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PathY5 > Lower GI pathology > Flashcards

Lower GI pathology Flashcards

1
Q

What are the types of GI pathology?

A

Congenital

Acquired
Mechanical
Infection
Inflammation
Ischaemia
Tumour

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2
Q

What are the general symptoms of large bowel pathology?

A

Disturbance of normal function (diarrhoea, constipation)
Bleeding
Perforation/fistula formation
Obstruction
+/- Systemic illness

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3
Q

What are congenital GI disorders?

A

Atresia/stenosis
Duplication
Imperforate anus

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4
Q

What is Hirschsprung’s disease?

A

Absence of ganglion cells in myenteric plexus,
Distal colon fails to dilate
80% male
Constipation, abdominal distension, vomiting, ‘overflow’ diarrhoea
Associated with Down’s syndrome (2%)
RET proto-oncogene Cr10 + others

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5
Q

How do you diagnose Hirschsprungs disease?

A

clinical impression
biopsy of affected segment.
hypertrophied nerve fibers but no ganglia.
Treatment: resection of affected (constricted) segment. (frozen section)

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6
Q

What are mechanical bowel disorders?

A

Obstruction
Adhesions
Herniation
Extrinsic mass
Volvulus

Diverticular disease

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7
Q

What is a volvulus?

A 
Complete twisting of a loop of bowel at mesenteric base, around vascular pedicle 
intestinal obstruction +/- infarction 
small bowel (infants) 
sigmoid colon (elderly)
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8
Q

What is the pathogenesis of diverticular disease?

A

High incidence in West
Low fibre diet
High intraluminal pressure
‘Weak points’ in wall of bowel
90% occur in left colon

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9
Q

What are the complications of diverticular disease?

A

Pain
Diverticulitis
Gross perforation
Fistula (bowel, bladder, vagina)
Obstruction

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10
Q

What are the inflammatory disorders of the large bowel?

A

Acute colitis
Infection (bacterial, viral, protozoal etc.)
Drug/toxin (esp.antibiotic)
Chemotherapy
Radiation

Chronic colitis
Crohn’s
Ulcerative colitis
TB

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11
Q

What are the infectious colitis’

A

Viral
Bacterial
Protozoal
Fungal

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12
Q

What are the effects of GI infection?

A

Secretory diarrhoea (toxin)
Exudative diarrhoea (invasion and mucosal damage)
Severe tissue damage + perforation
Systemic illness
(biopsy)

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13
Q

What is pseudomembranous colitis?

A

Antibiotic associated colitis
Acute colitis with pseudomembrane formation
Caused by protein exotoxins of C.difficile

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14
Q

How do you diagnose pseudomembranous colitis?

A

Histology: Characteristic microscopic features on biopsy
Laboratory: C. difficile toxin stool assay

Therapy: Metronidazole or Vancomycin

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15
Q

What is ischaemic bowel?

A

Acute or chronic
Most common vascular disorder of the intestinal tract
Usually occurs in segments in “watershed” zones, e.g. splenic flexure (SMA and IMA) and the rectosigmoid (IMA and internal iliac artery)
Mucosal, mural, transmural (perforation)

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16
Q

What is the aetiology of ischaemic colitis?

A

Arterial Occlusion: atheroma, thrombosis, embolism

Venous Occlusion: thrombus, hypercoagulable states

Small Vessel Disease: DM, cholesterol emboli, vasculitis

Low Flow States: CCF, haemorrhage, shock

Obstruction: hernia, intussusception, volvulus, adhesions

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17
Q

What is IBD?

A

Crohn’s disease or Ulcerative colitis
Diagnosis of exclusion

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18
Q

What is the aetiology of IBD?

A

?Genetic predisposition (familial aggregation, twin studies, HLA )
?Infection (Mycobacteria, Measles etc)
?Abnormal host immunoreactivity

->Inflammation

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19
Q

What are the clinical features of IBD?

A

Diarrhoea +/- blood
Fever
Abdominal pain
Acute abdomen
Anaemia
Weight loss
Extra-intestinal manifestations

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20
Q

Who gets Crohn’s?

A

Western populations
Occurs at any age but peak onset in teens/twenties
White 2-5x > non-white
Higher incidence in Jewish population
Smoking

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21
Q

Where is affected in Crohn’s?

A

Whole of GI tract can be affected (mouth to anus)
‘Skip lesions’
Transmural inflammation
Non-caseating granulomas
Sinus/fistula formation
‘Fat wrapping’
Thick ‘rubber-hose’ like wall
Narrow lumen
‘cobblestone mucosa’
Linear ulcers
Fissures
abscesses

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22
Q

What are the extra intestinal manifestations of Crohns?

A

Arthritis
Uveitis
Stomatitis/cheilitis
Skin lesions
Pyoderma gangrenosum
Erythema multiforme
Erythema nodosum

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23
Q

Who gets UC?

A

Slightly more common than Crohn’s
Whites > non-whites
Peak 20-25 years but can affect any age

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24
Q

What does UC cause?

A

Involves rectum and colon in contiguous fashion.
May see mild ‘backwash ileitis’ and appendiceal involvement but small bowel and proximal GI tract not affected.
Inflammation confined to mucosa
Bowel wall normal thickness
Shallow ulcers

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25
Q

What are the complications of UC?

A

Severe haemorrhage
Toxic megacolon
Adenocarcinoma (20-30 x risk)

26
Q

What are the extra intestinal manifestations of UC?

A

Arthritis
Myositis
Uveitis/iritis
Erythema nodosum, pyoderma gangrenosum
Primary Sclerosing Cholangitis (5.5% in pancolitis)

27
Q

What are the tumours of the colon and rectum?

A
  • Non-neoplastic polyps
  • Neoplastic epithelial lesions
  • Adenoma
  • Adenocarcinoma
  • Stromal tumours
  • Lipoma
  • Sarcoma
  • Carcinoid tumour
  • Mesenchymal lesions
  • Lymphoma
28
Q

What are the polyps of the colon?

A

Polyps - Non-neoplastic
(Hyperplastic)
Inflammatory (“pseudo-polyps”)
Hamartomatous (juvenile, Peutz Jeghers)

Polyps - Neoplastic
Tubular adenoma
Tubulovillous adenoma
Villous adenoma

29
Q

What are adenomas?

A

Excess epithelial proliferation + dysplasia
20-30% prevalence before age 40
40-50% prev. after age 60
Tubular
Villous
Tubulovillous

30
Q

What increases cancer risk in a polyp?

A

Size of polyp (> 4 cm approx 45% have invasive malignancy)
Proportion of villous component
Degree of dysplastic change within polyp

31
Q

What is the evidence of adenomas being a precursor to carcinomas?

A

High prevalence of adenoma = high prevalence of carcinoma
Colonic distribution similar
Peak incidence of adenomas 10 years before peak for Ca.
Residual adenoma near invasive Ca.
Risk proportional to no. of adenomas
Screening + removal of adenomas reduce Ca.

32
Q

What are the symptoms of adenomas?

A

Usually none
Bleeding/anaemia

33
Q

What are the familial syndromes linked to polyps?

A

(Peutz Jeghers)
Familial adenomatous polyposis
Gardner’s
Turcot
Hereditary non polyposis colon cancer

34
Q

What is FAP?

A

Autosomal dominant - average onset is 25 years old
Adenomatous polyps, mostly colorectal
Minimum 100 polyps, average ~1,000 polyps
chromosome 5q21, APC tumour suppressor gene
virtually 100% will develop cancer within 10 to 15 years; 5% periampullary Ca

35
Q

What is Gardeners syndrome?

A

Same clinical, pathological, and etiologic features as FAP, with high Ca risk

Distinctive extra-intestinal manifestations:

  • Multiple osteomas of skull & mandible, epidermoid cysts, desmoid tumors
  • Dental caries, unerrupted supernumery teeth
  • Post-surgical mesenteric fibromatoses
36
Q

What is HNPCC?

A

Uncommon autosomal dominant disease
3-5% of all colorectal cancers
1 of 4 DNA mismatch repair genes involved (mutation)
Numerous DNA replication errors (RER)

37
Q

How does HNPCC present?

A

Onset of colorectal cancer at an early age
High frequency of carcinomas proximal to splenic flexure
Poorly differentiated and mucinous carcinoma more frequent
Multiple synchronous cancers
Presence of extracolonic cancers (endometrium, prostate, breast, stomach)

38
Q

What are colorectal carcinomas?

A

98% are adenocarcinoma
Age: 60-79 years
If < 50yrs consider familial syndrome
Western population

39
Q

What is the aetiology of colorectal carcinomas?

A

Diet (low fibre, high fat etc)
Lack of exercise
Obesity

Familial
Chronic Inflammatory bowel disease

40
Q

What are the symptoms of colorectal carcinomas?

A

Bleeding
Change of bowel habit
Anaemia
Weight loss
Pain
Fistula

41
Q

How do you grade/ stage colorectal carcinomas?

A

Grade = level of differentiation

Dukes’ staging

TNM (tumour, nodes, metastases)

42
Q

How do you treat ischaemic bowel?

A

Resect

43
Q

Do hyperplastic polyps cause cancer?

A

No!

44
Q

What is this?

A

Hirschprungs disease

Similar to bowel obstruction but with Ileus findings due to aganglionosis

45
Q

What is this?

A

Volvulus

Bowel rotation and dilation

46
Q

What is this?

A

Diverticular disease (Barium enema)

Small outpouchings

47
Q

What is this?

A

Pseudomembranous (C Diff) Colitis

Wet Cornflake look

48
Q

What is this?

A

Diverticular disease

49
Q

What is this?

A

Pseudomembranous colitis

50
Q

What is this?

A

Ischaemic bowel

51
Q

What does this show?

A

Crohn’s Disease- Skip lesions

52
Q

What does this show?

A

Crohn’s Disease- Chronic inflammation and deep tissue damage

53
Q

What is this?

A

UC

Some continuous areas of damage with superficiality on microscopy.

54
Q

What does this show?

A

Hyperplastic polyps

55
Q

What is this?

A

Tubular adenoma

Many tube sections can be seen.

56
Q

What is this?

A

Villous adenoma

57
Q

What is this?

A

Familial Adenomatous Polyposis

58
Q

What is this?

A

Apple core lesion (colorectal carcinoma)

59
Q

What is this?

A

Colorectal carcinoma

60
Q

What are the levels of Duke’s Staging?

How do they predict Survival?

A

A = confined to mucosa (5yrSurv=95%+)

B1 = through muscularis propria (5yrSurv=67%)

B2 = transmural invasion, no lymph nodes involved (5yrSurv=54%)

C1 = In muscularis propria with lymph node metastases (5yrSurv=43%)

C2=transmural invasion, lymph nodes involved (5yrSurv=23%)

D = distant metastases (5YrSurv<10%)

PathY5 (98 decks)

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