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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)
(A) Inflammation
Cheilitis
Inflammation of the lips
(A) Inflammation
Glossitis
Inflammation of the tongue
(A) Inflammation
Gingivitis
Inflammation of the gums
(A) Inflammation
Periodontitis
Inflammation around teeth
(A) Inflammation
Dental caries
Tooth decay
(A) Inflammation
Sialadenitis
Inflammation of salivary glands
(A) Inflammation
Pharyngitis
Throat inflammation
(A) Inflammation
Eg. Fluorosis
Atrophic glossitis
“Strawberry tongue”
tooth staining
Glossitis - “geographic tongue”
due to S.pyogenes
Carcinoma of the Oral Cavity
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
(B) OESOPHAGUS
Oesophagitis -
Inflammation of oesophagus
(B) Reflux Oesophagitis (Gastroeosophageal reflux disease-GORD/GERD)
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
(B) Oesophageal varices
Dilated veins due to cirrhosis of the liver and portal hypertension
(B) Plummer-Vinson Syndrome
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
(B) Carcinoma of the Oesophagus
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%)
(B) Hiatus hernia
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
(C) STOMACH
Gastritis
Inflammation of gastric mucosa, acute or chronic in nature

Diagnosis: Endoscopy, confirmed by biopsy
(C) Acute (erosive) gastritis
-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
(C) Chronic gastritis
-Chronic Helicobacter-associated (hypertrophic) gastritis
-Most common form;
-Thickening of the gastric mucosa;
-Metaplasia often seen;
-Variable clinical effects with hypochlorhydria, hyperchlorhydria;
-Good prognosis
(C) Chronic atrophic (autoimmune) gastritis
-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
(C) Reactive gastritis
-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
(C) Peptic Ulcers
-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)
(C) Acute Peptic Ulcers
-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
(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
(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
(C) Adenocarcinoma of the Stomach
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
(D) SMALL INTESTINE
Diverticula:
Outpouchings in the walls of tubular organs, commonly occurring in the intestine
(D) Diverticulosis
diverticula present - often asymptomatic
(D) Diverticulitis
inflamed diverticula are present - symptomatic!
(D) True diverticulum
False diverticulum:
All layers of wall; Usually congenital
Only mucosal layer; Usually acquired
(D) Meckel’s Diverticulum:
Congenital;
Mostly asymptomatic;
Has pancreatic/gastric choristomata;
Meckel’s diverticulitis (“left-sided appendicitis”)
(D) Diverticulosis of the Jejunum:
False diverticula form in the jejunum, (multiple, solitary or few in number) and mostly symptomless
(D) Crohn’s Disease
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
(D) Malabsorption Syndrome
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
(D) Tumours
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)
(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
(E) Mucocoele of Appendix:
Obstruction of appendix without infection; Accumulation of mucus in the organ
(F) INFECTIONS OF SMALL & LARGE INTESTINE
Transmitted by contaminated food/water - cause diarrhoea, fever, ‘food poisoning’ symptoms
(F) Viruses:
Rotaviruses, caliciviruses (Norwalk viruses), enteric adenoviruses cause inflammation, gastroenteritis
(F) Bacteria:
-Salmonella typhi, Campylobacter jejuni cause direct damage to bowel
-Escherichia coli produces enterotoxin
-Yersinia causes ulceration, ileitis
(F) Protozoa
-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
(G) INTESTINAL OBSTRUCTION
Ileus = intestinal obstruction due to any cause
(G) Volvulus
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”
(G) Meconium ileus
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
(G) Intussusception
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
(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
(H) Diverticulosis of the Colon
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
(H) Benign Colonic Tumours
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
(H) Familial Polyposis Coli
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
(H) Other Inherited Benign Neoplasms
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
(H) Colonic Carcinoma
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%)
(H) Carcinoma of the Anal Canal
Rare tumour in middle to old age;
metastasizes early via lymphatics;
poor prognosis
(H) Haemorrhoids
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