Week 21 Pathology


  • Dilations in portosystemic veins due to increased pressure in portal venous system
  • Can rupture and lead to lifethreatening bleeding.
  • For cirrhotic patients with varices, bleed risk is 30%, reduced to 15% by treatment:
  • Primary
    • Non specific B blocker: propanolol
    • Endoscopic banding
  • Secondary
    • 80% will bleed again in 2yrs
    • Transjugular intrahepatic portosystemic shunting (TIPSS)


Barrett’s oesophagus.

  • Reversible change/metaplasia from squamous epithelium to columnar epithelium usually secondary to GORD.
  • Premalignant adenocarcinoma. With low-grade dysplasia, 6-monthly endoscopy for 1 year, followed by endoscopy at 2- to 3-yearly intervals (along with intensive medical therapy) has been suggested. There is much controversy over high-grade dysplasia, as approximately a quarter do not progress to cancer; oesophagectomy is associated with a mortality of 3-10% and high morbidity.


Peptic ulcers:

Gastri Duodenal
Site Gastric antrum, lesser curve Duodenum
Pathogenesis H pylori 80% H Pylori 90%, 4x as common,
Complications 50% asymptomatic
Mucosa reddened macroscopically, epithelia cell damage, inflammatory infiltrate(PMNs, eosinophils, lymphocytes, plasma cells) histologically Thought to reduce somatostatin production, increase parietal cell mass, reduced bicarb in duodenum.pathology- inflammed, haemorrhagic, friable vessels. Superficial mucosal defect. Not to the muscularis mucosa like GU.
  • RF: smoking, NSAIDs, stress), gastric malignancy, inflammation, GORD, NSAID, asprin, steroid use, Crohns, pancreatic cancer, lymphoma
  • Complications:
    • Bleeding
    • Perforation
    • Malignancy
    • Gastric outflow obstruction

Helicobacter pylori – G neg urease producing bacterium


Ca stomach:

  • Stromal tumours
    • Asymptomatic, surgically resected, imatinib(tyrosine kinase inhibitor) if unresectable. Slow growing.
  • Adenocarcinoma
    • 8th most fatal cancer in UK. High in Japan and Chile
    • Uk: 15/100 000, Peak incidence 50-70yo, M>W
    • Strong link to H pylori. (intrafamilial spread)
    • RF: high salt diet, smoking, H Pylori, family Hx, pernicious anaemia, reflux, caustic damage, RT, ulcers
    • Pathology: polypoid or ulcerating lesions with rolled edges and nearby intestinal metaplasia. Scattered type also there. Borrmann classification.
    • Clinical features: epigastric pain relieved by foods and antacids(like peptic ulcer), nausea, annorexia, weight loss, vomiting(esp if near pylorus), dysphagia(esp of near fundus), anaemia from occult blood loss.
    • 2/3 Patients present at stage 3 or 4. May have mets–> ascites, jaundice, bone, brain, lung symptoms. Virchows node.
    • 50% have epigastric mass + tenderness, virchow’s node, mets in 1/3
    • Associated with dermatomyositis, acanthosis nigricans.
    • Rx:
      • Surgical survival – 5yrs 30%
      • Surg combined with chemo-RT- better.
      • Overall survival at 5yrs 10%
  • Lymphoma
    • 10% of all gastric malignancies
    • Non Hodgkins
    • Presents like gastric carcinoma
    • Chemo + RT–> 75% 5yr survival
  • Gastric polyps
    • Removed due to premalignant potential
    • Most gastric carcinomas dont arise from polyps unlike in the colon.



  • Gut organisms invade appendix wall due to faecolith blocking or lympoidd hyperplasia or filarial worms.
  • Leading to
    • Oedema
    • Ischaemic necrosis
    • Perforation–> local abscess or generalised peritonitis


Infective gastroenteritis.

  • Causes
    • Staph aureus – toxin
    • Cholera – toxin
    • Shigella
    • E Coli – EHEC, ETEC, EIEC, EAEC
    • Rota virus
    • Adeno virus


Inflammatory bowel disease

  • Crohn’s disease.
    • Transmural granulomatous inflammation
    • Whole GIT
    • 50% terminal ileum
    • Proximal colon
    • Skip lesions
    • Prevalence: 75/100 000, Incidence: 7.5/100 000/yr, Smoking increases risk 3-4 times
    • Oral ulcers, abdo tenderness, RIF mass, perianal fistula/abscess/skin tags, anal/rectal strictures
    • Extra intestinal: clubbing, erethema nodosum, conjunctivitis, iritis, large joint arthritis, fatty liver, renal stones, osteomalacia, malnutrition.
    • Bowel: fat wrapping, LN in mesentry, irregular and thicker  large bowel
      Complications: Small bowel obstruction, toxic dilation, abscess, fistulae(10%), perforation, haemorrhage, carcinoma(rarer than UC).
  • Ulcerative colitis.
    • Colonic mucosa- continuous lesions
      • 50% just affect rectum- proctitis
      • 30% left sided colitis
      • 20% pan colitis
      • Never ascends past ileocaecal valve.
    • Haemorrhagic granular colonic mucosa. Punctate ulcers may extend deep into LP, Inflammation is normally not transmural.
    • Prevalence: 150/100 000, incidence 15/100 000/yr
    • 3x more common in non smokers, may relapse on quitting
    • Extraintestinal: clubbing, oral ulcers, erythema nodosum, conjunctivitis, iritis, large joint arthritis, fatty liver, renal stones, osteomalacia, nutritional defecits.
    • Severity: freq(4,6), bleeding, ESR(30), anaemia(11), HR(70), temp(37.8) (Truelove and Witts severity index criteria)
    • Back wash ilitis–> B12 def anaemia. (Backwash ileitis, the involvement of the terminal part of the ileum in ulcerative colitis following the ascent of the condition from the rectum)
    • Complications: perforation, bleeding, toxic colonic dilation, venous thrombosis, Colonic cancer(15% in 20yrs)


Bowel obstruction.

  • Causes.
    • Small bowel
      • 3-5cm
      • 60% adhesions
      • 15% hernias
      • 10% Crohns
      • 10% neoplasm
    • Large bowel:
      • >5cm
      • Neoplasm
      • Diverticulitis
      • Hernia
      • 10% Volvulus- 40% occur in preg. Seen more in institutionalised pts, makes bird’s beak appearance on AXR.
    • Intersusseption: most often in toddlers, if in adults usually due to cancer.



Diverticular disease:

  • Common in elderly
  • In 50% of >50yo
  • Commonly in colon, esp sigmoid
  • Diverticular disease means presence of diverticulum, diverticulitis means inflammation of diverticulum.
  • Associate to low fibre diet.
  • Weakness in colon wall. Protrusions of mucosa between muscle fibres.
  • Faeces obstructs diverticula–>stagnation, bacterial multiplication–> inflamm–>
  • Complications
    • Perforation–>abscess or generalised peritonitis, ileus, shock
    • Fistula–>disuria, vag discharge
    • Intestinal obstruction (after a few attacks), post op strictures.
    • Bleeding—-maybe massive- embolise or diathermy with adrenaline.
    • Abscesses- swinging fever, leucocytosis, local boggy rectal mass or not, always do abdo CT or US to check for abscesss including under the diaphragm.


Ca bowel:

  • Polyp like elevation above mucosa
    • Precursor(majority adenomas) to adenocarcinoma
    • Single, multiple, hundreds
    • Types
      • Adenoma- main source of colorectal cancers
      • Juvenile
      • Peutz Jeghers
      • Metaplastic- sigmoid and rectum, high neoplastic potential
      • Lymphoid
      • Inflam
  • Familial adenomatous polyposis- APC mutation(don’t slough off), auto dom.
    • Prophylactic colectomy.
    • Other cancers associates: thyroid, pancreas, hepatoblastomas, congen hypertrophy of retinal pigment epithelium.
  • Hereditary Non polyposis Colon cancer- MMR mutation.
  • PC:
    • Asymptomatic- most
    • Anaemia
    • Diarrhoea, hypokalaemia
    • Screening(FOB) and removal of polyps has reduced colon cancer deaths, though FOB isn’t very sensitive.

Factors affecting risk of malignant changes in adenoma

Higher Risk Lower Risk
Size >1.5cm <1cm
Type Sessille or flat Pedunculated
Histology Severe dysplasiaVillous Architecture Mild DysplasiaTubular Architecture
Squamous Metaplasia
Number Single Polyp Multiple Polyp


Colorectal Carcinoma

  • PC:
    • RHS lesion- anaemia(occult blood loss),
    • LHS lesion- obstruction/change in bowel habits with or without ab pain,
    • rectal/sigmoid have blood in stool, MASS in 60% (do DRE!!!.)
    • Intestinal ob in elderly.
    • Warning signs:  anorexia and weight loss, faecal incontinence, tenesmus and passing mucus per rectum.
  • RF: age, FHx, genetic, env(low fibre diet), IBD, polyposis syndromes, personal history of polyps or CC.
    • FAP: Germline mutations of the APC gene
    • HNPCC: germline mutations in any one of five mismatch repair (MMR) genes. Other cancers frequently occur in HNPCC, including endometrial, gastric, biliary tract, urinary tract, ovarian and small bowel malignancies.
  • Prevelance: 2nd biggest killer in Aus after lung ca, affect one in 2 by age 85. Slightly more in men. Average age of dx 60-65.
  • Path:  a polypoid mass with ulceration, spreads by direct infiltration through the bowel wall. It involves lymphatics and blood vessels with subsequent spread, most commonly to the liver. Synchronous tumours are present in 2% of cases.
  • Histology is adenocarcinoma with moderately to well differentiated glandular epithelium with mucin production. ‘Signet ring’ cells in which mucin displaces the nucleus to the side of the cell are characteristic.
    • Adenocarcinoma predominantly, Squamous cell carcinoma and adenosquamous carcinoma rare.
  • Duke’s Staging- A: confined to mucosa, B1: into but not through the muscularis propria, no nodal inv, B2: through MP but no nodes, C1: into but not through MP, nodes inv, C2: through MP, nodes inv, D: metastatic disease. 5yr survival at dx according to Duke’s: A-90%, B- 65%, C- 30%, D- <10%


Ischaemic gut

  • Disproportionate amount of pain compared to physical signs.
  • Cause – arterial inflow (embolism, thrombus, vasculitis, neoplasm), hypovolaemia/hypotension, obstructed venous outflow
  • Sudden abdo pain and vomiting,
  • Usually SMA, from AF
  • Abdomen usually distended and tender, bowel sounds absent.
  • Pt is hypotensive and ill–> surgery to resect gangrenous bowel. Upto 90% mortality (co morbidities, Multi organ failure, massive fluid and electrolyte loss post surg)–>survivors get short bowel syndrome.