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Cardio > Histopathology --> Colonic Pathology > Flashcards

Histopathology --> Colonic Pathology Flashcards

1
Q

• IBS

A

ill-defined (no associated inflammation).

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2
Q

• IBD:

A

Confirmed by use of faecal calprotection, which detects ulceration.

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3
Q

Crohn’s Disease → Epi

A
  • 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
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4
Q

Crohn’s Disease →

Definition

A

• 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

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5
Q

Crohn’s Disease →

Characteristic features

A

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

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6
Q

Crohn’s Disease →

Macroscopic examination

A
  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)
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7
Q

Crohn’s Disease →

Macroscopic examination as disease advances

A

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

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8
Q

Crohn’s Disease →

Complications

A
  • 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)
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9
Q

Crohn’s Disease →

Histopathology

A
  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
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10
Q

Crohn’s Disease →

Fibrosis and stricture formations

A

Caused by healing of the penetrating lesions

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11
Q

Crohn’s Disease →

Treatment

A 
5-Aminosalycilic acid
Steroids
Immunosuppressive drugs
Monoclonal antibodies against anti-TNF (Infliximab)
Surgery
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12
Q

Crohn’s Disease →

Anti-TNF used in

A

Primarily in patients with fistulae

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13
Q

Crohn’s Disease →

Problem with surgery

A

Neoterminal Ileum – the crohns starts to infiltrate other parts

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14
Q

Ulcerative Collitis →

Epi

A
  • 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.
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15
Q

Ulcerative Collitis → Histologically

A
  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
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16
Q

Ulcerative Collitis →Complications

A
  • Toxic megacolon
  • Perforation – in caecum (thinnest portion of bowel)
  • Massive haemorrhage
  • Colon Cancer (correlation with colonic involvement and duration of disease) → dysplasia and carcinoma
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17
Q

Ulcerative Collitis →Toxic Megacolon presentation

A
  • High Fever
  • Tachycardia
  • Diarrhoea
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18
Q

Ulcerative Collitis →Toxic Megacolon due to

A
  • Paralysis of the motor function of the transverse colon

* Mortality 30%

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19
Q

Ulcerative Collitis →Treatment

A
  • 5-ASA
  • Steroids
  • Immunosuppressive drugs High Fever
  • Tachycardia
  • Diarrhoea
  • Surgery (whole colon)
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20
Q

Ulcerative Collitis - Dysplasia and carcinoma proportional to

A

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

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21
Q

Colorectal Polyps → Definition

A

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

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22
Q

Colorectal Polyps → Classification

A

Inflammatory
Hamartomatous
Neoplastic
Others

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23
Q

Colorectal Polyps →Inflammatory

A

Pseudopolyps

Benign lymphoid polyps

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24
Q

Colorectal Polyps →Hamartomatous

A

Juvenile polyp

Peutz-Jegher

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25
Q

Colorectal Polyps →Neoplastic

A

Adenoma

Adenocarcinoma

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26
Q

Colorectal Polyps → Others

A

Hyperplastic
Lipoma
Leimyoma

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27
Q

Inflammatory Pseudopolyps: Pseudo because

A

Not ademonas

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28
Q

Inflammatory Pseudopolyps: Found in

A

UC and Crohns

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29
Q

Inflammatory Pseudopolyps: Macroscopically

A

Look like adenomas

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30
Q

Inflammatory Pseudopolyps: Microscopically

A

Inflammatory tissue, hyperplastic mucosa

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31
Q

Hamartomatous Polyps: Hamartoma

A

Benign tumour-like lesion

Two or more differentiated tissue elements normally present in the organ

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32
Q

Hamartomatous Polyps:Types

A

Juvenile

Peutzjegher

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33
Q

Hamartomatous Polyps: Juvenile

A

Most common paediatric

GI polyps

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34
Q

Hamartomatous Polyps:Peutz-Jegher

A

GI polyps

Pigmentations of oral mucosa, lips, palms genitalia

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35
Q

Juvenile Polyps: Histologically

A

Cystic glands with normal or inflamed epithelium

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36
Q

Juvenile Polyps: Germ Line

A

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

37
Q

Juvenile Polyps:Present in age

A

Children age 8 but in adults also

38
Q

Juvenile Polyps:Present in

39
Q

Juvenile Polyps: Clinical manifestations

A

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

40
Q

Peutz-Jeghers Polyps doinanceDominance

A

Autosomal dominant

41
Q

Peutz-Jeghers Polyps Occur

A

Throughout the GI tract

42
Q

Peutz-Jeghers Polyps Common in

A

Small bowel compared to large bowel

43
Q

Peutz-Jeghers Polyps Complications

A

Intussusception and partial or complete obstruction

44
Q

Peutz-Jeghers Polyps Adenoma/Carcinoma in PJP

A

Carcinoma develops from dysplastic foci (73% GI tract)

45
Q

Neoplastic Polyps: Adenoma definition

A

All are dysplastic
Disregulated proliferation
Failure to fully differentiate
Premalignant

46
Q

Neoplastic Polyps: Classification

A

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

47
Q

Neoplastic Polyps: Flat/Depressed

A

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

48
Q

Neoplastic Polyps Malignant potential of adenomas is proportional to

A

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

49
Q

Neoplastic Polyps Size

A

30% of villous adenomas >5cm may contain cancer)

Degree of dysplasia (severe)

50
Q

HyperPlastic Polyp: Commonest in

51
Q

HyperPlastic Polyp: Presentation

A

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

52
Q

HyperPlastic Polyp: Size

A

Small >5mm, sissile nodule

53
Q

HyperPlastic Polyp: Malignant potential

A

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

54
Q

Leiomyoma: Presents with

A

Intersusception

55
Q

Leiomyoma: Found in

A

Rectum, as well as jejunum, ileum

Muscularis Mucosa

56
Q

Leiomyoma: Symptoms

A

Anaemia
Bleeding due to ulceration
Epigastric pain

57
Q

Colorectal Cancer → Epi

A

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

58
Q

Colorectal Cancer → Location %

A

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

59
Q

Colorectal Cancer →Right Colon characteristics

A

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

60
Q

Colorectal Cancer →Left Colon characteristics

A

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

61
Q

Colorectal Cancer →Screening

A 
Colonoscopy:
1.	UC
2.	FAP/HNPCC
3.	Adenomatous Polyps
Faecal occult bloods (False positives) + 55 yrs
Flexible sigmoidoscopy
Genetic testing (close relatives)
62
Q

Colorectal Cancer → Spread

A

Direct
Lymphatic
Vascular (Liver, lungs, bones)

63
Q

Colorectal Cancer → Complications

A 
Obstruction
Perforation
Bleeding
Pericolic abscess
Fistulae
Intussusception
64
Q

Colorectal Cancer →Staging (see notes)

A

Dukes classification

TNM staging

65
Q

Colorectal Cancer → Survival Dukes @ 5 yrs

A 
A = 99%
B = 75%
C = 35%
66
Q

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

67
Q

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

A

Carcinoma develops younger

68
Q

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

A

Right sided

69
Q

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

A

Abnormalities in 4 mismatched repair genes (microsatellite instability)

70
Q

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

A

Amsterdam Criteria (see lecture notes)

71
Q

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

A

Relatively rare condition 1/8000

72
Q

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

A

Virtually all people with this condition will develop colon cancer

73
Q

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

A

Multiple polyps throughout the entire colon (up to thousands)

74
Q

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

A

Colectomy as thousand of polyps so cant do polpectomy

75
Q

Section 3 → Malabsorption Pathogenesis

A
  • 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
Q

Section 3 → Malabsorption Presentation

A 
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
Q

Section 3 → Malabsorption Investigations

A

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

78
Q

Section 3 → Malabsorption Serological tests

A 
IgA
•	Total
•	Anti tTG
Endomysial Antibody (EMA)
Deamidated gliadin peptide (DGP)
HLA typing
Anti tTG IgG – if IgA deficient
79
Q

Section 3 → Malabsorption Counselling

A

Gluten free diet and risk of untreated

80
Q

Section 3 → Malabsorption Duodenal biopsy

A

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
Q

Section 3 → Malabsorption Histology

A

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
Q

Section 3 → Malabsorption Guidelines

A

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
Q

Section 3 → Malabsorption Symptoms/Signs

A 
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
Q

Section 3 → Malabsorption Associated conditions

A 
Type 1 diabetes (>8%)
Selective IgA defiency (1.7-7.75)
Chromosome disorders e.g. downs + turners
Autoimmune thyroiditis
Autoimmune liver disease
Intussusception
85
Q

Section 3 → Malabsorption Family history

A

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

86
Q

Section 3 → Malabsorption Gluten rechallenge

A

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
Q

Section 3 → Malabsorption Treatment

A 
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
Q

Section 3 → Malabsorption Monitoring

A 
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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