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histopathology > GI disease > Flashcards

GI disease Flashcards

1
Q

Describe normal histology of the oesophagus

A

Squamous epithelium (proximal 2/3) and columnar epithelium (distal 1/3), joined by the squamo-columnar junction/ Z-line

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2
Q

Characteristics of reflux oesophagitis

A

GORD
Commonest cause of oesophagitis
Complications: ulceration, haemorrhage, haematemesis/melaena,
Barrett’s oesophagus, stricture, perforation
Los Angeles Classification
Tx: lifestyle changes (stop smoking, weight loss), PPI/H2 receptor
antagonists

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3
Q

Characteristics of Barrett’s oesophagus

A

Intestinal metaplasia of squamous mucosa to columnar epithelium (have goblet cells) following chronic GORD; upwards migration of the SCJ
Seen in 10% of those with symptomatic GORD
Can lead to adenocarcinoma: metaplasia → dysplasia → Ca

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4
Q

Characteristics of oesophageal adenocarcinoma

A

Associated with Barrett’s oesophagus so usually seen in distal 1/3
Other risk factors incl: smoking, obesity, prior radiation therapy
Most common in Caucasians, M»F

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5
Q

Characteristics of Squamous cell

oesophageal carcinoma

A

Associated with ETOH and smoking
Other risk factors incl: achalasia of cardia, Plummer-Vinson syndrome,
nutritional deficiencies, nitrosamines, HPV (in high prevalence areas)
6x more common in Afro-Carribeans, M>F
Usually found in middle 1/3 (50%). Upper 1/3 – 20%, Lower 1/3 – 30%
Presentation: progressive dysphagia (solids then fluids), odynophagia
(pain), anorexia, severe weight loss
Rapid growth and early spread (to LNs, liver and directly to proximal structures); palliative care

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6
Q

Characteristics of varices

A

Engorged dilated veins, usually due to portal HTN (back pressure)
Pt vomits units of blood
Emergency endoscopy -> sclerotherapy/banding

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7
Q

Describe normal histology of the stomach

A

Lined by gastric mucosa, columnar epithelium (mucin secreting) and glands.

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8
Q

Characteristics of gastritis

A

Acute (neutrophils) insult e.g. aspirin, NSAIDs, corrosives (bleach), acute H. pylori, severe stress (burns)
Chronic (lymphocytes and plasma cells) insult e.g. H-pylori tends to be Antral, AI e.g. pernicious anaemia, ETOH, smoking
Special types – Chemical (foveolar hyperplasia, chronic inflammation), Infection (CMV, HSV, strongyloides), Inflammatory Bowel Disease
Complications: Chronic gastritis may lead to gastric ulcer formation
It may also however result in intestinal metaplasia→ dysplasia →cancer

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9
Q

Characteristics of gastric ulcer

A

Breach through muscularis mucosa into submucosa.
Epigastric pain +/- weight loss
Worse with food (contrast with duodenal ulcer), relieved by antacids
RFs: H. pylori, smoking, NSAIDs, stress, delayed gastric emptying. Occurs mainly in elderly
Ix: Biopsy for H. pylori histology status. Punched out lesion with rolled margins.
Complications: anaemia (IDA) and perforation (erect CXR), malignancy

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10
Q

Characteristics of gastric lymphoma

A

Caused by H-pylori – chronic antigen stimulation

Rx: remove cause (H. pylori using triple therapy – PPI, Clarithromycin + Amox or Metro

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11
Q

Characteristics of duodenal ulcer

A

4 times more common than GU
Epigastric pain, worse at night
Relieved by food and milk
Occurs in younger adults
RFs: H. pylori, drugs, aspirin, NSAIDs, steroids, smoking, ↑ drugs, acid secretion
Complications: anaemia (IDA) and perforation (erect CXR)

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12
Q

Characteristics of coeliac disease

A

T cell mediated autoimmune disease ( DQ2, DQ8 HLA status)
Gluten intolerance results in villous atrophy and malabsorption
Presentation: young children (paeds) and Irish women (EMQs)
Symptoms (of malabsorption): steatorrhoea, abdo pain, bloating, n&v, ↓wt, fatigue, IDA, failure to thrive, rash (dermatitis herpetiformis)
Serological tests: Anti-endomysial ab (best sen and spec) , anti-tissue
transglutaminase (IgA), anti-gliadin (poor marker of disease control)
Gold standard Ix: upper GI endoscopy and duodenal biopsy (villous atrophy, crypt hyperplasia, lymphocyte infiltrate)
Rx: Gluten free diet
Around 10% progress to Duodenal T-cell lymphoma if not treated adequately

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13
Q

List some congenital GI diseases

A 
● Atresia
● Stenosis
● Duplication
● Imperforate anus 
● Hirschsprung’s disease – Absence of ganglion cells in myenteric plexus (80% males)
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14
Q

Categories of acquired GI disease

A

Mechanical
Inflammatory
Ischaemic

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15
Q

List some mechanical GI diseases

A

● Obstruction – caused by:
o Constipation!
o Diverticular disease = v. common
o Adhesions
o Herniation
o External mass (e.g. fetus, aneurysm, foreign body)
o Volvulus – complete twisting of bowel loop at mesenteric base around vascular pedicle,
small bowel (infants), sigmoid > caecal (elderly)
o Intussusception

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16
Q

List some inflammatory causes of GI disease

A

● Acute colitis – caused by:
o Infection (bacterial, viral, protozoal etc.) à diarrhoea v. common.
o Drug/toxin (esp. abx)
o Chemo/radiotherapy
● Chronic colitis – caused by:
o IBD: Crohn’s disease and ulcerative colitis
o TB

17
Q

Features of ischaemic GI disease

A

● Ischaemic colitis – arterial or venous occlusion, small vessel disease, low flow states,
obstruction
● Commonly in ‘Watershed areas’ eg: splenic flexure (SMA transition to IMA), rectosigmoid (IMA
transition to internal iliac).

18
Q

Pathophysiology of Crohn’s

A 
− Affects whole GI tract (mouth to 
anus), most common in terminal 
ileum and caecum.
− Patchy distribution: ‘skip 
lesions’. Areas of healthy mucosa lie above diseased mucosa -> ‘cobblestone 
appearance’
− First lesion =’aphthous ulcer’. 
These are deep ‘rosethorn 
ulcers.’ Can join together to form 
serpentine ulcers.
− Non-caseating granulomas
seen
− Transmural inflammation 
− Fistula/fissure formation common
19
Q

Pathophysiology of Ulcerative colitis

A 
− Extends proximally from 
rectum
− Continuous 
involvement of mucosa
− Small bowel not 
affected unless v. 
severe pancolitis 
causes ‘backwash 
ileitis’
− Extensive superficial broad 
ulcers 
− Inflammation superficial, 
confined to mucosa
− No granulomas/ fissures/ 
fistulae /strictures.
− Islands of regenerating 
mucosa bulge into lumen ->
pseudopolyps (can fuse to 
form mucosal bridges)
20
Q

Extra-GI manifestations of IBD

A

− Malabsorption & Fe def. Anaemia à stomatitis
− Eyes: uveitis (iris & ciliary body), conjunctivitis
− Skin: erythema nodosum (tender bruise-like swellings on shins),
pyoderma gangrenosum, erythema multiforme, digitial clubbing
− Joints: migratory asymmetrical polyarthropathy of large joints (15%),
sacroiliitis, myositis, ankylosing spondylitis
− Liver: pericholangitis, primary sclerosing cholangitis (UC>CD),
steatosis

21
Q

Complications of Crohn’s

A 
− Strictures (requiring bowel 
resection, often recurrent
− Fistulae
− Abscess formation
− Perforation
22
Q

Complications of UC

A 
− Severe haemorrhage
− Toxic megacolon -> perforation 
(damage to muscularis propria 
w/disruption of neuromuscular 
function à colonic dilatation)
− 30% require colectomy within 
3yrs for uncontrollable 
symptoms
− Adenocarcinoma (20-30x risk)
23
Q

Investigations for Crohn’s vs UC

A

Crohn’s
Systemic markers of inflammation
e.g. ESR, CRP, Barium contrast,
Endoscopy

UC
Rectal biopsy, flexible
sig/colonoscopy, AXR, stool culture

24
Q

Features of diverticular disease

A

High incidence in West probably due to low fibre diet. High intraluminal pressure results in
outpouchings at ‘weak points’ in wall of bowel (seen on barium enema CT or endoscopy). 90%
occur in left colon
Often asymptomatic, sometimes PR bleed
Complications: Diverticulitis: fever and peritonism; gross perforation, fistula,
obstruction (due to fibrosis)

25
Q

Features of carcinoid syndrome

A

• Diverse group of tumours of enterochromaffin cell origin, Produce 5-HT (serotonin)
• Commonly found in the bowel (but also lung, ovaries, testes)
• Usually slow growing
Investigation: 24hr urine 5-HIAA (main metabolite of serotonin)
Treatment: Octreotide (somatostatin analogue)

26
Q

Clinical findings of carcinoid syndrome and carcinoid crisis

A

Syndrome
Bronchoconstriction, flushing, diarrhoea

Crisis
Life threatening vasodilatation, Hypotension,
Tachycardia, Bronchoconstriction,
Hyperglycaemia

27
Q

Characteristics of colon adenomas

A
  • Benign dysplastic lesions that are the precursor lesion to most
    adenocarcinomas (although most remain benign)
    − Found in 50% >50yrs in Western world
    − Mostly asymptomatic so need regular surveillance if over 3.4cm 45%
    malignant change .
    − Classified based on architecture as tubular, tubulovillous or villous.
    − Villous adenoma (rare) à hypoproteinaemic hypokalaemia because they
    leak large amounts of protein and K.
    − Large size is most important risk factor for malignancy, in addition to
    degree of dysplasia and increased villous component.
    − Adenoma -> carcinoma progression ‘classical chromosomal instability
    sequence’
    o Normal colon: at risk mucosa after “first hit” mutation in 1st
    copy of APC gene (those with FAP born with this mutation)
    o At risk: adenoma after “second hit” mutation to remaining
    APC gene
    o Progression to carcinoma follows activation of KRAS, LOF
    mutations of p53
28
Q

Give examples of non-neoplastic polpys and their characteristics

A

Hamartomous polyp
Found sporadically in some genetic/acquired syndromes
Juvenile polyps are focal malformations of mucosa and lamina propria, vast
majority in those <5yrs old, mostly in rectum à bleeding. Usually solitary, but
up to 100 found in juvenile polyposis (AD) that may require colectomy to
stop haemorrhage.
Also seen in Peutz-Jeghers syndrome (AD - LKB1) = multiple polyps,
mucocutaneous hyperpigmentation, freckles around mouth, palms and
soles. Have increased risk of intussusception and of malignancy à regular
surveillance of GI tract, pelvis and gonads.

Hyperplastic polyp
een at 50-60yrs, thought to be caused by shedding of epithelium -> cell
buildup

Inflammatory
Pseudo-polyps e.g. IBD

29
Q

Epidemiology of colorectal cancer

A

2nd commonest cause of cancer deaths in UK.
Age 60-79 yrs
If found <50yrs consider familial syndrome.
Commoner in western population
98% are adenocarcinoma, 45% in rectum

30
Q

Aetiology, clinical features, investigations for colorectal cancer

A

Diet (↓fibre, ↑fat), Lack of exercise, Obesity, Familial syndromes, chronic IBD,
NSAIDS protective (COX2 over-expressed in 90%)
Right sided tumours: Fe def. anaemia, weight loss
Left sided tumours: change in bowel habit, crampy LLQ pain
Proctoscopy, sigmoidoscopy, colonoscopy, barium enema, bloods e.g. FBC,
CT/MRI
Carcinoembryonic antigen (CEA) – monitor disease

31
Q

Classification of colorecatal cancer

A

Duke’s Staging- helps determine Rx: (TNM staging also used)
A: confined to mucosa (5yr survival >95%)
B1: extending into muscularis propria (5yr survival 67%)
B2: transmural invasion, no lymph nodes involved (5yr survival 54%)
C1: extending to muscularis propria, with LN metastases (5yr survival 43%)
C2: transmural invasion, with lymph node metastases (5yr survival 23%)
D: distant metastases (5yr survival <10%)

32
Q

Familial syndromes in colorectal cancer

A

Familial adenomatous polyposis (FAP)
− 70% AD mutation in APC gene (C5q1), 30% AR mutation in DNA
mismatch repair genes
− Present 10-15yrs - >100 adenomatous polyps required for diagnosis,
usually 100-1000s seen. ALL will à adenocarcinoma if left untreated by
30yrs therefore most have prophylactic colectomy.
− Increased risk of neoplasia elsewhere, eg: ampulla of Vater and stomach
− At birth, hypertrophy of retinal pigment epithelium
Gardners – like FAP with extra intestinal features eg: osteoma’s, dental
caries

Hereditary non-polyposis colorectal cancer/Lynch syndrome (HNPCC)
− AD mutations in DNA mismatch repair genes
− Carcinomas usually in right colon, few polyps but fast progression to
malignancy therefore present usually <50yrs
− Associated with endometrial, ovarian, small bowel, transitional cell and
stomach carcinoma.

histopathology (7 decks)

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