OESOPHAGUS AND STOMACH

Lecture Outline

Oesophagus– Premalignant non-neoplastic disorders– Neoplasms– Causes of upper GI Haemorrhage

Stomach– Inflammatory disorders– Neoplasms

Oesophagus Congenital Abnormalities

– Plummer - Vinson Syndrome (Paterson - Kelly)

Webs Fe deficiency anaemia Atrophic glossitis

risk of malignancy

Oesophagus

Achalasia Cardia Decreased/loss of myenteric ganglion cells

– Aperistalsis resting tone LES

Dilatation Stasis Inflammation

– Neoplasia (5%)

Oesophagitis Reflux

– Bleeding– Ulceration– Stricture LES tone, alcohol, pregnancy, CNS

depression, obesity– Columnar metaplasia (Barrett’s)

10% risk of malignancy Infectious

– Candida- AIDS

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

Mallory-Weiss Syndrome Longitudinal tears at GEJ

– Partial or complete thickness Severe retching Alcoholic 5-10% of UGI bleed

Oesophageal Tumour

Benign– Leiomyomas

Malignant– Squamous cell carcinoma (90%)– Adenocarcinoma (10%)

Oesophageal Carcinoma6% of GIT cancers SCC

– >50 M:F= 2:1 B>W– Dietary factors

Vitamin deficiencies Zn deficiency Nitrites/nitroamines

– Lifestyle Cigarette Alcohol

Oesophageal Carcinoma Location (SCC)

– Middle1/3 -50%– Lower 1/3 –30%– Upper 1/3 –20%

Morphology– Polypoid/exophytic –60%– Excavating –25%– Flat –15%

Oesophageal Carcinoma

Adenocarcinoma– Barrett’s metaplasia*– Submucosal glands

Microscopy– SCC - keratin– Adeno – glands mucin

Stomach Gastritis

– Acute– Chronic

Acute – Superficial acute inflammation haemorrhage polymorphs superficial erosion

Acute Gastritis

Pathogenesis acid secretion HCO3

-

blood flow mucosal barrier

Acute GastritisAetiology NSAID/Aspirin

Alcohol Smoking ChemoRx drugs Uremia

•Stress•Trauma•Burns – Curling’s•Head injury – Cushing’s•Surgery

•Shock•Ischaemia•Sepsis

Acute Gastritis

Clinical Features Asymptomatic Pain Nausea/vomiting Haematemesis Melaema

Chronic GastritisAetiology Helicobacter pylori (90%)

Autoimmune (<10%)– Pernicious anaemia

Toxins - ETOH, Smoking

Bile Reflux (post-gastrectomy)

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

Chronic Gastritis Chronic mucosal inflammation

– Superficial or deep mucosal atrophy intestinal metaplasia No erosion

Gastric Tumours Benign

– Leiomyomas– Adenomas

Malignant– Adenocarcinoma (>90%)– Lymphomas (4%)– Endocrine cell tumours (3%)– Stromal tumours (2%)

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

Gastric Carcinoma Host factors

– CGIM ± H pylori– Partial gastrectomy– Adenomas

Genetic factors– Bld grp A– Family Hx– Lynch syndrome (HNPCC)

Gastric CarcinomaClassification Depth of invasion

– Early (95% 5YS) mucosal & submucosal LN

– Advanced (<15% 5YS) Morphology

– Exophytic– Flat (linitis plastica)– Excavated

Gastric CarcinomaClassification Histologic Types (Lauren Classification)

– Intestinal CGIM ± H pylori M:F =2:1, 55y

– Diffuse Spontaneous M:F =1:1, 48y

GIT Mesenchymal Tumours

Differentiation Stromal Tumours

(GIST) Smooth Muscle

(Leiomyosarcoma) Neurogenic

Causes of Upper GI Haemorrhage

SpecificOesophageal Gastric Varices Acute Gastritis Mallory Weiss Ulcers Neoplasia

Duodenal Ulcers

Non-specific

SMALL INTESTINE AND APPENDIX

Lecture OutlineSmall Bowel Peptic ulcer disease Causes and mechanisms of diarrhoea Clinicopathologic features of Crohns disease NeoplasmsAppendix Appendicitis Neoplasms and Multiple Endocrine

Adenopathy syndrome

Peptic Ulcer

Area of acid/pepsin digestion Relative or absolute acidity

Acid Secretion vs Mucosal Barrier

Peptic UlcerArea of acid/pepsin digestion Duodenum (70-75%) Antrum (20-25%) GEJ Multiple – ZE Meckel’s diverticulumRelative or absolute acidity vs mucosal

barrier

Peptic UlcerAetiologyM>F DU =3:1 GU =2:1 H. Pylori

– DU - 95%– GU –70%

NSAIDs (GU) Zollinger - Ellison Syndrome Other

Peptic UlcerMorphology <4cm Round/oval, punched out margins Clean base GU

– Lesser curve, antrum– Radiating rugal fold

DU– 1st part

Peptic Ulcer

Histology Fibrin and necrotic debris Non-specific inflammation Granulation tissue Scar tissue (fibrosis)

Peptic Ulcer

Complication Bleeding Perforation Obstruction Intractable pain ? Malignant change

– GU - <1%– DU - never

Enterocolitis

Diarrhoea mass, frequency and fluidity

DysenteryPainful, bloody diarrhoea( +low volume )

Diarrhoeal Disorders

Secretory Osmotic Exudative* Deranged Motility Malabsorption*

Infectious Enterocolitis

Viruses Rota - Infants Norwalk - Child., Adults Adeno

Damaged mature enterocytes are replaced by immature secretory cells => secretory and osmotic diarrhoea.

Bacterial Enterocolitis Preformed Toxins S. aureus, Vidrios, C. perfringens

Enterotoxins E. coli, V. cholerae

Enteroinvasive Salmonella, Shigella, C. jejuni, Yersinia

Parasitic Enterocolitis Protozoa

GiardiaCryptosporidia

HelminthsStrongyloidesAscarisHookworm

Malabsorption

Definition Sub-optimal absorption of fat, fat-soluble

and other vitamins, protein, carbohydrate, electrolytes, minerals and water.

Malabsorption Syndrome

Symptoms Diarrhoea - Bulky, Frothy, Greasy Weight Loss Abdominal Distention Borborygmi

MalabsorptionConsequences GIT - Diarrhoea Blood - Anaemia ( Fe, B12, Folate )

- Bleeding Musculoskeletal - Osteopenia, Tetany

(Ca, Mg, Vit D, Protein ) Endocrine Skin Nervous System

MalabsorptionCommon Causes

USA - celiac sprue- chronic pancreatitis- crohn’s disease

Ja - chronic pancreatitis

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

GIT AND HIV Malabsorption

Infectioncryptosporidia shigellaisospora CMVsalmonella HSV

Crohn’s Disease(Terminal ileitis, Regional enteritis)

Inflammatory Bowel Disease Chronic relapsing Granulomatous Unknown aetiology

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

Crohn’s Disease Transmural inflammation Segmental Noncaseating granulomas 50% Fissures and fistulas Mural fibrosis and strictures Creeping fat Lymphadenopathy Systemic manifestations

IBD Extra-GI Manifestations

Migratory polyarthritis

Sacroiliitis

Ankylosing spondylitis

Erythema nodosum

Clubbing

Small Intestine Tumours3 - 6 % of GIT tumours Benign

– Leiomyomas– Adenomas– Lipomas

Malignant– Adenocarcinomas– Endocrine cell tumours– Lymphomas– Stromal tumours

Endocrine Cell Tumours(Carcinoids)

Slow growing

Low malignant potential– “benign” - appendix, rectum– “malignant” - ileum, stomach, colon

Hamartomatous Polyps

Peutz Jegher/ Syndromemuscularis mucosa

Juvenile/ Syndromelamina propria(colon)

APPENDIX

Acute Appendicitis

Luminal obstruction(fecolith, tumour, worms)

Increased intraluminal pressure

Mucosal ischaemia

2o bacterial colonization

Acute Appendicitis

Morphology suppurative gangrenous empyema

Complications abscess perforation peritonitis septicaemia mucocele

Acute Appendicitis Mesenteric adenitis ( yersinia, virus )

Acute salpingitis

Ectopic gestation

Mittelschmerz

Meckel’s diverticulitis

Appendix Tumours

Mucinous cystadenoma/ carcinoma- pseudomyxoma peritonei

ECT - carcinoid

Adenocarcinoma

Multiple Endocrine Adenopathy (Neoplasia)

Hyperplasia and neoplasia of more than one endocrine gland

Autosomal dominant ( some recessive )

3 syndromes

MEA

I

pituitaryparathyroidpancreasadrenalPUD

II

pheomedullary ca

III

pheomedullary caganglioneuro

osteoma