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Year 5 Path Charis > Histopathology - Upper + Lower GI pathology > Flashcards

Histopathology - Upper + Lower GI pathology Flashcards

1
Q

Hirschsprung’s disease biopsy findings

A

Hypertrophied nerve fibres but no ganglia

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2
Q

Where is volvulus more likely to occur in
children
eldelry

A

children - small bowel

elderly - sigmoid colon

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3
Q

Where does diverticular disease occur more commonly?

A

90% occur in L colon

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4
Q

How does diverticular disease present in endoscopy

A

empty spaces - look at photo in lecture

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5
Q

Secretory diarrhoea vs exudative diarrhoea

A

secretory - toxin

exudative - invasion + mucosal damage

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6
Q

Histology of pseudomembranous colitis

A

Volcanic eruption of pus coming from the surface of the bowel at the mucosa

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7
Q

C. diff mx

A

Metronidazole (1)

Vancomycin (2)

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8
Q

Where is ischaemic colitis more likely to occur?

A

In watershed zones

Splenic flexure (SMA + IMA)
Rectosigmoid (IMA + internal iliac artery)
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9
Q

CD pathology

A

 Whole GIT can be affected (mouth to anus) – most common in terminal ileum + caecum (R side)

 Skip lesions  cobblestone appearance

 Transmural inflammation – entire thickness of the bowel wall

 Non-caseating granulomas – collections of macrophages but not necrotic or caseating (bottom L)
 Sinus/fistula/fissure formation common

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10
Q

CD extra-intestinal manifestations

A

Arthritis
Uveitis
Stomatitis/ cheilitis

Skin

  • Erythema nodosum
  • Erythema multiforme
  • Pyoderma gangrenosum
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11
Q

UC

A

Slightly more common than CD

Superficial inflammation confined to the mucosa
Bowel wall normal thickness
No granulomas
No abscesses/fissures/fistulae

Shallow ulcers
Pseudopolyps (islands of regenerating mucosa bulge into the lumen - can fuse to form mucosal bridges)

May see backwash ileitis + appendiceal involvement

bloody diarrhoea + mucus
crampy abdo pain relieved by defecation

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12
Q

Which conditions is UC associated with?

A

PSC

Adenocarcinoma

Toxic megacolon

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13
Q

UC mx

o Mild
o Moderate
o Severe
o For remission

A

o Mild – prednisolone + mesalazine (5 ASA)

o Moderate – prednisolone + 5- ASA + steroid enema BD

o Severe – admit, NBM, IVF, IV hydrocortisone, rectal steroids

o For remission – all 5-ASA (1st line), azathioprine (2nd line)

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14
Q

Carcinoid syndrome vs carcinoid crisis

A

Syndrome

  • Bronchoconstriction
  • Flushing
  • Diarrhoea

Crisis

  • Vasodilation
  • Hypotension
  • Tachycardia
  • Bronchoconstriction
  • Hyperglycaemia

caused by endochromaffin cell tumours which produce 5-HT commonly found in the bowel

Ix - 24h urine 5-HIAA (main metabolite of serotonin)
Mx - octreotide

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15
Q

Adenomas - RF for cancer

A
  • Large adenoma (most important RF)
  • Increased villous component
  • Dysplasia
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16
Q

Tubular adenoma vs villous adenoma macroscopic appearance

A

Look at pics on ppt (week 15)

Villous adenoma looks like a line of test tubes

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17
Q

How does an adenoma progress to a carcinoma?

A

o Normal colon  at risk mucosa after “first hit” mutation in 1st copy of APC (adenomatous polyposis coli) gene (those with FAP are born with this mutation)

o At risk  adenocarcinoma after “second hit” mutation remaining APC gene

o Progression to carcinoma follows activation of
KRAS
LOF
Mutations of p53

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18
Q

Peutz Jeghers mutation

A

AD

LKB1

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19
Q

Familial syndromes implicated in lower GI disease

A

• Peutz Jeghers

• FAP – Familial adenomatous polyposis
o Gardner’s
o Turcot

• HNPCC – hereditary non-polyposis colon cancer

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20
Q

FAP buzzwords

A

• FAP – Familial adenomatous polyposis

Chr 5q21 APC tumour suppressor gene

At birth –> hypertrophy of the retinal pigment epithelium

Young people getting colorectal cancer

At least 100 polyps required for dx
Average - 1000 polyps –> will develop into adenocarcinoma if not resected

Prophylactic colectomy

increased risk of cancer elsewhere - ampulla of Vater, stomach

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21
Q

What is Gardner’s syndrome?

A

o Same clinical/pathological/etiologic features as FAP with high cancer risk

o Distinctive extra-intestinal manifestations
 Multiple osteomas of skull + mandible
 Epidermoid cysts
 Desmoid tumours
 Dental caries, unerupted supernumerary teeth
 Post-surgical mesenteric fibromatoses

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22
Q

Most common hereditary colon cancer syndrome

A

HNPCC (hereditary non-polyposis colorectal cancer) / Lynch syndrome

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23
Q

HNPCC vs FAP

A

HNPCC is more common

In HNPCC there are few polyps, in FAP there are at least 100

In HNPCC there are multiple synchronous cancers (endometrium, ovary, small bowel, prostate, breast)

In HNPCC the mutation is in the DNA mismatch repair genes, in FAP the mutation is in the APC tumour suppressor gene

Both syndromes –> onset of colorectal cancer at an early age

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24
Q

Where are the carcinomas in HNPCC usually found?

A

R colon

proximal to the splenic flexure

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25
Q

Where is the mutation HNPCC ?

A

DNA mismatch repair genes

26
Q

Which staging system is used to stage colorectal cancer?

A
B1
B2
C1
C2
D
A

Duke’s staging system

A
Limited to mucosa

B1
Extends into muscularis propria, no lymph node involvement

B2
Transmural extension, no lymph node involvement

C1
Extends into muscularis propria + lymph node involvement

C2
Transmural extension + lymph node involvement

D
Distant mets

27
Q

Colorectal cancer mx

o Caecum, ascending colon, proximal transverse

o Transverse colon

o Descending colon + distal transverse

o Sigmoid cancer

o Rectal cancer/low sigmoid cancer
 <1-2cm above anal sphincter (lower 1/3 of rectum)
 >1-2cm above anal sphincter

• If it’s a transmural invasion

A

o Caecum, ascending colon, proximal transverse  R hemicolectomy

o Transverse colon  extended R hemicolectomy

o Descending colon + distal transverse  L hemicolectomy

o Sigmoid cancer  sigmoid colectomy

o Rectal cancer/low sigmoid cancer
 <1-2cm above anal sphincter (lower 1/3 of rectum)  abdomino-perineal resection
 >1-2cm above anal sphincter  anterior resection

• If it’s a transmural invasion you will likely get radiotherapy, chemotherapy + excision

28
Q

• What sort of colon polyps most commonly predispose to adenocarcinoma of the colon?

A

Adenomas

29
Q

What is the z line?

A

the point at which the epithelium of the oesophagus transitions from being squamous (proximal 2/3) to being columnar (distal 1/3)

30
Q

Where is H pylori gastritis usually found?

A

Antrum of the stomach + pyloric canal

31
Q

Difference between the body and the antrum of the stomach

A

glands in lamina propria

body - specialised (secrete acid + enzyme, produce IF)
No goblet cells*

antrum - non-specialised, produce gastrin

  • goblet cells are present in the intestine therefore presence of goblet cells in the stomach is a feature of intestinal metaplasia
32
Q

Normal villus: crypt ratio

A

> 2:1

33
Q

Layers of the oesophagus

A

o Epithelium  muscularis mucosa  submucosa with connective tissue + fat  muscularis externa (muscularis propria)

34
Q

Layers of the stomach

A

Mucosa (epithelium  lamina propria  muscularis mucosa)  submucosa  muscularis propria

35
Q

How would you describe the epithelium of the normal duodenum?

A

Glandular epithelium with goblet cells

Villous: crypt ratio –> >2:1

36
Q

Ulcer vs erosion

A

Ulcer = through muscularis mucosa (into submucosa)

Erosion = before muscularis mucosa, not past lamina propria (not into submucosa)

37
Q

What is Barret’s oesophagus?

A

The same as columnar lined oesophagus (CLO)

• Replacement of squamous epithelium by
metaplastic columnar epithelium

without goblet cells: gastric metaplasia (CLO)
with goblet cells: intestinal type metaplasia (CLO with IM)

Risk: can lead to adenocarcinoma (metaplasia -> dysplasia -> cancer)

38
Q

Define

metaplasia
dysplasia
cancer

A

1) Metaplasia = not pre-malignant because reversible (can progress to dysplasia)

 (2) Dysplasia = changes showing some of the cytological and histological features of malignancy but with NO invasion through the BM (this is the stage that screening identifies at)

 (3) Adenocarcinoma = abnormal cells invade through the BM

39
Q

2 pathways to development of GI cancer

A

 Adenoma-carcinoma pathway
o Lower GI
o Polyp pathway - adenomas becoming malignant

 Metaplasia-Dysplasia patway
o upper GI pathway
o Oesophagitis/ chronic gastritis –.> Metaplasia (i.e. CLO ± IM) –> dysplasia –> cancer

40
Q

Defining feature of SCC of the oesophagus

A

cells from keratin

(other histological features include:
Invasion of the submucosa
Cells have intracellular bridges)

41
Q

SCC vs adenocarcinoma of the oesophagus

A

SCC

  • Upper 2/3 of oesophagus (middle > lower > upper)
  • Developing countries
  • Smoking, Alcohol, HPV (16,18)

Adenocarcinoma

  • lower 1/3 of oesophagus
  • Developed countries
  • GORD, Barrett’s
42
Q

Histology of acute vs chronic gastritis

A

Acute = neutrophils

Chronic = lymphocytes, plasma cells

43
Q

Causes of acute vs chronic gastritis

A

Acute
Chemicals
Infection

Chronic ABCD
Autoimmune [body]
Bacterial [antrum]
Chemicals [antrum]
IBD
44
Q

What does presence of lymphoid follicles in a stomach biopsy indicate?

A

 Highly suggestive that the patient has had an H. pylori infection (i.e. the presence of lymphoid follicles is not part of the normal stomach mucosa)

H. pylori infection induces the development of lymphoid follicles in germinal centres –> MALT –> lymphoma

o If someone has H. pylori as well as lymphoma, you will see crypts that are full of neutrophils  good because if you treat H. pylori, the lymphoma could be reversed

45
Q

Helicobacter strain associated with chronic inflammation + cancer

A

cag-A-positive H.pylori

Needle like
appendage –> injects toxin into intercellular
junctions –> bacteria attach more easily

46
Q

2 types of cancer that arise from chronic stimulation by H pylori

A
  • CLO-IM-Dysplasia in the stomach  Adenocarcinoma (atrophic)
  • Chronic infection  Lymphoma (MALToma) (non-atrophic)
47
Q

Types of ulcers in

  • Antrum-predominant gastritis
  • Body-predominant atrophic gastritis
A
  • Antrum-predominant gastritis  duodenal ulcer

* Body-predominant atrophic gastritis  gastric ulcer

48
Q

Gastric ulcer mx

A

All ulcers should be biopsied to exclude malignancy

49
Q

Gastric vs duodenal ulcer

A

Gastric –> body of stomach, worse with food
Most are caused by H. pylori

Duodenal –> antrum of stomach, relieved with food
Almost all are cause by H. pylori

Duodenal ulcer 4x more common than gastric ulcer

50
Q

Why does gastric intestinal metaplasia happen?

A

In response to long term damage

isn’t cancerous/pre-cancerous but can lead to dysplasia + is associated with an increased risk of cancer

in intestinal metaplasia there will be goblet cells

51
Q

Commonest type of gastric cancer

A

Adenocarcinoma

52
Q

Treatment of H pylori

A

CAP (Clarithromycin, Amoxicillin, PPI)

53
Q

What are the two types of gastric adenocarcinomas?

A

• Intestinal
o Well-differentiated
o Mucin-containing big glands
o Big well-formed glands

• Diffuse
o Poorly differentiated
o Individual cancerous cells spread throughout the stomach
o Single cells with no attempt at gland formation
o Types = Linitis plastica, Signet ring cell carcinoma (spreads all over stomach)

54
Q

What type of lymphoma is MALT

A

B cell NHL

55
Q

How does H. pylori cause duodenal ulcers?

A

Almost all duodenal ulcers are caused by H. pylori

antrum predominant gastritis causes duodenal ulcers

H pylori –> antral infection –> increased stomach acid production –> acid spills over into duodenum –> chronic inflammation –> gastric metaplasia of the duodenal epithelium –> gastric epithelium in the duodenum can now become infected with H. pylori –> duodenitis + ulcer

56
Q

Normal range of intraepithelial lymphocytes

A

<20 lymphocytes per 100 enterocytes

57
Q

Coeliac disease classic histology findings

A

Villous atrophy (flattening/flat)
Normal villous: crypt ratio >2:1
Crypt hyperplasia
Increased intraepithelial lymphocytes

commonest cause = malabsorption

o Lymphocytes in coeliac disease are the cells that are causing damage to the villi

58
Q

What is coeliac disease?

A

T cell mediated autoimmune disease
Abnormal T cell response to gliadin

DQ2 DQ8 HLA associations

young children, Irish women

59
Q

Typical rash seen in coeliac disease

A

Dermatitis herpetiformis

60
Q

How do you diagnose coeliac disease?

A

Antibodies + imaging + biopsy

Antibodies

  • Anti-Endomysial (best sensitivity + specificity)
  • Anti - TTG (also check IgA since these are IgA ab and IgA deficiency might give you a false negative result)
  • Anti-gliadin ab

duodenal biopsy ON gluten free diet showing
Villous atrophy (flattening/flat)
Crypt hyperplasia
Increased intraepithelial lymphocytes

OFF gluten –> normal villi

61
Q

Most serious complication of coeliac disease

A

Enteropathy associated T cell lymphoma (EATL)

type of NHL

found in the duodenum

(n.b. lymphomas in the stomach are due to H. pylori and are B cell lymphomas)

62
Q

• Most oesophageal and gastric cancers arise from pre-existing adenomas – yes or no

A

o No – most gastric + oesophageal gastric cancers arise from a flat dysplasia pathway – chronic inflammation  metaplasia  dysplasia  cancer

o This statement would be true for colonic tumours (adenoma-carcinoma pathway)

Year 5 Path Charis (44 decks)

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