts begin at microscopic level
4.Initially cysts begin at microscopic level
31.Echinococcus Granulosus, which is true? (JS)
1.20% infected have liver lesions - F - liver is the most common organ of involvement (73%), followed by lung (14%), peritoneum (12%), kidney (6%). Can also involve spleen, CNS, orbit, bone, bladder, thyroid, prostate and heart.
2.Myocardial involvement is by antigen cross reaction rather than direct invasion - F -
3.Entry is by breach in skin and mucosal membranes - F - caused by ingestion of tapeworm eggs in dog faeces which hatch in the duodenum
4.Initially cysts begin at microscopic level - T - Cysts begin at microscopic size and progressively increase in size (can reach 10cm in 5 years)
32.Classic appearance of Mallory Weiss tear is
1.Linear at gastro-oesophageal junction
2.Linear with hiatus hernia
3.Undermined proximal mucosa
4.Circular at gastro-oesophageal junction
1.Linear at gastro-oesophageal junction
32.Classic appearance of Mallory Weiss tear is (JS)
1.Linear at gastro-oesophageal junction - T - Longitudinal tear at the GOJ, seen in alcoholics due to excessive vomiting and reflux of gastric contents.
2.Linear with hiatus hernia
3.Undermined proximal mucosa
4.Circular at gastro-oesophageal junction
33.Stomach cancer, which is not true
1.Benign ulcers on lesser curvature at antrum
2.Alcohol is not a risk factor
3.Most common is adenocarcinoma/ then lymphoma then carcinoid then GIST
4.Early gastric cancer is confined to mucosa/ submucosa with negative perigastric nodes
4.Early gastric cancer is confined to mucosa/ submucosa with negative perigastric nodes
33.Stomach cancer, which is not true (JS, TW & GC)
1.Benign ulcers on lesser curvature at antrum - T – gastric ulcers are predominantly located along the lesser curvature.
2.Alcohol is not a risk factor - T - Risk factors include Cigarette smoking, Diet (nitrites, smoked or salted foods, lack of fruit and veg), Chronic gastritis, H. pylori, Partial gastrectomy, Gastric adenomas, Barrett oesophagus, Family history, HNPCC
3.Most common is adenocarcinoma/ then lymphoma then carcinoid then GIST - T - Carcinoma (90-95%), Lymphoma (4%), Carcinoid (3%), Malignant stromal tumours (2%)
4.Early gastric cancer is confined to mucosa/submucosa without positive perigastric nodes - F - Early gastric carcinoma is defined as a lesion confined to the mucosa or submucosa, regardless of the presence or absence of perigastric lymph node metastases.
Changed option 4 from “with negative nodes” to make it less ambiguous.
34.In colonic polyps, which is true
1.Peutz jager is sporadic hamartomatous polyps
2.HNPCC not associated with adenoma
3.Most common type in adults is villous
4.Juvenile polyps occur in ileum
2.HNPCC not associated with adenoma
*LW: agree this is most likely true out of options; robbins states colonic malignancies not usually associated with pre exisiting adenomas.
34.In colonic polyps, which is true: (JS, GC & TW)
1.Peutz Jeger is sporadic hamartomatous polyps - F - Autosomal dominant syndrome (not sporadic) characterised by multiple hamartomatous polyps
2.HNPCC (Hereditary Nonpolyposis Colorectal Cancer) not associated with adenoma – T (not T anymore!) - HNPCC is characterised by familial carcinoma of the colon, affecting predominantly caecum and proximal colon, which DON’T arise within adenomatous polyps. Historically this is true, however, now shown to be due to a DNA mismatch repair gene, where there is either accelerated adenoma-Ca sequence or dysplasia in an area of flat mucosa. (Robbins). Like most sporadic colorectal carcinomas, Lynch syndrome carcinomas appear to evolve from adenomas, but when detected the adenomas tend to be larger, flatter, and more proximal. Adenoma-carcinoma sequence is thought to progress much more rapidly in Lynch syndrome (UpToDate).
3.Most common type in adults is villous - F - Tubular adenomas are the most common (90%) followed by tubulovillous (5-10%) then villous (1%)
4.Juvenille polyps occur in ileum F - Focal hamartomatous polyps found most frequently in the rectum in children younger than 5y
35.Crohns disease is not associated with
1.Hydronephrosis
2.Carcinoma
3.Hip arthropathy
4.Sclerosing cholangitis
5.Sclerosing peritonitis
5.Sclerosing peritonitis
35.Crohns disease is not associated with (JS)
1.Hydronephrosis - F - renal manifestations include stones, hydronephrosis, amyloid, cystitis and fistulas
2.Carcinoma - F - in ileum and colon, 4-20 times increased risk compared to general population
3.Hip arthropathy - F - AVN due to steroid treatment; enteropathic arthropathy
4.Sclerosing cholangitis - F - hepatobiliary manifestations include fatty infiltration, abscess, gallstones, cholecystitis, sclerosis cholangitis and bile duct carcinoma
5.Sclerosing peritonitis - T - asscociated with peritoneal dialysis
36.Choledochal cysts (T/F)
1.If jaundiced implies secondary stricture
2.Pain means pancreatitis
3.Primary abnormality is stricture with secondary proximal dilatation
36.Choledochal cysts T/F (TW) Robbins p887
1.If jaundiced implies secondary stricture - F - intermittent obstructive jaundice in 33-80% of patients. Uncommon cause of obstructive jaundice.
2.Pain means pancreatitis - F - chronic and intermittent abdominal pain appears to be most common presenting symptom (50-96%) in patients older than 2yo. Pancreatitis has been described in approx 20% of pts at diagnosis.
3.Primary abnormality is stricture with secondary proximal dilatation - F - may be congenital or acquired. Congenital - due to ductal plate malformation of large bile ducts. Anomalous junction of pancreatic duct and CBD proximal to duodenal papilla allows pancreatic enzyme refulx into CBD.
37.Patient sent for liver ultrasound, mother has primary biliary cirrhosis- which is true
1.Patient has 50% chance of having it
2.20% chance based on epidemiology
3.More likely to have it, if father has it
4.Has same risk as general population
37.Patient sent for liver ultrasound, mother has primary biliary cirrhosis- T/F (JS) - dodgy question
1.Patient has 50% chance of having it - F
2.20% chance based on epidemiology - F
3.More likely to have it, if father has it - F
4.Has same risk as general population - F –(this was previously thought to be the correct answer) not an inherited disorder, thought to have an autoimmune aetiology, disease of middle aged women with female to male ratio of 6:1
UpToDate:
The prevalence of primary biliary cirrhosis in females with 1 affected member is estimated to be 1000x greater than that of the general population.
Incidence of PBC in Australia is 25 per million (ie 1 in 40000 = 0.003%). Thus the risk with an affected family member (ie 1000x greater) is 1 in 40, or 2.5% chance.
38.Acute acalculous cholecystitis which is unlikely
1.Post partum
2.HIV positive
3.TPN
4.Amyloid
5.Post surgical
4.Amyloid
38.Acute acalculous cholecystitis which is unlikely (JS)
*LW:
1.Post partum - TRUE
2.HIV positive - TRUE
3.TPN - TRUE
4.Amyloid - False; not specifically listed in common risk factors, while all others are.
5.Post surgical - TRUE
WILD - Unsure about post partum?
39.Staging hepatocellular carcinoma, portal nodes negative, next most likely site is
1.Bone
2.Lungs
3.Adrenal
4.Brain
5.Spleen
2.Lungs
39.Staging hepatocellular carcinoma, portal nodes negative, next most likely site is (JS)
1.Bone
2.Lungs - T - most common site of mets (followed by adrenal, lymph nodes and bone) (Dahnert)
3.Adrenal
4.Brain
5.Spleen
40.Patient with ulcerative colitis with elevated CEA
1.Likely colon cancer
2.May be colon cancer, but also raised in ulcerative colitis active inflammation
2.May be colon cancer, but also raised in ulcerative colitis active inflammation
40.Patient with ulcerative colitis with elevated CEA (JS)
1.Likely colon cancer
2.May be colon cancer but also raised in UC active inflammation - T - produced in embryonic tissue of the gut, pancreas and liver. Elevated in 60-90% of colorectal, 50-80% of pancreatic and 25-50% of gastric and breast cancer. Also elevated in cirrhosis, hepatitis, UC, Crohns and in smokers. Lacks specificity and sensitivity for early cancer detection but can be used in prognosis and detection of recurrence.
3.Active ulcerative Colitis
41.Patient with elevated CA 125
1.Colon cancer
2.Ovarian cancer
3.Any ovarian pathology
3.Any ovarian pathology
41.Patient with elevated CA 125 (JS)
1.Colon cancer F
2.Ovarian cancer T surface epithelial tumours
3.Any ovarian pathology- T - elevated in ovarian cancer, endometrial, cervical, pancreatic, bronchial and breast cancer.
PID, endometriosis and first trimester pregnancy
Non-gynaecological: hepatic cirrhosis. acute peritonitis (esp TB), pancreatitis.
hepatoma, benign ovarian disease,
.
42.Amyloid, which is false
1.In TB is AA type
2.Causes Sago spleen and Lardaceous spleen
3.Seen in x% of patients with renal failure
3.Seen in x% of patients with renal failure
42.Amyloid, which is false (JS)
1.In TB is AA type - T - AA type is secondary amyloidosis - Crohns, JRA, Reiter syndrome, ank spond, familial Mediterranean fever, Sjogren, dermatomyositis, vasculitis, chronic osteomyelitis, TB, bronchiectasis, CF, SLE etc
2.Causes Sago spleen and Lardaceous spleen - T - Sago spleen refers to deposits of amyloid within splenic follicles producing tapioca-like granules. Lardaceous spleen is seen with fusion of the deposits giving rise to large maplike areas of amyloidosis
3.Seen in x% of patients with renal failure - F - although renal involvement is common, renal function compromise is rare (RG 2004;24(2):405-416). Get amyloid (joint deposition) if on hemodialysis (incidence 21% 2yr dialysis, 50% 4-7y, 90% 7-13y, 100% >13y).
43.Risk of Caecal carcinoma :
- 1% synchronous
- 0.1% synchronous
- 1% synchronous & metachronous
- 39% in the caecum and ascending colon
- 10% synchronous
43.Sep03.39 Risk of Caecal carcinoma : (TW)
1.1% synchronous - rate of synchronous CRC is about 5%.
2.0.1% synchronous
3.1% synchronous & metachronous - metachronous carcinoma occured in 2% of total, so metachronous and synchronous would be about 0.1%
4.39% in the caecum and ascending colon
5.10% synchronous
Info from Japanese Journal of Clinical Oncology 2003
44.What are risk factors for malignancy in a stomach ulcer ?
1.pernicious anaemia
2.Crohn’s disease
3.coeliac disease
4.H. Pylori
Answer: H.Pylori
Pathology outlines/Robbins
- Chronic H.pylori infection is recognized as the main cause of noncardia (distal) gastric cancer.
- PUD does not impart an increased risk of gastric cancer, but patients who have had partial gastrectomies for PUD have a slightly higher risk of developing cancer in the residual gastric stump, possibly due to hypochlorhydria, bile reflux, and chronic gastritis.
45.Crohn’s disease in counselling a sibling of risk
- 1% risk
- No increased risk
- 10% risk
- 10% risk
45.Crohn’s disease in counselling a sibling of risk (JS)
1.1% risk
2.No increased risk
3.10% risk - T - lifetime risk if either a parent or sibling is affected is 9% (Robbins)
46.Megaloblastic anaemia is not caused by :
1.Pernicious anaemia
2.Crohn’s disease
3.Coeliac disease
4.Pancreatic calcification
4.Pancreatic calcification
46.Megaloblastic anaemia is not caused by : (JS)
1.Pernicious anaemia - T - results in Intrinsic factor deficiency and therefore Vitamin B12 deficiency
2.Crohn’s disease - T - Ileitis can cause impaired absorption of Vit B12
3.Coeliac disease - T - Causes malabsorption
4.Pancreatic calcification – F - CME
**LJS - although also caused by panc insufficiency (panc enzymes allow cleavage of B12 from binder to allow it to bind intrinsic factor for SB absorption)
***LW:
All of above are listed as causes, hopefully option 5 was not a cause.
47.Sickle cell anaemia. An unusual feature would be
1.splenomegaly
2.splenic atrophy/ absent
3.fungal dacralitis
4.aplastic crises
3.fungal dacralitis
47.Sickle cell anaemia. An unusual feature would be (JS)
1.splenomegaly - T - splenomegaly is seen in children in the early phase of the disease
2.splenic atrophy/ absent - T - continued scarring causes progressive shrinkage - autosplenectomy
3.fungal dacralitis - F - dacrylitis is caused by vaso-occlusive crisis (hypoxic injury and infarction caused by sickling), which can be precipitated by infection
4.aplastic crises - T - refers to temporary cessation of bone marrow activity, usually triggered by parvovirus infection, with a rapid worsening of anaemia
48.HNPCC – barium enema is performed to look for
1.colonic carcinoma
2.polyps
1.colonic carcinoma
48.HNPCC – barium enema is performed to look for (JS)
1.Colonic carcinoma - T - HNPCC (Lynch syndrome) an AD condition, characterised by familial carcinomas of the colon, predominantly affecting the caecum and proximal colon. However the cancer DOES arise in adenomatous polyps (HNPCC – same rate of adenomas as general population, but higher rate of malignant transformation).
2.polyps
49.Coeliac disease. What is the least likely?
1.anti-gliadin antibodies
2.treatment prevents development of lymphoma
2.treatment prevents development of lymphoma
49.Coeliac disease. What is the least likely? (JS)
1.anti-gliadin antibodies - T - due to a sensitivity to gluten (gliadin)
2.treatment prevents development of lymphoma - F - there is a long term risk of malignant disease at 2 times the usual rate - intestinal lymphomas (including disproportionately high number of T-cell lymphomas) and GIT and breast cancers.
- Polycythemia Rubra Vera and splenomagaly —least likely
1.CML
2.ALL
3.Budd-Chiari
4.Cirrhosis
Answer: ALL (least likely)
PATHOLOGYOUTLINES
Clinical features
- 20% have document venous thrombosis, such as hepatic or portal vein thrombosis (associated Budd-Chiari).
Outcomes
- 2% develop AML.
- risk of leukemic transformation (ALL) is rare, except in patients treated with cytotoxic regimens.
ROBBINS
- Hepatic vein thrombosis/Budd-chiari is associated with polycythemia vera.
Budd-chiari is a cause of hepatic cirrhosis.
51.HCC with lymph node mets — commonest metastatic site ?
1.lung
2.pleura
3.bone
4.brain
1.lung
51.HCC with lymph node mets — commonest metastatic site ? (JS)
1.lung
2.pleura
3.bone
4.brain
52.Child for Ultrasound whose mother has PBC. What is the likelihood of PBC in child:
1.Patient has 50% chance of having it
2.20% chance based on epidemiology
3.More likely to have it, if father has it
4.Has same risk as general population
5. Increased risk.
Answer: Increased risk.
ROBBINS
PBC primarily a disease of middle-aged women, with a female predominance of 9:1. Peak incidence is 40-50 years of age.
Family members of PVC patients have an increased risk for development of the disease.
Autoimmune disorder, trigger unknown.
Most characteristic lab finding is Anti-mitochondrial antibodies.
No % or number quoted on robbins, statdx, pathologyoutlines, radiopeida.
53.With regards to Oesophageal Carcinoma which is FALSE
1.Barretts has x40 increased association of SCC
1.Barretts has x40 increased association of SCC
54.What are risk factors for malignancy in a stomach ulcer ?
1.Occurs in area of gastric atrophy
1.Occurs in area of gastric atrophy
55.Which of the following statements concerning gastrointestinal diseases is most correct?
1.The colon is the most common site for GIT lymphoma
2.Pseudomembranous colitis is due to toxins of clostridium difficile
3.Inflammatory pseudo-polyps are a characteristic feature of Crohn’s colitis
4.Apthous ulcers are a characteristic feature of ulcerative colitis
5.Juvenile polyps typically occur in the ascending colon.
2.Pseudomembranous colitis is due to toxins of clostridium difficile
55.Which of the following statements concerning gastrointestinal diseases is most correct? (JS)
1.The colon is the most common site for GIT lymphoma - F - Stomach (55-60%), small intestine (25-30%), proximal colon (10-15%) and distal colon (10%) with appendix and oesophagus rarely involved.
2.Pseudomembranous colitis is due to toxins of clostridium difficile - T - Caused by exotoxins A and B of C. difficle after antibiotic therapy
3.Inflammatory pseudo-polyps are a characteristic feature of Crohn’s colitis - F - associated with UC but can occur in Crohns
4.Apthous ulcers are a characteristic feature of ulcerative colitis - F - associated with Crohns
5.Juvenile polyps typically occur in the ascending colon. - F - hamartomatous malformations of mucosa, typically in the rectum
56.Which is NOT a hamartomatous/non neoplastic POLYP
1.Adenomatous
2.Peutz-Jeghers Syndrome
3.Hyperplastic
4.Inflammatory
5.Juvenile
1.Adenomatous
56.Which is NOT a hamartomatous/non neoplastic POLYP (JS)
1.Adenomatous - T – is neoplastic
2.Peutz Jegher - F – hamartoma
3.Hyperplastic - F – small epithelial polyps which arise at any age but are usually discovered in 6th and 7th decades, these are non-neoplastic with no adenomatous change
4.Inflammatory - F –
5.Juvenile - F – hamartomatous proliferation of lamina propria
57.32yo female. Presents for a barium enema. History of HNPCC. What is the referring physician looking for:
1.Inflammatory bowel disease
2.Colonic carcinoma
3.Hereditary neoplastic colonic polyposis
4.Strictures
5.Hamartoma
2.Colonic carcinoma
57.32yo female. Presents for a barium enema. History of HNPCC. What is the referring physician looking for: (JS)
1.Inflammatory bowel disease
2.Colonic carcinoma - T - HNPCC (Lynch syndrome) an AD condition, characterised by familial carcinomas of the colon, predominantly affecting the caecum and proximal colon.
3.Hereditary neoplastic colonic polyposis (tumours still pass through adenoma stage but this answer is incorrect)
4.Strictures
5.Hamartoma
HEREDITARY NONPOLYPOSIS COLORECTAL CANCER (HNPCC)
(Lynch Syndrome)
Autosomal dominant familial syndrome
Increased risk of colorectal cancer and extraintestinal cancer
Endometrial
GBM
58.Which is least likely in Crohn’s
1.Renal calculi
2.Cholangiocarcinoma
3.Biliary cirrhosis
4.Sclerosing cholangitis
5.Gallstones
3.Biliary cirrhosis
58.Which is least likely in Crohn’s (JS)
1.Renal calculi - F - urolithiasis in 5-10%
2.Cholangiocarcinoma - F - can develop bile duct and GB carcinoma (due to PSC)
3.Primary biliary cirrhosis - T - develop primary sclerosing cholangitis (not PBC)
4.Sacroilitis - F - ankylosing spondylitis in 3-16%
5.GIT malignancy - F - 4-20 times increased risk of colonic adenocarcinoma
59.Crohn’s colitis is not associated with
1.Fat wrapping
2.Aphthous ulcer
3.Cobblestone
4.Backwash ileitis
5.Fistulas
4.Backwash ileitis
59.Crohn’s colitis is not associated with (JS/SK)
1.Fat wrapping – F adherent creeping mesenteric fat
2.Aphthous ulcer – F punched out aphthous ulcers
3.Cobblestone – F mucosal cobblestoning due to ulcers & fissures with intervening normal mucosa
4.Backwash ileitis - T - ulcerative colitis
5.Fistulas - F
60.GIST tumours – which is correct?
1.Malignant > benign
2.Histological subtype most important in prognosis
3.Occur mainly in stomach and small bowel
4.Grow as an epithelial tumour
3.Occur mainly in stomach and small bowel
60.GIST tumours – which is correct? (TW)
1.Malignant > benign
2.Histological subtype most important in prognosis
3.Occur mainly in stomach and small bowel
4.Grow as an epithelial tumour
Location
70% stomach
30% small intestine
Rare in oesophagus and colon
May rarely occur in the ommentum and mesentery
90% are benign
either spindle cell or epithelioid
The spindle cell morphology is present in 70%–80%
61.H.Pylori which is least correct
1.G-ve spiral
2.Attaches to small bowel epithelium
3.In duodenal + gastric ulcers
4.Associated with MALT lymphoma
2.Attaches to epithelium
61.H.Pylori which is least correct
1.Gram negative spiral – T – spiral shaped, microaerophilic, gram negative bacterium.
2.Attaches to epithelium in the small and large intestine – F - adheres to gastric epithelium.
3.Role in gastric cancers – T – HP can cause chronic active gastritis and atrophic gastritis, early steps in the carcinogenesis sequence. Studies have shown a clear link between HP and gastric adenocarcinoma. Source of gastric cancer may not be from gastric epithelial cells themselves, but rather from bone-marrow derived cells that differentiate into gastric epithelial cells in the presence of HP (UTD).
4.Associated with MALT lymphoma – T – multiple studies have shown association, and MALToma remission following eradication of HP.
62.Which is most correct?
1.Angiodysplasia most commonly affects the sigmoid colon
2.short segment Hirschsprung most common in females
3.Meckel’s diverticulum is present on the mesenteric side
4.complications of necrotising enterocolitis include a stricture
5.pseudopolyps are a feature of Crohn’s disease
4.complications of necrotising enterocolitis include a stricture
62.Which is most correct? (JS)
1.Angiodysplasia most commonly affects the sigmoid colon - F - most often seen in the caecum or right colon
2.short segment Hirschsprung most common in females - F - more common in boys
3.Meckel’s diverticulum is present on the mesenteric side - F - form on the antimesenteric side of the small bowel
4.complications of necrotising enterocolitis include a stricture - T - complications of NEC include short bowel syndrome, malabsorption, strictures and recurrence of disease
5.pseudopolyps are a feature of Crohn’s disease - F - can occur in Crohns but more typical of UC
63.Patient has a peptic ulcer with increased serum gastrin levels, what would you scan for:
1.Pancreas and duodenum
2.Pancreas, duodenum and lymph nodes
3.Mass in duodenum
63.Patient has a peptic ulcer with increased serum gastrin levels, what would you scan for: (TW, GC, JS) Robbins p782
1.Pancreas and duodenum
2.Pancreas, duodenum and lymph nodes – T – although the majority of gastrinomas in ZES and MEN-1 are in the pancreas & 1st part of the duodenum, would presumably still search remainder of gastrinoma triangle, then nodes to assess for metastatic deposits.
3.Mass in duodenum – this would be highest yield place to search if only able to look at one area.
Gastrinoma triangle – region bounded by confluence of the cystic and common bile ducts superiorly, the 2nd and 3rd portions of the duodenum inferiorly, and the neck and body of the pancreas medially – 85% of gastrinomas.
In contrast to sporatic gastrinomas, which are usually solitary lesions, gastrinomas that occur in patients with ZES and MEN-1 are usually multiple, less than 5mm in size, and located in the proximal duodenum. In ZES most (75%) are in the 1st portion of the duodenum, 14% in the distal duodenum, 11% in jejunum.
64.With regards to carcinoid tumour, which is least correct:
1.Equal incidence to small bowel adenocarcinoma
2.Benign
3.Yellow, tan, circumscribed
4.Desmoplastic reaction
5.Dec order of incidence: appendix, SI, rectum
2.Benign
*LW: agree
More recent robbins has jejunum and ileum as > 40%, and appendix < 25%, while stat Dx has 90% of jejunal-ileal carcinoids being in ileum (of total 45%), while appendix only 16%.
So although option 5 is not true, I think option 2 is more incorrect, especially based on older Robbins data, likely from which question was written.
64.With regards to carcinoid tumour, which is least correct: (JS/SK)
1.Equal incidence to small bowel adenocarcinoma - T - 50% of SI malignant tumours
2.Benign - F - all are potentially malignant
3.Yellow, tan, circumscribed - T - characteristic feature is solid, yellow-tan appearance
4.Desmoplastic reaction - T - firm tumours due to desmoplastic reaction
5.Dec order of incidence: appendix, SI, rectum – T/F - appendix > SI > rectum > stomach > colon (not according to Robbins 8e p788 table 17-5!!)
65.Which of the following statements concerning gastrointestinal diseases is most correct:
1.The colon is the most common site for GIT lymphoma
2.Inflammatory pseudopolyps are a characteristic of Crohn’s colitis
3.Aphthous ulcers are a characteristic feature of ulcerative colitis
4.Juvenile polyps typically occur in the rectum
4.Juvenile polyps typically occur in the rectum
65.Which of the following statements concerning gastrointestinal diseases is most correct: (GC)
1.The colon is the most common site for GIT lymphoma F - stomach 50% > SB > colon > oesophagus; multicentric in 10-50%.
2.Inflammatory pseudopolyps are a characteristic of Crohn’colitis F - of UC; represent islands of regenerating mucosa.
3.Aphthous ulcers are a characteristic feature of ulcerative colitis F - of Crohn’s disease; focal mucosal ulcers resembling canker sores.
4.Juvenile polyps typically occur in the rectum T - hamartomatous proliferations; in general they occur singly and in the rectum. Usually large in kids under 5yo. (1-3cm), smaller in adults (called retention polyps). No malignant potential.
66.HNPCC: barium enema performed to look for:
1.Colonic carcinoma
2.Polyps
3.Detect colonic hamartoma
4.Hereditary neoplastic colonic polyposis
1.Colonic carcinoma
66.HNPCC: barium enema performed to look for: (JS)
1.Colonic carcinoma - T - HNPCC (Lynch syndrome) an AD condition, characterised by familial carcinomas of the colon, predominantly affecting the caecum and proximal colon. These don’t arise in adenomatous polyps.
2.Polyps
3.Detect colonic hamartoma
4.Hereditary neoplastic colonic polyposis
67.Benign gastric ulcer ?which feature is most likely:
1.Greater curvature
2.Heaped up edges
3.Radiating folds
4.Chronic atrophic gastritis -
Answer: Radiating folds
ROBBINS
- Classic Peptic ulcer is a round-oval sharply punched-out defect.
- mucosal margin may overhand the base slightly, but is usually level with the surrounding mucosa.
- Active ulcers may be lined by a thin layer of fibrinoid debris underlaid by a predominantly neutrophilic inflammatory infiltrate. Beneath this granulation tissue infiltrated with mononuclear leukocytes and a fibrous or collagenous scar forms the ulcer base.
- Scarring may involve the entire thickness of the wall and pucker the surrounding mucosa into folds that radiate outwards.
In contrast, heaped-up margins are more characteristic of cancers.
Peptic ulcer disease is a sequelae of H.pylori-Associated chronic gastritis.
Atrophic gastritis can be caused by both H.pylori-associated chronic gastritis as well as Autoimmune gastritis, however only H.pylori-associated gastritis is prone to Peptic ulcer disease.
68.Coeliac, which is true:
1.Flattened mucosa, elongated glands
2.Less than 2 times the risk of cancer -
1.Flattened mucosa, elongated glands
68.Coeliac, which is true: (JS)
1.Flattened villli, elongated glands – T - crypts are elongated, hyperplastic and tortuous but the overall mucosal thickness remains the same
2.At least 3 times the risk of cancer - F - there is a long term risk of malignant disease at 2 times the usual rate - intestinal lymphomas (including disproportionately high number of T-cell lymphomas) and GIT and breast cancers.
69.Crohn’s, associated findings, which is false:
1.PBC
2.Renal stones
3.Cancer
1.PBC
69.Crohn’s, associated findings, which is false: (JS)
1.Primary biliary cirrhosis - F - develop primary sclerosing cholangitis (not PBC)
2.Sacroilitis - T – seronegative spondyloarthropathy in 3-16%
3.Cholangiocarcinoma - T - can develop bile duct and GB carcinoma (due to PSC)
4.Renal calculi - T - urolithiasis in 5-10%
5.GIT malignancy - T - 4-20 times increased risk of colonic adenocarcinoma
70.Gastric marginal zone lymphoma, MALT oma, which is false:
1.They are a form of B cell lymphoma
2.They are most common in middle aged adults
3.Early dissemination is typical
4.They are associated with Helicobacter gastritis
5.They are associated with chronic inflammation secondary to autoimmune disorders
3.Early dissemination is typical
70.Gastric marginal zone lymphoma, MALToma, which is false: (JS)
1.They are a form of B cell lymphoma
2.They are most common in middle aged adults
3.Early dissemination is typical - F - they remain localised for prolonged periods at sites of origin with systemic spread late in their course
4.They are associated with Helicobacter gastritis
5.They are associated with chronic inflammation secondary to autoimmune disorders
71.Achalasia of the oesophagus, which is false:
1.Dilated vestibule
2.25% have a dilated oesophagus and colon with chagas
3.Oesophageal perforation common
4.Most oesophageal perforations are iatrogenic
71.Achalasia of the oesophagus, which is false: (JS)
1.Dilated vestibule - F - vestibule is the dilated region of the stomach just above the GOJ; in the region of the LOS which fails to relax in achalasia - beaked tapering at GOJ
2.25% have a dilated oesophagus and colon with Chagas – T -The digestive forms of the disease lead to megaesophagus and/or megacolon in approximately one third of chronic cases, of which 20-50% also present with an associated cardiopathy.
3.Oesophageal perforation is a complication – T - Pneumatic dilatation for achalasia carries a significant and recognized risk of esophageal perforation (5%).
4.Most oesophageal perforations are iatrogenic T –
72.Features of scleroderma include:
1.Upper third of oesophagus is preserved
2.Colon involvement rare
3.GIT involvement is rare
4.Oesophageal perforation is common
1.Upper third of oesophagus is preserved
72.Features of scleroderma include: (JS)
1.Upper third of oesophagus is preserved T - causes atony and aperistalsis of the lower 2/3 of oesophagus with patulous LOS and GOR
2.Colon involvement rare –F - colon is involved in 40-50% with pseudosacculations, eventual loss of haustra, marked dilatation and stercoral ulceration from retained faecal material
3.GIT involvement is rare – F - third most common manifestation (after skin and Raynaud’s), occurs in 40-45%
4.Oesophageal perforation is common - F - not mentioned in Dahnert, Primer or Mayo clinic book
73.H pylori: whole lot of facts about relationship in gastric ca and lymphoma (T/F):
1.10% asymptomatic
2.20% chronic gastritis
3.Not linked to gastric cancer and lymphoma
4.Previously called enterobacter lymphoma
73.H pylori: whole lot of facts about relationship in gastric ca and lymphoma T/F: (JS)
1.10% asymptomatic - F - colonisation rates increase with age, reaching 50% in asymptomatic adults over 50 years
2.20% chronic gastritis - F - H pylori is present in 90% of patients with chronic gastritis affecting the antrum
3.Not linked to gastric cancer and lymphoma - F - associated with gastric cancer and lymphoma (GC - H.pylori is the first bacterium classified as a carcinogen. MALToma: eradication of H.pylori with AB therapy often leads to regression of tumour cells, which seems to depend on cytokines secreted by H.pylori-specific T cells for teir growth and survival. H.pylori gastritis - chronic inflammation - gastric atrophy - intestinal metaplasia - dysplasia - adenoCa)
4.Previously called enterobacter lymphoma - F - can’t find this anywhere….
74.Elderly man with large bowel narrowing, biopsy showed segmental fibrosis and chronic inflammation, most likely:
1.Ischemia
2.Vasculitis
3.Carcinoma
1.Ischemia
74.Elderly man with large bowel narrowing, biopsy showed segmental fibrosis and chronic inflammation, most likely: (TW)
1.Ischemia - T - submucosal chronic inflammation and fibrosis can lead to stricture (in chronic ischemia).
2.Vasculitis
3.Carcinoma
75.Angiodysplasia, most likely:
1.Most common in sigmoid
2.Can’t be seen macroscopically because covered mucosa
3.Cause of 20% of significant lower GI bleeding, either as massive blood loss of chronic loss
4.Not associated with other GIT lesions or CVS abnormalities
3.Cause of 20% of significant lower GI bleeding, either as massive blood loss of chronic loss
75.Angiodysplasia, most likely: (JS)
1.Most common in sigmoid - F - most common in caecum and right colon
2.Can’t be seen macroscopically because covered mucosa - F - tortuous dilations of submucosal and mucosal blood vessels, separated from the intestinal lumen by only the vascular wall and a layer of attenuated epithelial cells
3.Cause of 20% of significant lower GI bleeding, either as massive blood loss of chronic loss - T - account for 20% of significant lower intestinal bleeding
4.Not associated with other GIT lesions or CVS abnormalities - F - associated with Meckel diverticulum & aortic stenosis (20%)
76.Known (or previous) strongyloides infection with oedema of the mucosa of ascending colon, what does it mean:
1.Autoinfection in the immunocompromised
2.Not related – only infects duodenum and SB
3.Ischaemia due to vascular invasion
1.Autoinfection in the immunocompromised
SCS: Dahert. Strongyloides hyperinfection syndrome. Extensive tissue invasion in immunocompromised. Thickened colon wall (due to florid transmural granulomatous inflammatory colitis causes by invasive larvae)
- Usually it just infects Duodenum and Jejunum (oedematous, irregular mucosal folds), duodenal stricture (3/4th portion).
-autoinfection: larve matures as it transits, re- enters via penetrating intestinal mucosa/perianal skin ans repeating life cycle.
-Life cycle: penetrates skin/mucous membranes. Passes from submucosal
Sites via lymphatics + venous circulation to lung. Larvae ascends bronchi into trachea after invading airway. Swallowed thus gets into alimentary tract.
76.Known (or previous) strongyloides infection with oedema of the mucosa of ascending colon, what does it mean: (TW) Robbins p391 & 805
1.Autoinfection in the immunocompromised - T - in contrast to other helminthic parasites, can complete life cycle entirely within human host. Autoinfection limited by intact immune respone, however in immunocompromised - can give rise to potentially fatal infection. During autoinfection, the rhabditiform (non-infectious) mature into filariform larvae (infectious) within the GIT - these can then penetrate the perianal skin or colonic mucosa to complete the cycle of autoinfection.
2.Not related – only infects duodenum and SB - F, but prob true in immunocompetent host - filariform larvae of Strongyloides stercoralia found in soil or in other materials contaminated with human faeces. Larvae penetrate skin and migrate hematogenously to lungs where they penetrate the alveolar air sacs. Larvae then ascent tracheobronchial tree and are swallowed. Then mature into adult worms and burrow into mucosa of duodenum and jejunum. Adult worms may life for up to 5y. Female adulte produces eggs, from which develop non-infectious larvae within the lumen of the GIT (which then pass into your turds).
3.Ischaemia due to vascular invasion - F - oedema and inflammation secondary to invasion
Endoscopy can show: duodenum - oedema, brown discoloration of mucosa, erythrmatous spots, subepithelial haemorrhage, and megaduodenum; colon - loss of vascular pattern, oedema, apthous ulcers, erosions, serpiginous ulcerations, and xanthoma-like lesions; stomach - thickened folds and mucosal erosions.
77.Oesophageal narrowing in patient with CML, which is most likely:
1.CML recurrence
2.Graft verses host disease
3.Thrombocytopenia or something
????
78.20 yo with 20 colonic polyps, suspect FAP, which is most likely:
1.Need >100 polyps
2.Attenuated FAP
3.Polyps in Peutz Jegher restricted to SB
4.Normal patients…inheritance, sporadic mutations are rare
5.Thyroid cancer and mastoid osteoma in Gardners
2.Attenuated FAP
78.20 yo with 20 colonic polyps, suspect FAP, which is most likely: (TW)
1.Need >100 polyps - F - attenuated FAP can have <100; classic FAP needs > 100
2.Attenuated FAP - T - (UTD) attenuated from of FAP - affected patients have fewer than 100 colorectal adenomas and a delayed onset of colorectal cancer. Polyposis typically develops in 2nd or 3rd decate of life. Similarly high risk, but with older average age of cancer (54yo).
3.Polyps in Peutz Jegher restricted to SB - F - small intestine 64%, colon 64%, stomach 49%, rectum 32%.
4.Normal patients…inheritance, sporadic mutations are rare
5.Thyroid cancer and mastoid osteoma in Gardners - F - 20 colonic polyps. Gardners = FAP + benign manifestations: osteomas and dental abnormalities; cutenous lesions; desmoid tumors; congenital hypertrophy of th retinal pigment; adrenal adenomas; nasal angiofibromas. And malignant manifestations: extra-colonic malignancies duodenal; thyroid; pancreatic; gastric; CNS; hepatoblastoma; small bowel distal to duodenum; possibly adrenal.
79.Adenocarcinoma distal oesophagus, most likely:
1.Barrett’s oesophagus
1.Barrett’s oesophagus
