Pathology of Oesophagus, Stomach and Appendix
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Transcript of Pathology of Oesophagus, Stomach and Appendix
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OESOPHAGUS AND STOMACH
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Lecture Outline
Oesophagus– Premalignant non-neoplastic disorders– Neoplasms– Causes of upper GI Haemorrhage
Stomach– Inflammatory disorders– Neoplasms
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Oesophagus Congenital Abnormalities
– Plummer - Vinson Syndrome (Paterson - Kelly)
Webs Fe deficiency anaemia Atrophic glossitis
risk of malignancy
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Oesophagus
Achalasia Cardia Decreased/loss of myenteric ganglion cells
– Aperistalsis resting tone LES
Dilatation Stasis Inflammation
– Neoplasia (5%)
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Oesophagitis Reflux
– Bleeding– Ulceration– Stricture LES tone, alcohol, pregnancy, CNS
depression, obesity– Columnar metaplasia (Barrett’s)
10% risk of malignancy Infectious
– Candida- AIDS
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Oesophageal Varices Porto-systemic anastomosis
– Cirrhosis– Bud-Chiari syndrome– Hepatic vein thrombosis– Portal vein thrombosis– Veno-occlusive disease (VOD)
Complication– Rupture- <50% of UGI bleed– Cause of death of 50% of
alcoholics
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Mallory-Weiss Syndrome Longitudinal tears at GEJ
– Partial or complete thickness Severe retching Alcoholic 5-10% of UGI bleed
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Oesophageal Tumour
Benign– Leiomyomas
Malignant– Squamous cell carcinoma (90%)– Adenocarcinoma (10%)
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Oesophageal Carcinoma6% of GIT cancers SCC
– >50 M:F= 2:1 B>W– Dietary factors
Vitamin deficiencies Zn deficiency Nitrites/nitroamines
– Lifestyle Cigarette Alcohol
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Oesophageal Carcinoma Location (SCC)
– Middle1/3 -50%– Lower 1/3 –30%– Upper 1/3 –20%
Morphology– Polypoid/exophytic –60%– Excavating –25%– Flat –15%
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Oesophageal Carcinoma
Adenocarcinoma– Barrett’s metaplasia*– Submucosal glands
Microscopy– SCC - keratin– Adeno – glands mucin
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Stomach Gastritis
– Acute– Chronic
Acute – Superficial acute inflammation haemorrhage polymorphs superficial erosion
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Acute Gastritis
Pathogenesis acid secretion HCO3
-
blood flow mucosal barrier
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Acute GastritisAetiology NSAID/Aspirin
Alcohol Smoking ChemoRx drugs Uremia
•Stress•Trauma•Burns – Curling’s•Head injury – Cushing’s•Surgery
•Shock•Ischaemia•Sepsis
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Acute Gastritis
Clinical Features Asymptomatic Pain Nausea/vomiting Haematemesis Melaema
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Chronic GastritisAetiology Helicobacter pylori (90%)
Autoimmune (<10%)– Pernicious anaemia
Toxins - ETOH, Smoking
Bile Reflux (post-gastrectomy)
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Chronic GastritisMorphology Autoimmune (type A)
– Diffuse, body and fundus– More severe– Atrophy, auto-antibodies & parietal cell loss
H. pylori-associated (type B)– Focal or diffuse, antral and body– Polymorph infiltration– Lymphoid nodule formation
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Chronic Gastritis Chronic mucosal inflammation
– Superficial or deep mucosal atrophy intestinal metaplasia No erosion
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Gastric Tumours Benign
– Leiomyomas– Adenomas
Malignant– Adenocarcinoma (>90%)– Lymphomas (4%)– Endocrine cell tumours (3%)– Stromal tumours (2%)
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Gastric Carcinoma M:F =2:1 Japan, Chile, Costa Rica Predisposing factors
– Environmental factors Diet
– preserved/smoked/salted foods fresh fruits and vegetables
Low socioeconomic status Cigarette smoking
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Gastric Carcinoma Host factors
– CGIM ± H pylori– Partial gastrectomy– Adenomas
Genetic factors– Bld grp A– Family Hx– Lynch syndrome (HNPCC)
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Gastric CarcinomaClassification Depth of invasion
– Early (95% 5YS) mucosal & submucosal LN
– Advanced (<15% 5YS) Morphology
– Exophytic– Flat (linitis plastica)– Excavated
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Gastric CarcinomaClassification Histologic Types (Lauren Classification)
– Intestinal CGIM ± H pylori M:F =2:1, 55y
– Diffuse Spontaneous M:F =1:1, 48y
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GIT Mesenchymal Tumours
Differentiation Stromal Tumours
(GIST) Smooth Muscle
(Leiomyosarcoma) Neurogenic
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Causes of Upper GI Haemorrhage
SpecificOesophageal Gastric Varices Acute Gastritis Mallory Weiss Ulcers Neoplasia
Duodenal Ulcers
Non-specific
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SMALL INTESTINE AND APPENDIX
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Lecture OutlineSmall Bowel Peptic ulcer disease Causes and mechanisms of diarrhoea Clinicopathologic features of Crohns disease NeoplasmsAppendix Appendicitis Neoplasms and Multiple Endocrine
Adenopathy syndrome
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Peptic Ulcer
Area of acid/pepsin digestion Relative or absolute acidity
Acid Secretion vs Mucosal Barrier
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Peptic UlcerArea of acid/pepsin digestion Duodenum (70-75%) Antrum (20-25%) GEJ Multiple – ZE Meckel’s diverticulumRelative or absolute acidity vs mucosal
barrier
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Peptic UlcerAetiologyM>F DU =3:1 GU =2:1 H. Pylori
– DU - 95%– GU –70%
NSAIDs (GU) Zollinger - Ellison Syndrome Other
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Peptic UlcerMorphology <4cm Round/oval, punched out margins Clean base GU
– Lesser curve, antrum– Radiating rugal fold
DU– 1st part
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Peptic Ulcer
Histology Fibrin and necrotic debris Non-specific inflammation Granulation tissue Scar tissue (fibrosis)
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Peptic Ulcer
Complication Bleeding Perforation Obstruction Intractable pain ? Malignant change
– GU - <1%– DU - never
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Enterocolitis
Diarrhoea mass, frequency and fluidity
DysenteryPainful, bloody diarrhoea( +low volume )
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Diarrhoeal Disorders
Secretory Osmotic Exudative* Deranged Motility Malabsorption*
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Infectious Enterocolitis
Viruses Rota - Infants Norwalk - Child., Adults Adeno
Damaged mature enterocytes are replaced by immature secretory cells => secretory and osmotic diarrhoea.
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Bacterial Enterocolitis Preformed Toxins S. aureus, Vidrios, C. perfringens
Enterotoxins E. coli, V. cholerae
Enteroinvasive Salmonella, Shigella, C. jejuni, Yersinia
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Parasitic Enterocolitis Protozoa
GiardiaCryptosporidia
HelminthsStrongyloidesAscarisHookworm
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Malabsorption
Definition Sub-optimal absorption of fat, fat-soluble
and other vitamins, protein, carbohydrate, electrolytes, minerals and water.
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Malabsorption Syndrome
Symptoms Diarrhoea - Bulky, Frothy, Greasy Weight Loss Abdominal Distention Borborygmi
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MalabsorptionConsequences GIT - Diarrhoea Blood - Anaemia ( Fe, B12, Folate )
- Bleeding Musculoskeletal - Osteopenia, Tetany
(Ca, Mg, Vit D, Protein ) Endocrine Skin Nervous System
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MalabsorptionCommon Causes
USA - celiac sprue- chronic pancreatitis- crohn’s disease
Ja - chronic pancreatitis
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Unusual Causes Celiac disease (Gluten-sensitive enteropathy,
Nontropical sprue)– Rare in nonwhites
Tropical Sprue (Post-infectious Sprue)– Caribbean (not Ja), South and Central America
Whipple’s Disease– Whites 30 - 40 yrs
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GIT AND HIV Malabsorption
Infectioncryptosporidia shigellaisospora CMVsalmonella HSV
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Crohn’s Disease(Terminal ileitis, Regional enteritis)
Inflammatory Bowel Disease Chronic relapsing Granulomatous Unknown aetiology
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Crohn’s Disease
Mouth to anus Genetic determinants: HLA-B27 ? infectious ? immune mediated Any age peaks 50 - 60 F > M white = 2 - 5x nonwhites Jews 2 - 5x non-Jews
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Crohn’s Disease Transmural inflammation Segmental Noncaseating granulomas 50% Fissures and fistulas Mural fibrosis and strictures Creeping fat Lymphadenopathy Systemic manifestations
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IBD Extra-GI Manifestations
Migratory polyarthritis
Sacroiliitis
Ankylosing spondylitis
Erythema nodosum
Clubbing
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Small Intestine Tumours3 - 6 % of GIT tumours Benign
– Leiomyomas– Adenomas– Lipomas
Malignant– Adenocarcinomas– Endocrine cell tumours– Lymphomas– Stromal tumours
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Endocrine Cell Tumours(Carcinoids)
Slow growing
Low malignant potential– “benign” - appendix, rectum– “malignant” - ileum, stomach, colon
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Hamartomatous Polyps
Peutz Jegher/ Syndromemuscularis mucosa
Juvenile/ Syndromelamina propria(colon)
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APPENDIX
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Acute Appendicitis
Luminal obstruction(fecolith, tumour, worms)
Increased intraluminal pressure
Mucosal ischaemia
2o bacterial colonization
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Acute Appendicitis
Morphology suppurative gangrenous empyema
Complications abscess perforation peritonitis septicaemia mucocele
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Acute Appendicitis Mesenteric adenitis ( yersinia, virus )
Acute salpingitis
Ectopic gestation
Mittelschmerz
Meckel’s diverticulitis
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Appendix Tumours
Mucinous cystadenoma/ carcinoma- pseudomyxoma peritonei
ECT - carcinoid
Adenocarcinoma
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Multiple Endocrine Adenopathy (Neoplasia)
Hyperplasia and neoplasia of more than one endocrine gland
Autosomal dominant ( some recessive )
3 syndromes
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MEA
I
pituitaryparathyroidpancreasadrenalPUD
II
pheomedullary ca
III
pheomedullary caganglioneuro
osteoma
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