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Stomach pathology - Coggle Diagram

- - - - extension of superficial erosions
      - often multiple
        
        1-2cm
      - punched out, clean base
      - stress
        
        ICU
        
        curling
        
        cushings - vagal
        
        prophylactic PPIs
      - extreme hyperacidity
        
        zollinger-ellison
        
        hypergastrinaemia 2° to gastrin secreting neoplasm
        
        multiple
        
        antrum, D1, jejunum
    - - pathogenesis
        
        excessive acid production
        
        but many hypersecretors of acid do not get ulcers and those with ulcers may not have raised acid levels
        
        initially respond to anti-acid treatment but freq. relapse
        
        mucosal defence against acid attack is important
        
        failure means ulcers can result from normal or decreased quantities of acid
      - gross appearance
        
        80% solitary
        
        1-3cm in diameter, some larger
        
        round to oval
        
        punched out, straight walls, overhang base
        
        depth varies - may penetrate entire wall
        
        duodenal
        
        90% in first part
        
        ant. wall more than post.
        
        gastric
        
        predominantly on lesser curvature
        
        rugae puckered towards them
        
        chronic healing by fibrosis
  - - - barretts oesophagus
      - gastroenterostostomy stoma
      - meckels diverticulum
  - - - increases up to 35yr
      - aicd is elevated or normal
      - helicobacter in almost all
      - eating makes better
      - more
    - - less
      - increases with age
      - acid levels normal or low
      - 70% with helicobacter
      - eating makes worse
  - - - dyspepsia
        
        epigastric pain-one finger point
        
        related to meals
        
        can be relieved by food
    - - perforation peritonitis
      - penetration-adjacent organ
      - haemorrhage
        
        shock
        
        haematemesis
        
        melena
        
        anaemia
      - stenosis/stricture
      - malignant change
        
        rare in gastric, never in duodenal
- - - - haemorrhage into mucosa
      - sloughing of superficial mucosal epi.
    - - may be asymptomatic
      - epigastric pain
      - nausea and vomiting
      - haematemesis or melena
    - - irritants and stress
      - heavy NSAID use (esp. aspirin)
      - excessive alcohol
      - heavy smoking
      - chemotherapy
      - uraemia - renal failure
      - systemic inf. - salmonellosis
      - severe stress
      - ischaemia and shock
      - neurotrauma (cushings ulcer, vagal)
    - - oedema
      - vasodilation
      - erythematous
      - hyperemia
      - intra-mucosal haemorrhage
      - erosions
        
        limited above muscularis mucosae
        
        superficial
        
        often multiple
  - - - less than 10% of chronic gastritis
      - majority of HLO negative chronic gastritis
      - autoantibodies
        
        parietal cells
        
        intrinsic factor
      - gland centred
        
        reduced acid
        
        stimulates gastrin release
        
        hypergastrinaemia
        
        reduced intrinsic factor
        
        B12 deficiency(pernicious anaemia)
      - fundus and body
      - atrophy
        
        reduced acid
        
        carcinogens
        
        intestinal metaplasia
        
        ^RR of adenocarcinoma
    - - most common cause of chronic gastritis
      - gram neg, spiral, flagellated
      - in surface mucin pits?
      - binds to surface cells
      - virulence
        
        colonisation
        
        urease
        
        flagella
        
        adhesins
        
        immune escape
        
        flagella
        
        CagA
        
        VacA
        
        cytopathic effects
        
        suppress phagocytosis
        
        nutrient release
      - gastritis resolves after eradication
      - found only on gastric epi - antrum and pylorus
      - histology
        
        organisms on surface epi
        
        chronic infl.
        
        lymphoid follicle formation
      - Clinical patterns depend on
        
        pathogen factors
        
        host factors
        
        blood group a
        
        cytokine and receptor gene polymorphisms
        
        2 patterns
        
        antral gastritis
        
        99%
        
        reduced somatostatin
        
        ^gastrin
        
        ^acid
        
        risk of duodenal ulcer
        
        pan gastritis
        
        1%
        
        multifocal
        
        antrum and body
        
        atrophy
        
        no significant ^ acid
        
        intestinal metaplasia
        
        risk of gastric adenocarcinoma
        
        10-15% of those infected get PUD
        
        gastric carcinoma risk 1-3%
        
        lymphoma risk
    - - post surgery/motility disorder
        
        reflux
        
        cholecystectomy
        
        by-pass
      - bile acids irritant
      - oedema, vasodilation, scant leucocytes
      - neck cells prolif. to replace lost cells
      - NSAIDs and alcohol similar
    - - lymphocytes
      - plasma cells
      - +/- neutrophils
    - - atrophy
      - intestinal metaplasia
    - - often few or none
      - upper abd. discomfort
      - nausea&vomiting
- - - - due to TGFalpha production
      - resulting in excess mucous production
    - - epigastric pain
      - N&V
      - anorexia
      - protein losing enteropathy
        
        hypoalbuminaemia and oedema
    - - may be self-limitng when
        
        post-infectious in children
        
        protracted in adults
  - - - chronic liver disease
      - chronic kidney disease
- - - - reactive/hyperplastic
      - neoplastic
        
        epithelial
        
        adenomas
        
        benign glandular epi neoplasma
        
        uncommon in western but relatively freq. in Japan
        
        ^ and those with high incidence of gastric cancer
        
        if polypoid
        
        strong potential for malignant change
        
        40% have carcinoma on micro exam
        
        flat adenomas
        
        lower malignant potential
        
        adenocarcinomas
        
        pathogenesis
        
        patients with antibodies to pylori have higher risk of gastric cancer
        
        polymorphisms in IL-1 beta gene cluster
        
        diet, preserved food- bad, fresh food -good, oxidative stress, luminal vit c
        
        Th1/2 balance - Th1 encourages pre-neoplastic changes -atrophy, metaplasia
        
        intestinal helminth inf. from Th1 to Th2 - may be protective against gastric cancer
        
        mesenchymal/soft tissue tumours
        
        majority
        
        gastrointestinal stromal tumours
        
        spindle cells
        
        interstitial pacemaker cells of Cajal
        
        C-Kit or PDGFRA tyrosine kinase mutations
        
        spectrum from benign to malignant
        
        most benign
        
        30% malignant
  - - - intestinal type
        
        glands
        
        high prevalence areas e.g Japan
        
        assoc. with
        
        H.pylori
        
        these inf. are falling so so is this cancer
        
        autoimmune gastritis
        
        intestinal metaplasia
        
        low acid, altered flora, carcinogens, preserved food
        
        elderly
        
        haematogenous spread
        
        Wnt, APC signalling, CDNK2 cyclin derangement
      - diffuse type
        
        low prevalence areas
        
        signet ring single cells
        
        CDH1 familial and sporadic
        
        P53
        
        intracellular mucin displaces/deforms nucleus
        
        diffuse infiltration and serosal spread
        
        linitis plastica, leather bottle stomach
        
        worse prognosis than intestinal
    - - if confined to mucosa or submucosa
        
        better prognsosi
      - all gastric ulcers must be regarded as potentially malignant
      - Virchow's node
        
        left supraclavicular LN as a sign of metastic malignancy from gastric cancer
      - Irish node
      - sister mary joseph node
    - - 5-10%
      - weight loss, dyspepsia and abd. pain
      - gastric mucosa devoid of lymphocytes
      - H.Pylori Th2 response lymphoid follicles with germinal centres and intra-epi lymphocytes
      - B-cell origin
        
        arise from MALT
        
        closely related to H.pylori inf.
      - most are high grade diffuse large b cell lymphomas
      - MALTomas
        
        t11:18, t1:14, t14:18
        
        some regress after pylori eradication
        
        diffuse to polypoid
        
        freq. nodal involvement
- - - - pyloric sphincter
      - pyloric canal
    - - muscular hypertrophy of pyloric circular muscle coat
    - - projectile vomiting
        
        2nd or 3rd week