Upper GIT II
Luigi TornilloPathoBasic 09.09.2014
Pathology
• Esofagus : inflammation II– Infectious esophagitis– Drug esophagits– Radiation esophagitis
• Stomach : inflammation II– Drug gastritis– Granulomatous gastritis– Lymphocytic gastritis
Esophagus: inflammation
• GERD• Eosinophilic esophagitis• Infective
– Candida– CMV, HSV– Immunocompetent: measles, scarlet,
dyphteria– Immunodeficient: HIV, HZV, HPV, HHV6, varied
bacteria & fungi• Drugs, Toxic• Radiation esophagitis• GvHD
Herpes Infection
• Immunocompromised– HIV, transplant.
Immunosupp. therapy, tumors
• Immuncompetent (?)– Children, elderly,
pregnancy• Dysphagia, odinophagia• Middle, lower esophagus• Punched -out ulcers,
multiple vesicles
Herpes Infection
• Ulcer edge• Mixed inflammatory infiltrate (also
macrophages )• Multinucleated epithelial cells with viral
inclusions (IHC)• „Dirty “ background
Candida Infection
• Immunocompromised– HIV, transplant.
Immunosupp. therapy, tumors
• Immuncompetent (?)– Children, elderly,
• Dysphagia , odinophagia• Whitish , bleeding
membranes
Riddell, 2nd ed
Drug (pill) esophagitis
• Elderly pat., M/F 1/2• Swallowing pills dry
– KCL, NSAIDs, ASA, Tetracyclines, iron, biphosphonates, quinidine
• Focal, mid esophagus• Histology not specific ,
(Acute ) GvHD
• Rare, upperesophagus
• Apoptoticepithelial cells
• Scantymononuclearinfiltrate
Radiation esophagitis
• If chemoradio more frequent
• Smaller epithelial cells
• Nuclear alterations
• Submucosal changes
• Bizarre endothelia
Stomach : inflammation II
Lymphocytic gastritis
• IEL (> 25/100), surface and foveolae
• 1% of gastroscopies• Sometimes focal• Varioliform , large
mucosal folds
• Infections ( HP, HIV)• Immune-mediated
– Celiac disease,Crohn, CVID
• Tumors• Drugs (of course...)
– Ticlodipine
CD3 CD8
Granulomatous gastritis
• Crohn (<5%, not specific)– NB: FAG
• Infection– HP, TBC, Syphilis, Histoplasmosis
• Vasculitis , Amyloid , Rheumatoid, Sarcoid , Foreign material
• Malignancy
Stomach: Granulomas
• Neutrophils = recent• Eosinophils = parasite• Compact with no gastritis = sarcoidosis• Compact with gastritis = Crohn• Necrosis = infection • Ulcer = foreign body (?)
Iatrogenic gastropathies
Erosions/ulcersNSAID, KCl, alendronate, colchicine, biphosph., Fe, steroids
Hemorragic gastritisNSAID, KCl, antibiotics, biphosph., Fe, steroids, kayexalate, taxol
Reactive (chemical) gastropathy
NSAID
Pariet. Cell Hyp., FGP PPI
Ep. Atypia („dysplastic“) Chemotherapy (5FU, mytomicine )
Lymphocytic gastritis Ticlodipine
Pathologie
Epithelial apoptosis
• PPI• Colchicine• Conditioning/chemo• Mycophenolate• Cave: GVHD• Antrum• Glands neck
Non-specific pill inflammation(esophagus and stomach )
• KCL, alendronate, doxycycline, quinidine, iron, kayexalate, taxol, NSAID
• Neutrophilic inflammation
• Ulcer, strictures
Pathologie
Pathologie
Drug: lymphocytic gastritis
Drug / Chemical Gastropathy
• NSAID• Proliferative
compartment• Regeneration• Large nuclei
(„atypical“)
Pathologie
„Dysplastic“ changes (colchicine)
Pathologie
Gastric GvHD
• Scantyinflammation , mostlymononuclear
• Apoptosis– Corpus (neck,
surface)– Rare in antrum
(deep!)
Autoimmune gastritis
„Immune -mediated progressive destruction of parietal cells leading to reduced acid production and reducedor absent intrinsic factor (IF)“
Riddell, 2nd Ed., 2014
Autoimmune gastritis
• Antiparietal cell antibodies, achlorhydria , prevalent body
• HP involved (cross -reaction?)
• Other autoimmune diseases
Autoimmune gastritis
• Pebbled appearance to mucosa• Corpus -predominant, mild
activity• Intestinal and/or pancreatic
metaplasia , los s of parietal and chief cells
• ECL in corpus, G cell in antrum
2 clusters 5 cells/mm or HPF
< 0,5mm5 or more micronodularhyperplasia
Gastric atrophy
“Absence of glands that should normally be present in the gastric area in question, irrespective of what replaces them ”
• Nothing (“empty lamina propria ”)• Fibrosis• Other glands not native to the area
Gastric atrophy : meaning
• Antrum– No meaning
• Corpus, mild to moderate– Hypochlorhydria
• Corpus, severe– Severe hypochlorhydria, achlorhydria– Vit. B 12 malabsorption
Gastric atrophy : report
• Reporting gastric atrophy only if it issevere and in corpus
• Essential separate biopsies of corpus
• Severe extensive metaplasia : surveillance
• Shepherd et al. (eds.), Morson & Dawson‘sGastrointestinal Pathology, 5th ed., Hoboken , NY, 2013
• Riddell & Jain (eds.), Riddell‘s GastrointestinalPathology and its Clinical Implications, 2nd ed., Philadelphia, PA, 2014
• Liacouras et al., J Allergy Clin Immunol, 2011; 128(1):3–20.e6
• Straumann A, Dig Dis Sci, 2013;31:6–9• Almashat SJ et al, Sem Diagn Pathol, 2014; 31:
89-99 • Maguire and Sheehan , Histopathology,
2012;60:864-79• Parfitt & Driman , Human Pathology, 2007; 38:
527– 536
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