Lower GI Pathology Flashcards

1
Q

Name and describe some congenital pathologies of the lower GI tract

A
  • Atresia (duodenal or biliary)
  • Stenosis
  • Duplication
  • Imperforate anus
  • Hirschsprung’s disease (absence of ganglionic cells in myenteric plexus, males, obstruction, managed with resection, associated with Down’s)
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2
Q

Classify the acquired diseases of the lower GI tract

A

Mechanical

  • Constipation
  • Diverticular disease
  • Adhesions
  • Herniations
  • External masses (foetus, foreign body, tumour)
  • Volvulus (twisting of bowel, sigmoid>caecal
  • Intussusception

Inflammatory

  • Acute (infectious, drug induced, iatrogenic)
  • Chronic (IBD, TB)

Ischaemic

  • Ischaemic colitis (arterial/venous occlusion, low blood flow, small vessel disease, obstruction)
  • Watershed areas (splenic flexure - SMA to IMA or rectosigmoid - IMA to IIA)
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3
Q

Describe the epidemiology, aetiology, pathophysiology, clinical features, complications, investigations and management of Crohn’s disease

A

Epidemiology

  • Western population
  • Onset in 20s, F>M
  • Whites
  • Smoking

Aetiology
Unknown

Pathophysiology

  • Whole GI tract (mouth to anus)
  • Skip lesions, cobblestone appearance
  • Non-caseating granulomas
  • Transmural inflammation

Clinical features

  • Intermittent diarrhoea
  • Pain and fever

Complications

  • Strictures
  • Fistulae
  • Abscesses
  • Perforation

Investigations

  • ESR, CRP
  • barium contract and endoscopy

Management

  • Mild: prednisolone
  • Severe: IV hydrocortisone, metronidazole
  • Additional: azathioprine, methotrexate, infliximab
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4
Q

Describe the epidemiology, aetiology, pathophysiology, clinical features, complications, investigations and management of ulcerative colitis

A

Epidemiology

  • More common that CD
  • Onset at 20-25 years

Aetiology
Unknown

Pathophysiology

  • Extends proximally from anus
  • Continuous lesions
  • Does not affect small bowel, unless backwash ileitis
  • Superficial inflammation, confined to the mucosa
  • No granulomas or fistulae or fissures

Clinical features

  • Bloody diarrhoea and mucus
  • Crampy abdominal pain, relieved by defecation
  • Pseudopolyps

Complications

  • Toxic megacolon and perforation
  • Severe haemorrhage
  • 30 percent will need colectomy within 3 years
  • 20-30x risk of adenocarcinoma

Investigations

  • Rectal biopsy
  • Flexible sigmoidoscopy
  • Stool culture

Management

  • Mild: prednisolone and mesalazine
  • Moderate: prednisolone and mesalazine and steroid enemas
  • Severe: admit, NBM, IV fluids, IV hydrocortisone and rectal steroids
  • Remission: mesalazine and azathioprine
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5
Q

What are the extra-gastrointestinal manifestations of IBD

A
  • Malabsorption and iron deficiency anaemia
  • Eyes: uveitis, conjunctivitis
  • Skin: erythema nodosum, pyoderma gangrenosum, erythema multiforme
  • Joints: migratory asymmetrical polyarthropathy of large joints
  • Liver: primary sclerosing cholangitis (UC)
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6
Q

Describe diverticular disease

A

Higher incidence in western populations due to the low fibre diet resulting in a high intraluminal pressure causing outpouchings at the weak points. 90 percent will occur in the left colon.

Complications include infection, perforation, fistula formation and obstruction

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7
Q

Describe how to classify tumours of the colon and the rectum

A
  • Non-neoplastic polyps
  • Neoplastic polyps
  • Colorectal cancer
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8
Q

Describe some non-neoplastic polyps

A

Hamartomatous

  • Found sporadically
  • Juvenile polyps found mostly in rectum and can cause bleeding
  • Usually
  • Juvenile polyposis can cause more than 100 polyps
  • Seen in Peutz-Jegher’s syndrome

Hyperplastic

  • Seen in the elderly
  • Caused by the shedding of the epithelium, causing cell build-up

Inflammatory
- Seen in ulcerative colitis

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9
Q

Describe neoplastic polyps

A

These are adenomas which are benign but are the precursor to most adenocarcinomas.

  • Found in half of those over 60
  • Classified based on architecture: tubular, tubulovillous, villous
  • Villous is rare, and can cause hypoproteinaemia and hypokalaemia
  • Size associated with malignancy risk
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10
Q

Describe some familial syndromes which predispose to colorectal cancer

A

Familial adenomatous polyposis (FAP)

  • 70 percent have a mutation in the APC gene in mismatch repair genes
  • Present at 10-15 years with >100 adenomatous polyps
  • Will become adenocarcinoma if untreated
  • Treated with a prophylactic colectomy

Gardner’s syndrome

  • Like FAP with extra GI symptoms
  • Osteomas
  • Dental caries

Hereditary non-polyposis colorectal cancer (HNPCC)

  • Carcinomas in the right colon
  • Few polyps but a fast progression to malignancy
  • Associated with gynaecological cancers, TCC, small bowel cancers
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11
Q

Describe the epidemiology, aetiology, clinical features, investigations, classification and management of colorectal cancer

A

Epidemiology

  • 2nd most common cancer killer in the UK
  • Present in those 60-79
  • 98 percent are adenocarcinomas

Aetiology

  • low fibre and high fat diet
  • Obesity
  • Chronic IBD
  • NSAIDs are protective (COX2 is overexpressed in 90 percent of the cases)

Clinical features

  • Iron deficiency anaemia
  • Weight loss
  • Change in bowel habit
  • Crampy pain
  • Blood in stool

Investigations

  • Proctoscopy, sigmoidoscopy, colonoscopy, barium enema
  • FBC
  • CT?MRI
  • Carcinoembryonic antigen (CEA)

Classification

  • Duke’s staging system A to D, with worse prognosis as you go down
  • A: confined to mucosa
  • B1: extending to muscularis, no lymph nodes
  • B2: transmural, no lymph nodes
  • C1: extending to muscularis, with lymph nodes
  • C2: transmural, with lymph nodes
  • D: distant metastasis

Management

  • Surgery depending on location and size of cancer
  • Radiotherapy to reduce local recurrence
  • Chemotherapy in palliative cases
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