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Flashcards in Histopathology --> Colonic Pathology Deck (88):
1

• IBS

ill-defined (no associated inflammation).

2

• IBD:

Confirmed by use of faecal calprotection, which detects ulceration.

3


Crohn’s Disease → Epi


• Common in North America and Northern Europe
• Prevalence from 30 to 100 per 100000
• Family history common, relative risk for a sibling is 13-36 x normal population
• Maximal incidence in young adults 15-30 years

4


Crohn’s Disease →
Definition

• Any portion of the GI tract can be affected but pattern of anatomical involvement is important
→ 40-50% involvement of both terminal ileum and caecum
→ 20% of patients disease confined to the colon

5


Crohn’s Disease →
Characteristic features

Discontinuous or “skip” lesions on colonoscopy or barium studies are characteristic

6


Crohn’s Disease →
Macroscopic examination

1. Involved bowel potions and associated mesentery thickened and oedematous
→ Small bowel has serosa in crohns = fat surrounds serosa (characteristic of crohns) = fat wrapping.
2. Mucosal lesion typically begins as a superficial ulcer → Apthas ulcer (surface)

7


Crohn’s Disease →
Macroscopic examination as disease advances

Ulcers enlarge, deepen and eventually coalesce to form transverse and longitudinal ulcers, giving “cobblestone” appearance.

8


Crohn’s Disease →
Complications

• Inflammatory mass and anastomotic stricture in a patient with Crohns disease.
• Inflammatory adhesions
• Perforation (very rare)
• Perirectal disease (perianal fistulas and abscesses)
• Malabsorption
• Small bowel adenocarcinoma (difficult to treat)

9


Crohn’s Disease →
Histopathology

1. Transmural inflammation
2. Non-necrotising granulomas (40-60%)
3. Crypt abscess with pus
4. Ulcers may penetrate deeply forming fissures in the muscularis propria leading to abscess and fistula formation – small bowel can attach to large @ wrong point

10


Crohn’s Disease →
Fibrosis and stricture formations

Caused by healing of the penetrating lesions

11


Crohn’s Disease →
Treatment

5-Aminosalycilic acid
Steroids
Immunosuppressive drugs
Monoclonal antibodies against anti-TNF (Infliximab)
Surgery

12


Crohn’s Disease →
Anti-TNF used in

Primarily in patients with fistulae

13


Crohn’s Disease →
Problem with surgery

Neoterminal Ileum – the crohns starts to infiltrate other parts

14

Ulcerative Collitis →
Epi

• Common in North America and Northern Europe
• Prevalence – 35-50 in 100000
• Family history is common, relative risk for a sibling is 7-17.
• Maximal incidence in young adults in young adults 20-50 yrs. Second peak 60-70 yrs.

15

Ulcerative Collitis → Histologically

1. Crypt abscesses with neutrophils within the crypt, in the crypt wall and in the lamina propria → stops here
2. Crypt architerual distortion, with gland branching

16

Ulcerative Collitis →Complications

• Toxic megacolon
• Perforation – in caecum (thinnest portion of bowel)
• Massive haemorrhage
• Colon Cancer (correlation with colonic involvement and duration of disease) → dysplasia and carcinoma

17

Ulcerative Collitis →Toxic Megacolon presentation

• High Fever
• Tachycardia
• Diarrhoea

18

Ulcerative Collitis →Toxic Megacolon due to

• Paralysis of the motor function of the transverse colon
• Mortality 30%

19

Ulcerative Collitis →Treatment

• 5-ASA
• Steroids
• Immunosuppressive drugs High Fever
• Tachycardia
• Diarrhoea
• Surgery (whole colon)

20

Ulcerative Collitis - Dysplasia and carcinoma proportional to

Extent and duration of disease = with biliary disease if you pouch = fistula form.
→ Inflamm in pelvis difficult to manage

21

Colorectal Polyps → Definition


Proturbent growth – from surface not specific for underlying pathology
Epithelial (very common)
Mesenchymal (uncommon)
Benign or Malignant

22

Colorectal Polyps → Classification

Inflammatory
Hamartomatous
Neoplastic
Others

23

Colorectal Polyps →Inflammatory

Pseudopolyps
Benign lymphoid polyps

24

Colorectal Polyps →Hamartomatous

Juvenile polyp
Peutz-Jegher

25

Colorectal Polyps →Neoplastic

Adenoma
Adenocarcinoma

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Colorectal Polyps → Others

Hyperplastic
Lipoma
Leimyoma

27

Inflammatory Pseudopolyps: Pseudo because

Not ademonas

28

Inflammatory Pseudopolyps: Found in

UC and Crohns

29

Inflammatory Pseudopolyps: Macroscopically

Look like adenomas

30

Inflammatory Pseudopolyps: Microscopically

Inflammatory tissue, hyperplastic mucosa

31

Hamartomatous Polyps: Hamartoma

Benign tumour-like lesion
Two or more differentiated tissue elements normally present in the organ

32

Hamartomatous Polyps:Types

Juvenile
Peutzjegher

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Hamartomatous Polyps: Juvenile

Most common paediatric
GI polyps

34

Hamartomatous Polyps:Peutz-Jegher

GI polyps
Pigmentations of oral mucosa, lips, palms genitalia

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Juvenile Polyps: Histologically

Cystic glands with normal or inflamed epithelium

36

Juvenile Polyps: Germ Line

SMAD4 mutation (18q21-2) (25-30%)

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Juvenile Polyps:Present in age

Children age 8 but in adults also

38

Juvenile Polyps:Present in

Rectum

39

Juvenile Polyps: Clinical manifestations

Bleeding (up to 95%), prolapse (because its in the rectum).

40

Peutz-Jeghers Polyps doinanceDominance

Autosomal dominant

41

Peutz-Jeghers Polyps Occur

Throughout the GI tract

42

Peutz-Jeghers Polyps Common in

Small bowel compared to large bowel

43

Peutz-Jeghers Polyps Complications

Intussusception and partial or complete obstruction

44

Peutz-Jeghers Polyps Adenoma/Carcinoma in PJP

Carcinoma develops from dysplastic foci (73% GI tract)

45

Neoplastic Polyps: Adenoma definition

All are dysplastic
Disregulated proliferation
Failure to fully differentiate
Premalignant

46

Neoplastic Polyps: Classification

Tubular – tubular growth
Tubulovillous -outgrowth
Villous – more than 75% villous

47

Neoplastic Polyps: Flat/Depressed

High malignant potential (even if small)
High incidence of severe dysplasia
Associated with familial colon cancer syndromes, HNPCC (50%) or FAP

48

Neoplastic Polyps Malignant potential of adenomas is proportional to

Villosity (25-85%) of villous adenomas may contain cancer

49

Neoplastic Polyps Size

30% of villous adenomas >5cm may contain cancer)
Degree of dysplasia (severe)

50

HyperPlastic Polyp: Commonest in

Adults

51

HyperPlastic Polyp: Presentation

Asymptomatic, any age but increase in 60s and 70s, mostly rectosigmoid

52

HyperPlastic Polyp: Size

Small >5mm, sissile nodule

53

HyperPlastic Polyp: Malignant potential

Benign, no malignant potential unless they are mixed (hyperplastic – adenomatous polyps, Serrated Aenomas) – disorder of maturation rather than proliferation.

54

Leiomyoma: Presents with

Intersusception

55

Leiomyoma: Found in

Rectum, as well as jejunum, ileum
Muscularis Mucosa

56

Leiomyoma: Symptoms

Anaemia
Bleeding due to ulceration
Epigastric pain

57

Colorectal Cancer → Epi

Peaks a 75-80 yrs
Carcinoma colon F>M
Carcinoma rectum M>F

58

Colorectal Cancer → Location %

Right colon 25%
Left colon 15%
Rectosigmoid 50% (status of carcinogens)

59

Colorectal Cancer →Right Colon characteristics

Polypoid
Mass
Discomfort/anaemia (premenopausal and male – find out why?)

60

Colorectal Cancer →Left Colon characteristics

Anular, obstructing
Bleeding/mucus
Colicky pain
Change of bowel habit

61

Colorectal Cancer →Screening

Colonoscopy:
1. UC
2. FAP/HNPCC
3. Adenomatous Polyps
Faecal occult bloods (False positives) + 55 yrs
Flexible sigmoidoscopy
Genetic testing (close relatives)

62

Colorectal Cancer → Spread

Direct
Lymphatic
Vascular (Liver, lungs, bones)

63

Colorectal Cancer → Complications

Obstruction
Perforation
Bleeding
Pericolic abscess
Fistulae
Intussusception

64

Colorectal Cancer →Staging (see notes)

Dukes classification
TNM staging

65

Colorectal Cancer → Survival Dukes @ 5 yrs

A = 99%
B = 75%
C = 35%

66

Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Dominance

Dominant

67

Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Age

Carcinoma develops younger

68

Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Location

Right sided

69

Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Genetics

Abnormalities in 4 mismatched repair genes (microsatellite instability)

70

Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Identifying HNPCC

Amsterdam Criteria (see lecture notes)

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Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Epi

Relatively rare condition 1/8000

72

Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Without intervention

Virtually all people with this condition will develop colon cancer

73

Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Characterised by

Multiple polyps throughout the entire colon (up to thousands)

74

Familial colorectal Cancer Syndrome: HNPCC (hereditary non-polyposis carcinoma) Surgery

Colectomy as thousand of polyps so cant do polpectomy

75

Section 3 → Malabsorption Pathogenesis


• Autoimmune condition
• Immunological response to gluten and related prolamines
• Causing villous atrophy of the lining of the small bowel
• Genetically susceptible people
• Heavily dependent on human leukocyte antigen (HLA) → specifically HLA DQ2 and DQ8 haplotypes

76

Section 3 → Malabsorption Presentation

2 categories:
1. Classical
• Symptoms of malabsorption
→ Weight loss
→ Chronic diarrhoea
→ FTT
2. Non-classical
• IBS type symptoms
→ Abdominal pain
→ Altered bowel habit
→ Anaemia

77

Section 3 → Malabsorption Investigations

Serological tests
Duodenal biopsy
Ensure counselling is carried out prior to testing

78

Section 3 → Malabsorption Serological tests

IgA
• Total
• Anti tTG
Endomysial Antibody (EMA)
Deamidated gliadin peptide (DGP)
HLA typing
Anti tTG IgG – if IgA deficient

79

Section 3 → Malabsorption Counselling

Gluten free diet and risk of untreated

80

Section 3 → Malabsorption Duodenal biopsy

Via endoscopy
3 + biopsy
• Previously beyond D2
• Now also recommended biopsies from D1
Location of each biopsy must be communicated with the pathologist
Different normal architecture of the villi in D1

81

Section 3 → Malabsorption Histology

Modified Marsh criteria
1. Increased IELs with norma villous architecture (MARSH type 1) is non-specific for CD but diagnosis strengthened by strongly positive serology]
2. Increased IELs with crypt hyperplasia (Marsh type 2) compatible with CD: diagnosis strengthened by positive serology; if serology negative, reconsider CD after exclusion of other disorders
3. MOST IMPORTANT → The most important → villous atrophy with crypt hyperplasia and increased intraepithelial lymphocytes (IELS) >30/100 epithelial cells – characteristic CD

82

Section 3 → Malabsorption Guidelines

Joint BSPGHAN and Coeliac UK guidelines for the diagnosis and management of coeliac disease in children.
Increasing prevalence
• Estimated 1/100 people
• 10-20% of this figure are diagnosed
No current universal screening but the new guidelines suggest that we should have a low threshold for investigating
• Symptomatic children
• Associated conditions

83

Section 3 → Malabsorption Symptoms/Signs

Persistent diarrhoea
Constipation
Faltering growth/weight gain
Abdominal pain/distension
Dental enamel defects
Delayed menarche
Unexplained anaemia/ iron deficient
Dermatitis herpetiformis
Osteporosis/path fracture
Recurrent apthous stomatitis
Unexplained liver disease
Weakness

84

Section 3 → Malabsorption Associated conditions

Type 1 diabetes (>8%)
Selective IgA defiency (1.7-7.75)
Chromosome disorders e.g. downs + turners
Autoimmune thyroiditis
Autoimmune liver disease
Intussusception

85

Section 3 → Malabsorption Family history

First-degree relative (10%)
HLA-matching sibling (30%-40)
Monozygotic twin (70%)

86

Section 3 → Malabsorption Gluten rechallenge

3 months gluten challenge prior to testing
Minimum of 4-6 weeks if symptomatic
Needs to be adequate gluten in diet 10-15g/day
Follow up for 2 years post challenge with serology at 6 monthly intervals

87

Section 3 → Malabsorption Treatment

Gluten free diet (GFD) diet after diagnosis
• Food with gluten 20 ppm or less
• Education to improve compliance
Lifelong dietician input
• Within 2 weeks of diagnosis
• FU 3-6 monthly
Case summary in notes
Advise families to join coeliac UK
Pneumococcal vaccine
Aimto normalise serology within 12 months

88

Section 3 → Malabsorption Monitoring

Paeds gastroenterologist and paeds dietician
Symptoms
Growth
Adherence to GFD
Bloods:
• Micronutrient status
• Calcium and iron
• Anti TTG antibodies
Transition to adult care when appropriate

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