Upper and Lower GI Flashcards by Ashlyn Stackhouse

oesophageal histology showing polymorphonuclear infiltrates.

oesophagitis

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commonest cause of oesophagitis

can cause complications such as ulceration, strictures, barrets oesophagus and perforation

GORD

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oesophageal histology showig necrotic slough, inflammation and neutrophil exudate. no fibrosis or scarrying at base.

ACUTE ulcer

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re-epithelialisation - metaplastic change of squamous to columnar cells, usually with goblet cells (intestinal type mucosa)

Barrett’s oesophagus

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glandular carcinoma that is associated with Barrett’s seen in the distal 1/3 of the oesophagus. risk factors include smoking, obesity and radiation therapy

Adenocarcinoma of the oesophagus

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Presents with progressive dysphagia, odynophagia, anorexia and severe weight loss. associated with plummer vinson, nutritional deficiencies, HPV. usually found in the middle oesophagus. assocaited with eTOH and smoking.

Squamous cell oesophageal carcinoma.

rapid growth, early spread

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inflammation and infiltration of PMN into gastric mucosa. 5 causes:

acute gastritis

aspirin, NSAIDS, corrosives, H.Pylori, alcohol

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complcation of gastritis

may develop ulcers, or metaplstic –> dysplastic changes (including goblet cell metaplasia)
potential to become cancer

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causes of chronic gastritis in the antrum

NSAIDS, bile reflux

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causes of chronic gastritis in the body of the stomach

autoimmune

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histology of chornic gastritis

lymphocytic infiltrates +/- neutrophils (acute on chronic)

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most important cause of chronic gastritis, can lead to development of gastric adenocarcinoma or MALToma.

H. pylori
causes 8x increase risk of gastric ca
cAg A +ve -= more virulent form, injects toxin into intercellular junctions

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Other infective causes of chronic gastritis

CMV, strongyloides

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epigastric pain +/- weight loss
worse with food
relieved by antacids
punched out lesion with rolled margins
breech through muscularis mucosa into the submucosa

Gastric ulcer

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caused by chronic antigenic stimulation of the B cell marginal zone lymphocytes

MALToma

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soft tissue tumour that arises from the intersitial cellf of Cajal. benign but can have malignant transformation.

GIST

Gastrointestinal stormal tumour

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Adenocarcinoma of the stomach with well differentiated cells and goblet cells. looks like intestinal mucosa

Intestinal type adenocarcinoma

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adenocarcinoma with poorly differentiaated cells, fixed rigid stomach. includes signet ring cell carcinoma

Diffuse adenocarcinoma

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caused by increased gastric acid spilling into the duodenum, causing inflammation and gastric metaplasia

duodenitis

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epigastric pain, worse at night, relieved by food and milk.
occcurs in younger adults

neutrophil infiltrates

duodenal ulcer

RFs drugs, asprion, NSAIDS, steroids, smoking
H.pylori can form ulcers in the duodenum is gastric metaplasia has occured
NB - GASTRIC metaplasia, not INTESTINAL-TYPE metaplasia as seen in barretts and gastric.

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histology of the duodenum showing villous atrophy, crypt hyperplasia and increased intraepithelial lymphocytes

Coeliac

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other cause of malabsorption

Tropical sprue

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percentage of coeliac disease that progresses to duodenal MALT

10%

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serological test with best sens and spec fo coeliac

anti-endomysial abs

anti-ttG also good (IgA)

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presents with signs and symptoms of GI obstruction in young babies, mostly male. assocayed with Down's syndrome RET proto oncogene biopsy shows hypertrophied nerve fibres but no ganglia

Hirschsprung's disease

inflammatory bowel disease with MZ twin concordance 50%. deep rosethorn ulcersa which can join to form serpentine ulcers. transmural inflammation

Crohns

rubberhose thick wall, fat wrapping around lumen and abcesses common. most commonly presents in the terminal ileum and caecum.

Crohns

IBD Associated with primary sclerosing cholangitis.

IBD w 20-30x risk of adenocarcinoma

IBD w superficial inflammation confined to the mucosa, no granulomas, fissures/fistulae.

IBD that affects the whole GI tract from mouth to anus, has patchy distribution with skip lesions and areas of healthy mucosa overlying diseased tissue.

Crohns | cobblestone appearance

non-caseating granulomas seen in this IBD

Crohns

presents with bloody diarrhoea, mucus, crampy abdo pains relieved by defecation. associated with PSC

NOD2/CARD15 gene defects may be seen in this condition

Crohns

managment of mild attacks of Crohns

pred

severe attacks of crohns - Rx

IV hydrocortison, metronidazole

additional immunomodulating therapies used in crohns

Methotrexate Infliximab Azathioprine go MIA when you have Crohns

Rx of mild UC

pred + mesalazine (5-ASA)

rx of moderate UC:

pred + 5-ASA + steroid enema bd

rx of severe UC

admit, NBM, IV fluids and hydrocortisone, rectal steroids | Remission - 5-ASA, 2nd line Azathioprine

outpounching of the bowel at weak spots. can lead to rupture, fistulae, infection and scarring.

Diverticular disease

cornflake slough appearance of the bowel. histology shows 'volcano explosion' inflammatory cells.

Pseudomembranous colitis

causes of pseudomembranous coliotis

C.diff overgrowth - exotoxins - clindamycin - ceftriaxone - ciprofloxacin

Rx of pseudomembranous colitis

metronidazole po | 2nd line - vanc

high incdience in the west due to low fibre diet. high intraluminal pressure leads to outpounchings in weak points of the bowel wall. 90% occur in left colon.

diverticular disease. | seen on barium enema CT or endoscopy

fever and peritonism with a history of diverticular disease

diverticulitis

tumours of enterochromaffin cell origin, produce 5-HT. commonly found in the bowel but also lung, ovaries, testes.

Carcinoid syndrome

symptoms of carcinoid syndrome

bronchoconstriction flushing diarrhoea

investigation to diagnose carcinoid syndrome

24hr urine 5-HIAA (main metabolite of serotonin)

main complication of carcinoid syndrome

carcinoid crisis: | life-threatening vasodilation, tachycardia, hypotension, bronchoconstriction and hyperglycaemia

Rx of carcinoid syndrome

octreotide

non neoplastic polyp of the colon/rectum, found sporadically in some genetic/acquired conditions. focal malformations of the mucosa and lamina propria. usually found in children or in patients with peutz-jegher syndrome.

hamartomatous polyps

multiple focal malformations of the mucosa and lamina propria, found in <5year old, mostly in the rectum. causes some bleeding, usually solidary but up to 100 can be found in this particular AD condition.

Juvenile polyposis

non-neoplastic polyps that are seen at 50-60 yearsm thought to be caused by shedding of the epithelium. Related to damage, everyone has them to some extent.

hyperplastic polyps

benign dysplastic lesions that are precursors to most adenocarcinomas (although the vast majority remain benign)

adenoma

hypoproteinaemic hypokalaemia is caused by what type of adenoma

villous adenoma

what are the three types of adenoma | v

villous tubular tubulovillous

most important risk factor for malignancy in adenoma (3)

large size degree of dysplasia increased villous component

FAP gene mutation

70% AD mutation APC, Chr5q21. 30% AR mutation in DNA mismatch gene.

progression of adenoma --> carcinoma requires activation of

k ras | LOF and p53 mutations

histology of adenoma

excess epithelial proliferation, dysplasia. dark and hypermitotic but has NOT invaded BM

AD-LKB1 mutation causing multiple hamartomatous polyps, mucocutaneous hyperpigmentation, freckles around the mouth and on the palms and soles. increased risk of intussusception and malignancy.

Peutz Jeghers

98% of colorectal cancers are ...

adenocarcinomas

iron deficiency anaemia, weight loss are associated with colorectal cancer located on...

right side of colon

left sided colorectal cancer present with

change in bowel habit, crampy LLQ pain

classification staging system used for colorectal cancer

Duke's staging

Dukes staging (summary) A-D

``` A = mucosa (5yr = 95%) B = musc propria/transmural, NO LN C = musc propria/transmural + LN D = distant mets (5yr survival 10%) ```

Histology: colorectal ca (general)

disordered archictecture, dark purple mitotic figures, big nucleus, reactive stromal changes. invades through BM.

average age of onset of FAP

25 years of age - present with >100 adenomatous polyps (req for diagnosis) usuallys 1000s seen.

what percentage of pts with FAP will progress to adenocarcinoma if left untreated?

100% in 30 years

Gardners syndrome

FAP + extra-intestinal features: osteomas, dental caries

AD mutations in DNA mismatch repair genes, cause of 3-5% of all colorectal cancer. caners are usually in the right colon. few polyps but fast progression to malignancy.

HNPCC

HNPCC - other associated cancers

ovarian, small bowel, transitional cell and stomach carcinoma - multile synchronous ca.

treatment of FAP

prophylactic colectomy

early age colorectal cancer (<50yo) especially proximal to the splenic flexure. tumours are poorly differentiated and often mucinous. associated with other cancers such as endometrial and ovarian ca.

HNPCC (Lynch)

Upper and Lower GI Flashcards

(75 cards)