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53 Cards in this Set
- Front
- Back
(A) ORAL CAVITY
Inflammation Stomatitis |
Inflammation of oral cavity (lips & buccal cavity)
Mainly due to viruses or fungi (HSV Type 1, EBV, Coxsackievirus, Candida albicans) |
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(A) Inflammation
Cheilitis |
Inflammation of the lips
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(A) Inflammation
Glossitis |
Inflammation of the tongue
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(A) Inflammation
Gingivitis |
Inflammation of the gums
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(A) Inflammation
Periodontitis |
Inflammation around teeth
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(A) Inflammation
Dental caries |
Tooth decay
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(A) Inflammation
Sialadenitis |
Inflammation of salivary glands
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(A) Inflammation
Pharyngitis |
Throat inflammation
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(A) Inflammation
Eg. Fluorosis Atrophic glossitis “Strawberry tongue” |
tooth staining
Glossitis - “geographic tongue” due to S.pyogenes |
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Carcinoma of the Oral Cavity
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Includes carcinomata of:
-Lips (esp lower); -Tongue; -Buccal mucosa; -Pharynx; -Higher incidence in males Aetiology: -Smoking (esp pipe); -Chronic irritation (eg. ill-fitting dentures); -Carcinogenic substances (eg. betel nuts) Morphology: -Usually begins as leukoplakia (a dysplasia); -Progresses to invasive squamous cell carcinoma Treatment: -Surgical excision; -Radiotherapy Prognosis: -Very poor |
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(B) OESOPHAGUS
Oesophagitis - |
Inflammation of oesophagus
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(B) Reflux Oesophagitis (Gastroeosophageal reflux disease-GORD/GERD)
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Reflux of gastric acid into lower oesophagus;
burning pain/heartburn, dyspepsia, dysphagia Persistence of reflux causes metaplasia from squamous to glandular epithelium containing goblet cells (ie. Barrett’s oesophagus, may lead to adenocarcinoma) Infections: Candida albicans esp in immunosuppression |
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(B) Oesophageal varices
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Dilated veins due to cirrhosis of the liver and portal hypertension
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(B) Plummer-Vinson Syndrome
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Sideropenic dysphagia; (Lack of iron + difficulty in swallowing/eating)
Aetiology: -Congenital; -Almost always in females Abnormal oesophageal peristalsis coupled with oesophageal strictures and mucosal webs causes dysphagia Symptomatology: -Atrophic glossitis; -Iron deficiency anaemia leading to koilonychia (spoon-shaped nails) Complications: -Severe anaemia; -Carcinoma of the oesophagus |
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(B) Carcinoma of the Oesophagus
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Aetiology:
-Smoking; -Consumption of alcohol; -Chronic oesophagitis; -Geographical, racial factors (China, Japan); -Plummer-Vinson syndrome; -Carcinogenic foods? Morphology: -Squamous cells carcinoma; -Adenocarcinoma less common Symptomatology: -Dysphagia (late!); -Pain, choking sensations, loss of weight; -haematemesis Diagnosis: -Barium meal and X-rays; -Biopsy via an oesophagoscopy Treatment: -Surgery (but often impossible!); -Radiotherapy is palliative; -Chemotherapy ineffective Prognosis: -Grave (5yr survival <10%) |
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(B) Hiatus hernia
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A protrusion of part of the stomach into the thoracic cavity through the diaphragmatic hiatus
Sliding hiatus hernia (95%) Vs rolling (paraoesophageal) hiatus hernia (5%) (see Fig 13.2 in text book) Aetiology: -Congenital weakness in diaphragm; -Obesity and overloading of the stomach; -Late pregnancy Symptomatology: -Same as reflux oesophagitis (burning pain/heartburn, dyspepsia, dysphagia) Diagnosis: -Barium meal, X-rays, endoscopy Treatment: -Avoiding alcohol; -Eating small meals; -Weight reduction; -Antacids; -Surgery |
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(C) STOMACH
Gastritis |
Inflammation of gastric mucosa, acute or chronic in nature
Diagnosis: Endoscopy, confirmed by biopsy |
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(C) Acute (erosive) gastritis
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-Usually due to very heavy acute alcohol ingestion
-Characterized by erosions; -Typical acute inflammation; -“Indigestion”, dyspepsia, epigastric pain, tenderness Results: -Usually resolution with regeneration of mucosa; -Occasionally progression to ulcers or chronic gastritis |
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(C) Chronic gastritis
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-Chronic Helicobacter-associated (hypertrophic) gastritis
-Most common form; -Thickening of the gastric mucosa; -Metaplasia often seen; -Variable clinical effects with hypochlorhydria, hyperchlorhydria; -Good prognosis |
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(C) Chronic atrophic (autoimmune) gastritis
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-Auto-immune disease with autoantibodies against the parietal cells (90%) & intrinsic factor (60%)
-Severe atrophy of mucosa; -Iron deficiency anaemia and pernicious anaemia develops; -Common in females -Incidence increasing with increasing age; -Predisposes to gastric cancer; -Poor prognosis |
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(C) Reactive gastritis
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-Chemical or reflux gastritis;
-occurs when alkaline duodenal fluid (containing bile) refluxes into lower part of stomach -Seen in patients with prolonged administration of non-steroidal anti-inflammatory drugs (NSAIDs), or with damaged pyloric sphincter; -Good prognosis |
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(C) Peptic Ulcers
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-A peptic ulcer is a benign, localized defect consisting of a deep excavation of any part of the GIT mucosa beyond the muscularis mucosae.
-May be acute or chronic -Most common site: Duodenum (due to hypersecretion of acid), followed by stomach (regurgitated bile due to pyloric incompetence, H. pylori, NSAIDS) & oesophagus (reflux of gastric secretions) |
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(C) Acute Peptic Ulcers
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-Progression of acute (erosive) inflammation of mucosa;
-alcohol, aspirin consumption; -H.pylori infection; -NSAIDs -Ulcers heal without much scarring, mucosa regenerates; -May progress to form a chronic peptic ulcer |
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(C) Chronic Peptic Ulcers
Aetiology & symptomology |
-Usually 30-45 years;
-Duodenal ulcers affect males more; -Gastric ulcers are more prevalent in women Aetiology: -Imbalance between protective mechanisms and aggressive factors; -Genetic factors; -Cigarette smoking; -Hypersecretion of acid (e.g. stress, neurogenic factors, Zollinger-Ellison syndrome) -Decreased mucosal blood supply, decreased mucus production; -Helicobacter pylori infection Symptomatology: -Dyspepsia, nausea, heartburn, belching Gnawing pain in epigastrium, 1-3 hours after meals (gastric) -Steady, aching pain in mid-epigastrium or slightly off centre to right, 2-4 hours after meals (duodenal) -Pain relieved by food or antacids -Succussion splash; Vomiting, diarrhoea or constipation |
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(C) Chronic Peptic Ulcers
Sequelae, Diagnosis, Treatment, Prognosis |
Sequelae:
-Most heal but ~50% recur; -Stenosis (“hour glass” stomach); -Haemorrhage (may lead to shock); -Melaena: tarry black stools; -Haematemesis: Vomiting of blood; Perforation, sterile peritonitis due to acid; -Malignancy may supervene in gastric or oesophageal ulcers (NOT duodenal!) Diagnosis: -Gastroduodenoscopy & biopsy; -Barium swallow and X-rays; -Microbiological investigation Treatment: -Antibiotics for Helicobacter infection if microbiologically confirmed; -Antacids, etc for symptomatic relief; -Surgery (for complicated cases); Prognosis: -Very good |
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(C) Adenocarcinoma of the Stomach
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More common in males (≈ 50 yrs)
Aetiology: -Diet (smoked, salt-preserved and pickled foods – generation of nitrosamines) -Genetics (Blood group A) -H.pylori infection -Racial/geographical factors (related to diet/genes: Japan, China, Finland, Chile) -Premalignant diseases (chronic peptic ulcer, chronic atrophic gastritis, benign tumours- adenomatous polyps) Spread: -Direct to serosa; -Lymphatic early; -Transcoelomic to other organs in abdomen; -Blood to liver/lungs/bone Symptomatology: -Tumours present late; -Early warning signs very non-specific (“indigestion”; vague epigastric discomfort); Gradual onset of weight loss; -Haematemesis, melaena, anaemia; -Nausea, vomiting; -Back pain (pancreatic involvement) Diagnosis: -Gastroscopy, biopsy; -Barium meal, X-rays; Treatment: -Surgery – gastrectomy; (~50% of diagnosed tumours inoperable); -Radiotherapy/chemotherapy not very effective; Prognosis: Grave |
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(D) SMALL INTESTINE
Diverticula: |
Outpouchings in the walls of tubular organs, commonly occurring in the intestine
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(D) Diverticulosis
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diverticula present - often asymptomatic
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(D) Diverticulitis
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inflamed diverticula are present - symptomatic!
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(D) True diverticulum
False diverticulum: |
All layers of wall; Usually congenital
Only mucosal layer; Usually acquired |
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(D) Meckel’s Diverticulum:
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Congenital;
Mostly asymptomatic; Has pancreatic/gastric choristomata; Meckel’s diverticulitis (“left-sided appendicitis”) |
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(D) Diverticulosis of the Jejunum:
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False diverticula form in the jejunum, (multiple, solitary or few in number) and mostly symptomless
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(D) Crohn’s Disease
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May occur anywhere in GIT but most commonly in ileum (regional ileitis); More common in women (20-60yrs)
Relapsing-remitting, chronic granulomatous inflammatory disorder Aetiology: Idiopathic, although the pathogenesis is thought to be autoimmune Morphology: Transmural granulomatous inflammation (skip lesions/cobblestone pattern) Complications: Ileus; Mucosal & deeper ulceration; fissure & fistula formation; “Rubber hose intestine” Symptomatology: Clinically confused with ulcerative colitis, Abdominal pain, slight fever (≈75 % cases); May present as acute appendicitis; Intermittent diarrhoea, weight loss; Recurrent anorectal fistulae; Vitamin B12 deficiency, anaemia; Steatorrhoea (due to malabsorption) Diagnosis: Clinical presentation; Endoscopic biopsy; Barium enema, X-rays; Raised ESR and leukocytosis, anaemia Treatment: Antibiotics, steroids, Vit B12 supplements; Modify diet; Surgical excision, repair, colostomy Prognosis: Variable; Permanent remission, premalignant in colon |
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(D) Malabsorption Syndrome
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Poor absorption of foodstuffs and products of their digestion from the intestine
Due to: -pancreatic insufficiency; -parasitic & worm infestation; -resection of ileum; -Crohn’s disease; -liver disease; -Coeliac disease (gluten enteropathy): Autoantibodies to gluten (protein found in wheat, rye, barley, oats) causes mucosal atrophy & inflammation, malabsorption, steatorrhoea |
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(D) Tumours
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Rare eg. Lipomas, Leiomyomas, Carcinoid Tumour (Argentaffinoma)
Carcinoid tumour derived from the amine precursor uptake and decarboxylation (APUD) cells: secrete serotonin Carcinoid syndrome due to serotonin excess: Flushing of the face (with alcohol); Cyanosis, diarrhoea, ascites, oedema; Bronchospasm (resembling asthma attack) |
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(E) APPENDIX
Acute appendicitis: |
Typically in young people, male/female;
Acute inflammatory condition presenting as an “acute abdomen”; Surgical emergency – appendectomy (NB: 10% normal), otherwise may rupture, peritonitis, death Aetiology: Obstruction thought to occur first by faecolith/swallowed foreign objects (e.g. pips, seeds) then 2o infection |
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(E) Mucocoele of Appendix:
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Obstruction of appendix without infection; Accumulation of mucus in the organ
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(F) INFECTIONS OF SMALL & LARGE INTESTINE
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Transmitted by contaminated food/water - cause diarrhoea, fever, ‘food poisoning’ symptoms
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(F) Viruses:
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Rotaviruses, caliciviruses (Norwalk viruses), enteric adenoviruses cause inflammation, gastroenteritis
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(F) Bacteria:
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-Salmonella typhi, Campylobacter jejuni cause direct damage to bowel
-Escherichia coli produces enterotoxin -Yersinia causes ulceration, ileitis |
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(F) Protozoa
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-Giardia lamblia infection of small bowel (due to contaminated water), causes malabsorption
-Entamoeba histolytica (spread by food/water contaminated with stools) causes dysentery-like symptoms |
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(G) INTESTINAL OBSTRUCTION
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Ileus = intestinal obstruction due to any cause
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(G) Volvulus
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Twisting or rotation of a loop(s) of bowel and mesentery through at least 180˚, resulting in ileus
Vascular obstruction may then progress to gangrene of the bowel; “Acute abdomen” |
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(G) Meconium ileus
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Meconium is the thick, sticky, greenish-black first stool of a newborn
Intestinal obstruction by the meconium is termed meconium ileus – seen in 10-20% cases of cystic fibrosis |
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(G) Intussusception
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Invagination of one portion of intestine into the lumen of the bowel immediately distal to it (“telescoping” effect”)
Most common site is at ileocaecal valve (ileum invaginates into caecum); Results: Similar to volvulus |
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(H) COLON
Ulcerative colitis |
Chronic inflammation of the mucosa of the colon (sigmoid, rectum most commonly) - pseudopolyp formation
Aetiology: Idiopathic, non-granulomatous, active chronic inflammatory disease Autoimmunity implicated = non-specific ulcerative colitis NB: Specific ulcerative colitis is an infection with Entamoeba histolytica (= amoebic dysentery) Morphology: In between ulcers, hyperplasia of mucosa leads to pseudopolyp formation (for both types) Non-specific ulcerative colitis: Symptomatology: Similar to Crohn’s disease; intermittent diarrhoea, anaemia, weight loss; in some individuals also iritis, stomatitis, arthritis, skin rashes, anaemia Diagnosis: Clinical presentation; Colonoscopy & biopsy; Barium enema & X-rays; Stool examination & culture (to exclude amoebic/bacterial colitis) Treatment: A high calorie, high protein diet, no milk intake may control diarrhoea; Corticosteroids decrease inflammation; Blood transfusion, electrolyte replenishment, parenteral nutrition; Surgery: Colectomy Prognosis: Variable; long standing disease may lead to colon cancer |
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(H) Diverticulosis of the Colon
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Multiple false diverticula form in the colon (through weak points of muscle), especially in the rectum and sigmoid
Incidence: Very common (~50% >60 yrs on ‘Western’ diet); M:F equal Aetiology: Low fibre, red meat, high saturated fats, highly processed foods; Chronic constipation; Abnormal peristalsis, hypertrophy of colonic muscle (abnormal contractility of muscularis propria) Symptomatology: Vague Ssx of abdominal discomfort; Alterations in bowel habit Complications: Acute abdomen (esp. with perforation); fistula, abscess formation Diagnosis: Sigmoidoscopy (excludes rectal carcinoma and ulcerative colitis); Barium enema, X-rays Treatment: Diverticulosis - diet alteration; Laxatives; Diverticulitis - antibiotics, surgery |
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(H) Benign Colonic Tumours
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Incidence:
Very common, sigmoid colon and rectum; more common in males, ≈ 55 years Morphology: Adenomatous polyps ≈90% of lesions; Villous adenomata ≈10% of lesions; All premalignant! Symptomatology: Often asymptomatic Incidental diagnosis in a routine colonoscopy; Haemorrhage; Alteration of bowel habit Complications: Premalignant! The larger (esp > 2 cm diam), flatter, more villous the lesion, the greater the risk Diagnosis: Clinical presentation; Colonoscopy & biopsy; Barium enema, X-rays Treatment: Diathermy via colonoscopy; Surgical resection |
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(H) Familial Polyposis Coli
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Autosomal dominant. Hundreds of benign adenomatous polyps form in GIT (mostly colon, rectum)
Develop in adolescence, early adulthood; If not there by ≈40 yrs, they will not develop Predisposes to carcinoma within 15-20 years |
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(H) Other Inherited Benign Neoplasms
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Peutz-Jeghers syndrome : Autosomal dominant; benign polyps; harmatomas in small & large intestine; increased melanin pigmentation in the mucocutaneous junctions, around mouth; predisposes to carcinoma of colon
Gardner’s syndrome : Autosomal dominant; benign polyps; osteomas; predisposes to carcinoma of colon Turcot’s syndrome: Autosomal recessive; benign polyps; Malignant gliomas; predisposes to carcinoma of colon |
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(H) Colonic Carcinoma
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Incidence: Very common, >55 years, up to twice as common in men
Aetiology: Genetic factors “Western” diet, low fibre, high saturated fats, highly processed foods, red meats Chronic constipation Clostridium paraputrificum metabolism of bile acids (some biles derivatives are carcinogenic), Premalignant diseases ie. Familial polyposis coli: Gardner’s syndrome; Benign, solitary tumours; Peutz Jegher’s syndrome; Turcot’s syndrome; Ulcerative colitis; Crohn’s disease; Previous colonic cancer Sites: rectum and sigmoid most common Morphology: Fungating, polypoid, ulcerative, mucoid, infiltrating, annular Histopathology: Most are well differentiated adenocarcinomata (NB: mucus secreting) Spread: Direct local - involves wall; Lymphatic - involves draining nodes; Haematogenous - to liver and lungs Symptomatology: Changes in bowel habit, Dyspepsia and vague abdominal pain Mucus and blood (occult faecal blood, haemochezia) in faeces, Intestinal obstruction, Anaemia with fatigue, lassitude and weakness, Perforation, peritonitis, 2˚ bacterial infection, fistula formation, cachexia Diagnosis: Colonoscopy & biopsy; Barium enema and X-rays Treatment: Surgical resection, colostomy; Stapling anastomosis preserves normal defaecation Prognosis: TNM score combined with Duke’s staging system (see Figure 13.16 in prescribed text) Duke’s stage A: Tumour in mucosa, submucosa (5-year survival is ~93%) Duke’s stage B: Tumour in all layers (5-year survival is ~72-85%) Duke’s stage C: Tumour in lymph nodes (5-year survival is ~44-83%) Duke’s stage D: Tumour with distant metastases (5-year survival is 8%) |
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(H) Carcinoma of the Anal Canal
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Rare tumour in middle to old age;
metastasizes early via lymphatics; poor prognosis |
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(H) Haemorrhoids
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Varicosities in the venous channels of the internal haemorrhoidal plexi; Very common in developed world
Aetiology: Diet, chronic constipation, obesity, pregnancy and portal HT all predispose Symptomatology: Pain, haemorrhage, anaemia, rectal prolapse Treatment: Haemorrhoidectomy |