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Histopath > Upper and Lower GI > Flashcards

Upper and Lower GI Flashcards

1
Q

oesophageal histology showing polymorphonuclear infiltrates.

A

oesophagitis

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2
Q

commonest cause of oesophagitis

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

A

GORD

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3
Q

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

A

ACUTE ulcer

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4
Q

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

A

Barrett’s oesophagus

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5
Q

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

A

Adenocarcinoma of the oesophagus

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6
Q

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.

A

Squamous cell oesophageal carcinoma.

rapid growth, early spread

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7
Q

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

A

acute gastritis

aspirin, NSAIDS, corrosives, H.Pylori, alcohol

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8
Q

complcation of gastritis

A

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

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9
Q

causes of chronic gastritis in the antrum

A

NSAIDS, bile reflux

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10
Q

causes of chronic gastritis in the body of the stomach

A

autoimmune

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11
Q

histology of chornic gastritis

A

lymphocytic infiltrates +/- neutrophils (acute on chronic)

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12
Q

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

A

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

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13
Q

Other infective causes of chronic gastritis

A

CMV, strongyloides

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14
Q 
epigastric pain +/- weight loss
worse with food
relieved by antacids
punched out lesion with rolled margins
breech through muscularis mucosa into the submucosa
A

Gastric ulcer

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15
Q

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

A

MALToma

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16
Q

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

A

GIST

Gastrointestinal stormal tumour

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17
Q

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

A

Intestinal type adenocarcinoma

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18
Q

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

A

Diffuse adenocarcinoma

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19
Q

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

A

duodenitis

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20
Q

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

neutrophil infiltrates

A

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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21
Q

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

A

Coeliac

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22
Q

other cause of malabsorption

A

Tropical sprue

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23
Q

percentage of coeliac disease that progresses to duodenal MALT

A

10%

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24
Q

serological test with best sens and spec fo coeliac

A

anti-endomysial abs

anti-ttG also good (IgA)

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25
Q

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

A

Hirschsprung’s disease

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26
Q

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

A

Crohns

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27
Q

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

A

Crohns

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28
Q

IBD Associated with primary sclerosing cholangitis.

A

UC

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29
Q

IBD w 20-30x risk of adenocarcinoma

A

UC

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30
Q

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

A

UC

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31
Q

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.

A

Crohns

cobblestone appearance

32
Q

non-caseating granulomas seen in this IBD

A

Crohns

33
Q

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

A

UC

34
Q

NOD2/CARD15 gene defects may be seen in this condition

A

Crohns

35
Q

managment of mild attacks of Crohns

A

pred

36
Q

severe attacks of crohns - Rx

A

IV hydrocortison, metronidazole

37
Q

additional immunomodulating therapies used in crohns

A

Methotrexate
Infliximab
Azathioprine

go MIA when you have Crohns

38
Q

Rx of mild UC

A

pred + mesalazine (5-ASA)

39
Q

rx of moderate UC:

A

pred + 5-ASA + steroid enema bd

40
Q

rx of severe UC

A

admit, NBM, IV fluids and hydrocortisone, rectal steroids

Remission - 5-ASA, 2nd line Azathioprine

41
Q

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

A

Diverticular disease

42
Q

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

A

Pseudomembranous colitis

43
Q

causes of pseudomembranous coliotis

A

C.diff overgrowth - exotoxins

  • clindamycin
  • ceftriaxone
  • ciprofloxacin
44
Q

Rx of pseudomembranous colitis

A

metronidazole po

2nd line - vanc

45
Q

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.

A

diverticular disease.

seen on barium enema CT or endoscopy

46
Q

fever and peritonism with a history of diverticular disease

A

diverticulitis

47
Q

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

A

Carcinoid syndrome

48
Q

symptoms of carcinoid syndrome

A

bronchoconstriction
flushing
diarrhoea

49
Q

investigation to diagnose carcinoid syndrome

A

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

50
Q

main complication of carcinoid syndrome

A

carcinoid crisis:

life-threatening vasodilation, tachycardia, hypotension, bronchoconstriction and hyperglycaemia

51
Q

Rx of carcinoid syndrome

A

octreotide

52
Q

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.

A

hamartomatous polyps

53
Q

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.

A

Juvenile polyposis

54
Q

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.

A

hyperplastic polyps

55
Q

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

A

adenoma

56
Q

hypoproteinaemic hypokalaemia is caused by what type of adenoma

A

villous adenoma

57
Q

what are the three types of adenoma

v

A

villous
tubular
tubulovillous

58
Q

most important risk factor for malignancy in adenoma (3)

A

large size
degree of dysplasia
increased villous component

59
Q

FAP gene mutation

A

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

60
Q

progression of adenoma –> carcinoma requires activation of

A

k ras

LOF and p53 mutations

61
Q

histology of adenoma

A

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

62
Q

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.

A

Peutz Jeghers

63
Q

98% of colorectal cancers are …

A

adenocarcinomas

64
Q

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

A

right side of colon

65
Q

left sided colorectal cancer present with

A

change in bowel habit, crampy LLQ pain

66
Q

classification staging system used for colorectal cancer

A

Duke’s staging

67
Q

Dukes staging (summary) A-D

A 
A = mucosa (5yr = 95%)
B = musc propria/transmural, NO LN
C = musc propria/transmural + LN
D = distant mets (5yr survival 10%)
68
Q

Histology: colorectal ca (general)

A

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

69
Q

average age of onset of FAP

A

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

70
Q

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

A

100% in 30 years

71
Q

Gardners syndrome

A

FAP + extra-intestinal features: osteomas, dental caries

72
Q

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.

A

HNPCC

73
Q

HNPCC - other associated cancers

A

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

74
Q

treatment of FAP

A

prophylactic colectomy

75
Q

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.

A

HNPCC (Lynch)

Histopath (13 decks)

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