Drsapna Harsha, profile picture
Uploaded byDrsapna Harsha
PPTX, PDF20,695 views

Stomach pathology lecture

The normal gastric mucosa contains mucus-secreting cells in the cardia, acid-producing and pepsin-producing cells in the fundus and body, and hormone-producing cells in the pylorus. The stomach functions to mix and start digestion of food, activate enzymes, destroy bacteria, and absorb nutrients, alcohol, water, and vitamins. Common pathologies of the stomach include peptic ulcers, gastritis, tumors, and congenital anomalies like pyloric stenosis. Chronic gastritis is often caused by H. pylori infection and can lead to atrophy, intestinal metaplasia, and increased cancer risk over time if not treated.

Embed presentation

Downloaded 911 times
1 / 123
2 / 123
3 / 123
4 / 123
5 / 123
6 / 123
7 / 123
8 / 123
9 / 123
10 / 123
11 / 123
12 / 123
13 / 123
14 / 123
15 / 123
16 / 123
17 / 123
18 / 123
19 / 123
20 / 123
21 / 123
22 / 123
23 / 123
24 / 123
25 / 123
26 / 123
27 / 123
28 / 123
29 / 123
30 / 123
Most read
31 / 123
32 / 123
33 / 123
34 / 123
35 / 123
36 / 123
37 / 123
38 / 123
39 / 123
40 / 123
Most read
41 / 123
42 / 123
43 / 123
44 / 123
45 / 123
46 / 123
47 / 123
48 / 123
49 / 123
50 / 123
51 / 123
52 / 123
53 / 123
54 / 123
55 / 123
56 / 123
57 / 123
58 / 123
59 / 123
60 / 123
61 / 123
62 / 123
63 / 123
64 / 123
65 / 123
66 / 123
67 / 123
68 / 123
69 / 123
70 / 123
71 / 123
72 / 123
73 / 123
74 / 123
75 / 123
76 / 123
77 / 123
Most read
78 / 123
79 / 123
80 / 123
81 / 123
82 / 123
83 / 123
84 / 123
85 / 123
86 / 123
87 / 123
88 / 123
89 / 123
90 / 123
91 / 123
92 / 123
93 / 123
94 / 123
95 / 123
96 / 123
97 / 123
98 / 123
99 / 123
100 / 123
101 / 123
102 / 123
103 / 123
104 / 123
105 / 123
106 / 123
107 / 123
108 / 123
109 / 123
110 / 123
111 / 123
112 / 123
113 / 123
114 / 123
115 / 123
116 / 123
117 / 123
118 / 123
119 / 123
120 / 123
121 / 123
122 / 123
123 / 123
Dr Sapna M
NORMAL ANATOMY/ HISTOLOGY
Stomach - Normal 3
The normal gastric mucosa  Cardia – mainly mucus-secreting cells  Fundus (body) – acid producing parietal cells, pepsin producing chief cells  Pylorus – hormone (gastrin) production 4
Stomach - Normal 5
6
7
Stomach  Functions ◦ Mix food ◦ Reservoir ◦ Start digestion of  Protein  Nucleic acids  Fats ◦ Activates some enzymes ◦ Destroy some bacteria ◦ Makes intrinsic factor – B 12 absorption ◦ Destroys some bacteria ◦ Absorbs  Alcohol  Water  Lipophilic acid  B 12 8
Bezoar  A bezoar is a mass found trapped in the gastrointestinal system (usually the stomach), though it can occur in other locations.  A pseudobezoar is an indigestible object introduced intentionally into the digestive system.  There are several varieties of bezoar, some of which have inorganic constituents and others organic.
Stomach pathology  Congenital anomaly – pyloric stenosis  Inflammatory conditions – gastritis, peptic ulcers  Tumors 10
Pyloric stenosis  In 95% of infants with pyloric stenosis the age at presentation is between 3 and 12 weeks of life, typically between 3 and 8 weeks.  Pyloric stenosis has been reported in neonates within the first day of life. 11
12
etiology  3 in 1,000 live births  more commonly in males  30 percent of cases occur in firstborn  genetic predisposition  Sibling has 5 times more incidence  environmental factors  Neonatal hypergastrinemia and gastric hyperacidity may have a role 13
CLINICAL MANIFESTATIONS  The classic presentation of IHPS is the three- to six-week-old baby who develops immediate postprandial, non-bilious, often projectile VOMITING and demands to be re-fed soon afterwards  (a "hungry vomiter"). 14
Palpable mass  The mass is most easily felt immediately after emesis because it may otherwise be obscured by a distended antrum and/or tensed abdominal muscles 15
Pancreatic heterotopia  Pancreatic tissue outside boundaries of pancreas without anatomic or vascular connections to pancreas ● Also called ectopic pancreas ● Present in 0.5% to 14% of autopsies ● Due to displacement of pancreatic tissue during embryonic development 16
17
Inflammatory Disease of Stomach 18
Definition  The term gastritis is used to denote inflammation associated with mucosal injury.  . 19
20
Pathophysiology The mechanisms of mucosal injury in gastritis is thought to be an imbalance of aggressive factors  acid production or pepsin and defensive factors  mucus production  bicarbonate  and blood flow 21
Protective factors vs. hostile factors 22
Gastritis Acute Chronic 23
Classification of gastritis Acute Chronic •H pylori gastritis •Other infective gastritis – bacteria, virus, fungi, parasite •Acute non infective gastritis •Type A- autoimmune •Type B- h pylori related •Type AB- environmental •Chemical – reflux gastritis •Uncommon forms 24
Acute & Chronic Difference ◦ Acute refers to short term inflammation ◦ Acute refering to neurophilic infiltrate ◦ Chronic referring to long standing forms ◦ Chronic referring to mononuclear cell infiltrate especially lymphocyte and macrophages 25
Acute Gastritis  Definition ◦ An acute mucosal inflammatory process, with neutrophilic infiltrate, that is usually transient. ◦ There may be hemorrhage into the mucosa or sloughing of the mucosa. ◦ Severe erosive form is an important cause of severe GI bleeding 26
Etiology ◦ Frequently associated with, among others:  heavy use of NSAIDS, especially aspirin  excessive alcohol consumption  heavy smoking  severe stress e.g. trauma, burns, surgery  Ischemia  Systemic infection ◦ Often, idiopathic 27
NSAIDs NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins 28
Smoking  Promotes gastritis & ulcer occurrence  Increases the likelihood of ulcer complications  Mechanisms ◦ Stimulate gastric acid secretion ◦ Stimulate bile salt reflux ◦ Causes alteration in mucosal blood flow ◦ Decrease mucus secretion ◦ Reduces prostaglandin synthesis ◦ Decrease pancreatic bicarbonate secretion 29
Acute Gastritis - Pathogenesis 30 All above Factor Acid secretion + back diffusion + Bicarbonate buffer + Blood flow Disruption of Mucus layer + Direct Mucosal Injury Acute Gastritis
Stages of Acute Gastritis  Acute superficial gastritis Inflammation of superficial gastric mucosa.  Acute erosive gastritis Destruction of multiple small zones of superficial mucosa.  Acute Gastric Ulceration Destruction of full thickness of mucosa 31
Mucosal congestion ,edema inflammation & ulceration ACUTE GASTRITIS - MORPHOLOGY 32
Acute Gastritis - Morphology Ranges from edema with neutrophil infiltration, vascular congestion,& an intact epithelium, to erosion (mucosal defect that does not cross the muscularis mucosa) and hemorrhage. 33
Acute Gastritis  Gastric mucosa demonstrates infiltration by Neutrophils 34
35
Acute Gastritis  diffusely hyperemic gastric mucosa  causes for acute gastritis ◦ alcoholism ◦ drugs ◦ infections, etc. 36
Complications: Malignancy Hemorrhage Perforation  Obstruction 37
Chronic Gastritis  Definition ◦ Chronic mucosal inflammatory changes leading to atrophy and metaplasia (usually without erosions)  Dysplasia and ultimate neoplasia are complications. 38
Chronic Gastritis Type B Antral Gastritis Type A Autoimmune gastritis 39
40
Type B (Antral Gastritis) ◦ 90% of patients with antral chronic gastritis: Helicobacter pylori infected  Motile, gram negative curvilinear rods that elaborate urease (buffers gastric acid) & toxins and have adhesins to bind to the epithelium.  Pathogenesis ◦ H. pylori (urease  NH4 + + toxins) + Host (acid + peptic enzymes)  Chronic Inflammation ◦ Antibodies  Gland destruction + Mucosal atrophy   acid   intrinsic factor (which can lead to pernicious anemia) 41
Helicobacter pylori infection
H. pylori – silver stain 43
H. pylori – giemsa stain 44
H. pylori – H & E stain 45
Pathogenetic qualities of H.pylori; Adheres to gastric epithelium Lives within mucous gel layer overlying gastric epithelium Penetrates intercellular junctions Invades gastric glands and canaliculi of parietal cells Secretes urease to produce ammonia, which protects it from gastric acid Produces cytotoxins that may play role in pathogenicity Induces epithelial cytolysis and disrupts intercellular junctions Increases permeability of mucous layer to hydrogen ions and pepsin Enables gastric acid and pepsin to create ulcer craters Evades host immune defenses Damages tissue. 46
47
Noninvasive Urea Breath Test (UBT) Blood test Invasive Biopsy Urease TestHistology
Culture Stool antigen test Upper gastrointestinal (upper GI) X-ray Other tests Endoscopy
Helicobacter gastritis  2 patterns of infection ◦ Diffuse involvement of body and antrum (“pan gastritis” associated with diminishing acid output) ◦ Infection confined to antrum (antral gastritis, associate with increased acid output) 50
Type A (Auto immune) Etiology ◦ Autoimmune - antibodies to parietal cells, gastrin receptor, intrinsic factor, and H+,K+ ATPase  <10% of cases of chronic gastritis  Possible autosomal dominant inheritance 51
Morphology of chronic gastritis  Chronic inflammatory cell infiltration  Mucosal atrophy  Intestinal (goblet cell) metaplasia Seen in Helicobacter and autoimmune gastritis (not chemical) 52
Autoimmune gastritis  Autoimmune gastritis - pernicious anemia  Chronic atrophic gastritis is associated with Ab’s - intrinsic factor - patietal cell  bright green IF- in the parietal cells of the gastric mucosa. 53
Autoimmune Gastritis -Morphology PJ Goldblatt, MD Diffuse mucosal damage of the body and fundic mucosa. Antrum less involved. 54
Chronic Gastritis  Clinical Features ◦ Usually only a few symptoms: nausea, vomiting, upper abdominal discomfort ◦ Autoimmune  Hypo to achlorhydria (severe loss of parietal glands)  Hypergastrinemia  10% have pernicious anemia 55
Clinical Complications ◦ Autoimmune:  Often seen in association with other autoimmune disorders (Hashimoto thyroiditis, Addison disease, and type I diabetes)  Significant risk for the development of gastric carcinoma (2-4%) and endocrine tumors (carcinoid tumor) 56
Chronic Gastritis Morphology ◦ Varying degrees of mucosal damage possible ◦ Mucosal lesions are reddened, with thickened rugae ◦ Atrophied rugae in long-standing cases ◦ Lymphocytes and plasma cell infiltrate; neutrophils indicate “active” inflammation (may or may not be present) 57
◦ Regeneration - constant feature ◦ Metaplasia - mucosa of antral and body-fundic regions converts to columnar absorptive cells and goblet cells (intestinal metaplasia) ◦ Atrophy - marked loss of glands ◦ Dysplasia – precursor lesion to gastric cancer in atrophic gastritis 58
Sydney System of Grading Chronic Gastritis 1. Site: Antral, Corporal mucosa 2. Grading of: (Mild, Moderate, Marked)  H-Pylori  Chronic inflammation  Activity  Atrophy  Intestinal metaplasia *Normal lymphocytes & plasma cells in lamina propria = up to 5/HPF *No Neutrophils in lamina propria
Peptic Ulcer Disease
Peptic Ulcer Disease  Condition characterized by ◦ Erosion of GI mucosa resulting from digestive action of HCl and pepsin
Peptic Ulcer Disease  Ulcer development ◦ Lower esophagus ◦ Stomach ◦ Duodenum ◦ 10% of men, 4% of women
Types  Acute ◦ Superficial erosion ◦ Minimal erosion  Chronic ◦ Muscular wall erosion with formation of fibrous tissue ◦ Present continuously for many months or intermittently
Peptic Ulcer Disease Etiology and Pathophysiology  Develop only in presence of acid environment  Excess of gastric acid not necessary for ulcer development  Person with a gastric ulcer has normal to less than normal gastric acidity compared with person with a duodenal ulcer
Peptic Ulcer Size – variable; 0.3 – 4 cm in diameter Shape - round to oval Sharply demarcated, clean-cut, punched-out area with clean base Margins are usually level with surrounding mucosa or slightly elevated due to edema; the mucosa is undermined at the edges Radiating mucosal rugae 80% are solitary, 80% occur in the duodenum, of which 90% in the first part of the duodenum on the anterior wall’ within a few centimeter of the pyloric ring. 19% occur in the stomach(usually at the lesser curvature at the border of the body and antrum. 65
Gastric Ulcer- Endoscopic Appearance 66
Gastric Ulcer- Gross Appearance Sharply punched-out Large, mucosal defect or ulcer Radiating mucosal folds 67
Acute Gastric Ulcer 68
Giant gastric ulcer 69
Duodenal Peptic Ulcers- Gross 70
Microscopy:  Overhanging gastric mucosal margins (A)  Necrotic fibrinoid debris (B)  Acute inflammatory infiltrate (C)  Granulation tissue (D)  Fibrotic scarred base (E) 71 A B C, D E
Ulcer Base  Superficial thin layer of necrotic fibrinoid debris  Zone of inflammatory infiltrate with neutrophils  Zone of granulation tissue with dilated blood vessels and lymphocytes  Zone of fibrous scarring 72
73
Gastric ulcerDuodenal Ulcer middle age 50-60Any age specially 30-40Age More in maleMore in maleSex SameStress job eg. ManagerOccupation Epi. Can radiate to back Epigastric , discomfortPain Immediately after eating 2-3 hours after eating & midnight Onset EatingHungerAgg.by
Gastric ulcerDuodenal Ulcer Lying down or vomitingEatingRelived by Few weeks1-2 monthsDuration Common(to relieve the pain) UncommonVomiting Pt. afraid to eatGoodAppetite Avoid fried foodGood , eat to relieve the painDiet wt. LossNo wt. lossWeight 60%40%Hematemesis 40%60%Melena
GASTRIC TUMORS  BENIGN:  POLYPS (HYPERPLASTIC vs. ADENOMATOUS)  LEIOMYOMAS (Same gross and micro as sm. muscle)  LIPOMAS (Same gross and micro as adipose tissue)  MALIGNANT  (ADENO)Carcinoma  LYMPHOMA  POTENTIALLY MALIGNANT  G.I.S.T. (Gastro-Intestinal “Stromal” Tumor)  CARCINOID (NEUROENDOCRINE)
WHO GASTRIC NEOPLASMS  Epithelial Tumors:  Adenomatous polyps  Adenocarcinoma (papillary, tubular, mucinous, signet ring, adenosquamous, unclassified),  Small cell, Carcinoid (neuroendocrine)  Nonepithelial Tumors: Leiomyooma, Leimyosarcoma,  Schwannoma, GIST, Granular Cell Tumor, Kaposi sarcoma  Malignant Lymphomas:
What is gastric cancer?
GC is not far from us…… Napoleon‘s gastric cancer：tumor found on the lesser curvature of the stomach: What cause? How to treat? Ambition is never content, even on the summit of greatness. He conquered the larger part of Europe, but he could not conquer gastric cancer
How to diagnose What is epidemiology and etilogy What is the pathology How to treat Content
How to diagnose What is epidemiology and etilogy What is the pathology How to treat Content
GC Worldwide incidence Male 16.4 Female 8.2 Male 36.3 Female 16.9 Male 77.9 Female 33.3 Male 10.8 Female 4.9 Male 43.6 Female 19.0 Male 5.9 Female 2.6 Male 11.5 Female 4.3 Male 18.6 Female 13.3 Male 8.4 Female 4.0 Eastern Europe Japan Australia/ New Zealand China Northern Africa Southern Africa Central America Western Europe North America In terms of geographic distribution, high rates apply to Japan, China and Eastern Europe and low rates to North America. Almost 40% of cases occur in China . Pazdur R et al. Cancer management: A multidisciplinary approach. edition,2002
Gastric Cancer H. pylori Precancerous changes Genetic factors Diet Etiological Factors of GC
Precancerous changes  precancerous diseases  chronic atrophic gastritis  gastric ulcer  gastric polyps  gastric remnant  precancerous lesion  atypical hyperplasia
“The new study suggest he was chronically infected with the bacteria Helicobacter pylori.” “full of salt-preserved foods but sparse in fruits and vegetables-- common fare for long military” H. pylori Genetic factors “his father had also died of stomach cancer which led to the theory that he had inherited the disease.” Diet Precancerous changes Why Napoleon died of GC chronic atrophic gastritis?
How to diagnose What is epidemiology and etilogy What is the pathology How to treat Content
Early gastric cancer  Defined as a tumor confined to the mucosal or submucosal layer, with or without lymph node metastasis
Advanced gastric cancer  invasion depth beyond submucosal layer
Morphology SITE - Favoured location is the lesser curvature of the antropyloric region Gastric carcinoma is classified on the basis of - depth of invasion - macroscopic growth pattern - histologic subtype
ADENOCARCINOMA GROWTH PATTERNS
Gross: Linitis plastica carcinoma diffusely infiltrates the entire gastric wall without forming an intraluminal mass. The wall of the stomach is typically thickened to about 2-3 cm. and has a leathery, inelastic consistency.
Lauren classification Intestinal type --- associated with most environmental risk factors --- carries a better prognosis --- shows no familial history  Diffuse type --- consists of scattered cell clusters with poor prognosis
Intestinal type gland formation by malignant cells, Gastric carcinoma. Diffuse type demonstrating signet-ring carcinoma cells.
Bormann classifications  Gross classification phymatoid type ulcerative type infiltrative ulcerative diffuse infiltrative type
Histology classification  Adenocarcinoma occupy 95%  Lymphomas 2%  Carcinoids 1%  Adenocathomas 1%  Squamous cell 1%
TNM classification ——T  Primary tumor: depth of tumor invasion Tx- cannot be assessed T0- no evidence Tis- carcinoma in situ, no invasion of lamina T1- invades lamina propria or submucosa T2- invades muscularis or subserosa T3- penetrates serosa, no adjacent structure T4- invades adjacent structures
T:Primary tumor  Direct extension into omentum, pancreas, diaphragm, transverse colon, and duodenum.  If lesion extends beyond wall to a free peritoneal surface, peritoneal involvement is frequent.
TNM classification ——N  Regional Lymph Nodes NX- cannot be assessed N0- no nodes N1- mets in 1-6 regional nodes N2- mets in 7-15 regional nodes N3- mets in more than 15 regional nodes
TNM classification ——M  Distant metastasis MX- cannot be assessed M0- no distant metastases M1-distant metastases
Spread Patterns  Direct invasion  Lymph node dissemination  Blood spread  Intraperitoneal colonization
Special term  Blumer shelf A shelf palpable by reactal examination, due to metastatic tumor cells gravitating from an abdominal cancer and growing in the rectovesical or rectouterine pouch  Krukenberg tumor A tumor in the ovary by the spread of stomach cancer
What is the classification for Napoleon , GC “The scientists suggest that Napoleon died from a T3N1M0 (stage IIIA) gastric cancer. This means the tumour (T3) had spread to some local lymph nodes (N1) near the stomach, but had not spread or metastased (M0) to other organs. The prognosis for such tumours is known to be very poor. ”
How to diagnose What is epidemiology and etilogy What is the pathology How to treat Content
Clinical manifestation Early Gastric Cancer  Asymptomatic or silent 80%  Peptic ulcer symptoms 10%  Nausea or vomiting 8%  Anorexia 8%  Early satiety 5%  Abdominal pain 2%  Gastrointestinal blood loss <2%  Weight loss <2%  Dysphagia <1%
Clinical manifestation Advanced Gastric Cancer  Weight loss 60%  Abdominal pain 50%  Nausea or vomiting 30%  Anorexia 30%  Dysphagia 25%  Gastrointestinal blood loss 20%  Early satiety 20%  Peptic ulcer symptoms 20%  Abdominal mass or fullness 5%  Asymptomatic or silent <5%
Special signs  Linitis plastica: --- diffusely infiltrating with a rigid stomach  Virchow’s node: --- left supraclavicular lymph node  Sister Mary Joseph’s node: --- umbilical lymph node  prerectal pouch mass (Blumer shelf) --- seeding metastasis
Sister Mary Joseph’s node
Laboratory tests  Assists in determining optimal therapy.  CBC identifies anemia, with may be caused by bleeding, liver dysfunction, or poor nutrition.  30% have anemia.  Tumor markers CEA:carcino-embryonic antigen CA19-9:carbohydrate antigen CA724:carbohydrate antigen
Imaging Studies  Endoscopic diagnosis --- biopsy needed for definitive diagnosis  Endoscopic screening --- general population or high risk persons
How to diagnose Napoleon , GC Endoscopic diagnosis? Endoscopic Ultrasonography? CT scan? Preoperative staging ...... Why?
How to diagnose What is epidemiology and etilogy What is the pathology How to treat Content
G.I.S.T. TUMORS  Can behave and/or look benign or malignant  Usually look like smooth muscle, i.e., “stroma”  Are usually POSITIVE for c-KIT (CD117), i.e., express this antigen on immunochemical staining, the tumor cells are derived from the interstitial cells, of Cajal, a “neural” type of cell
G.I.S.T. TUMORS  c-KIT (receptor for stem cell factor) mutations  platelet-derived growth factor receptor-a. (PDGFRA) mutations  tyrosine kinase inhibitor (STIS71) has been shown to be effective in treatment
GIST 114
CARCINOID TUMOR  arise from the diffuse components of the endocrine system  majority are found in the GI tract, and more than 40% occur in the small intestine  tracheobronchial tree and lungs
Gastric carcinoids  release peptide and nonpeptide hormones to coordinate gut function  carcinoids are intramural or submucosal masses that create small polypoid lesions
Carcinoid tumor 117
119
The most important prognostic factor for GI carcinoid tumors is location Foregut carcinoid tumors  rarely metastasize and are generally cured by resection Midgut carcinoid tumors  Aggressive, greater depth of local invasion, increased size, and presence of necrosis and mitosis are associated with poor outcome Hindgut carcinoids occur in appendix & rectum  in appendix almost uniformly benign < 2cm  Rectal carcinoid rarely metastsize
GASTRIC LYMPHOMA Primary :  Mucosa (gut)-associated lymphoid tissue tumor Previously called MALToma, MALT-type lymphoma, or MALT lymphoma, Now called Extranodal marginal zone B-cell lymphoma of MALT type lymphoepithelial lesion (LEL) is a hallmark Secondary spread from adjacent lymph nodes
 Peptic ulcers  Gastric carcinoma 122
123

More Related Content

PPTX
Ulcerative intestine
bySaurav Singh
 
PPTX
INFLAMMATORY BOWEL DISEASE PATHOLOGY.pptx
byMona Rashed
 
PPTX
Pathology of Upper GIT
byShashidhar Venkatesh Murthy
 
PPTX
liver pathgology.pptx
bygimspathcme2022
 
PDF
CELLULAR ADAPTATIONS
byIra Bharadwaj
 
PPT
02 cardiac pathology
bymed_students0
 
PPTX
IHD - TA L2.pptx
byDrSamiyahSyeed
 
PPT
Neoplasia 1-csbrp
byPrasad CSBR
 
Ulcerative intestine
bySaurav Singh
 
INFLAMMATORY BOWEL DISEASE PATHOLOGY.pptx
byMona Rashed
 
Pathology of Upper GIT
byShashidhar Venkatesh Murthy
 
liver pathgology.pptx
bygimspathcme2022
 
CELLULAR ADAPTATIONS
byIra Bharadwaj
 
02 cardiac pathology
bymed_students0
 
IHD - TA L2.pptx
byDrSamiyahSyeed
 
Neoplasia 1-csbrp
byPrasad CSBR
 

What's hot

PPT
Stomach pathology
byRawalpindi Medical College
 
PPT
Perforated peptic ulcers
bySefeen Geris
 
PPT
Pathology of stomach
byDr Saifeldenn Hussein Elyass
 
PPT
L7 chronic gastritis f
byMohammad Manzoor
 
PPTX
Disorders of the stomach
byEngidaw Ambelu
 
PDF
Lecture 19 pancreatitis - Pathology
byAreej Abu Hanieh
 
PPTX
Crohn's disease signs,symptoms,Morphology
byMohammad Manzoor
 
PPTX
Abdominal tuberculosis
bySir Salimullah Medical College, Mitford Hospital
 
PPTX
Barrett's Oesophagus for the Histopathologist.
byDr. Varughese George
 
PPT
Esophageal disorders
byMohammad Manzoor
 
PPT
Stomach pathology
byraj kumar
 
PPTX
Acute & chronic gastritis
byVerdah Sabih
 
PPTX
Acute cholecystitis.pptx
byPradeep Pande
 
PPT
Small and large intestine pathology
byraj kumar
 
PPTX
Acute and Chronic gastritis
byDr. Aryan (Anish Dhakal)
 
PPTX
Malabsorption syndromes
bySaikat Mandal
 
PPT
Pathology of the Esophagus
byNaagavishal Barkam
 
PPT
Git pathology m scyear2011 12
byForensic Pathology
 
PPTX
Diasease of small intestine
byNur Idris
 
PPTX
Hepatomegaly
byDr. Armaan Singh
 
Stomach pathology
byRawalpindi Medical College
 
Perforated peptic ulcers
bySefeen Geris
 
Pathology of stomach
byDr Saifeldenn Hussein Elyass
 
L7 chronic gastritis f
byMohammad Manzoor
 
Disorders of the stomach
byEngidaw Ambelu
 
Lecture 19 pancreatitis - Pathology
byAreej Abu Hanieh
 
Crohn's disease signs,symptoms,Morphology
byMohammad Manzoor
 
Abdominal tuberculosis
bySir Salimullah Medical College, Mitford Hospital
 
Barrett's Oesophagus for the Histopathologist.
byDr. Varughese George
 
Esophageal disorders
byMohammad Manzoor
 
Stomach pathology
byraj kumar
 
Acute & chronic gastritis
byVerdah Sabih
 
Acute cholecystitis.pptx
byPradeep Pande
 
Small and large intestine pathology
byraj kumar
 
Acute and Chronic gastritis
byDr. Aryan (Anish Dhakal)
 
Malabsorption syndromes
bySaikat Mandal
 
Pathology of the Esophagus
byNaagavishal Barkam
 
Git pathology m scyear2011 12
byForensic Pathology
 
Diasease of small intestine
byNur Idris
 
Hepatomegaly
byDr. Armaan Singh
 

Similar to Stomach pathology lecture

PPTX
Gastritis final
byAamir Sharif
 
PPT
Lect 4- gastric disorder
byMohanad Aljashamy
 
PPT
Gastitis,treatment, symptoms, 4042024.ppt
byddjumanalieva97
 
PDF
Gastritis
byDr. Suman Chaudhary
 
PPT
5-DISEASES OF THE STOMACH AND DUODENUM.ppt
byJabbar Jasim
 
PPT
Gastric disorder
byMohanad Mohanad
 
PPTX
10.dyspepsia, peptic ulcer disease gastrities new.pptx
byAbdulkadirHasan
 
PPTX
Lec 2 gastritis, gastric neoplasm
byimrana tanvir
 
PPTX
Benign diseases of stomach and management
byMehmood Rehman
 
PPTX
Stomach.pptx pathology of stomach lecture notes by wachemo university.every o...
bymekahussen90
 
PPT
Lect 4- gastric disord
byMohanad Mohanad
 
PPT
Lect 4- gastric disorder
byMohanad Mohanad
 
PPTX
PEPTIC ULCER DISEASE medical management.pptx
byMayankrajkarn
 
PPTX
3 gastritis.pptx
bycolmanny
 
PPTX
Diseases of stomuch 1.pptx
byAbdirahmaan6
 
PPTX
24. GASTRITIS gastritis gastritis gastritis.pptx
bymuhammadbarakatalata
 
PPTX
Gastritis
byKofiNtiBaffourAboagy
 
PDF
non neoplastic disease of stomach
byamiliannisa
 
PDF
5_Stomach_Gastro¬intestinal_bleeding,_bezoars_and_foreign_body_in.pdf
byAnsaraMariam
 
PPT
2.stomach
byPNK SINGH
 
Gastritis final
byAamir Sharif
 
Lect 4- gastric disorder
byMohanad Aljashamy
 
Gastitis,treatment, symptoms, 4042024.ppt
byddjumanalieva97
 
Gastritis
byDr. Suman Chaudhary
 
5-DISEASES OF THE STOMACH AND DUODENUM.ppt
byJabbar Jasim
 
Gastric disorder
byMohanad Mohanad
 
10.dyspepsia, peptic ulcer disease gastrities new.pptx
byAbdulkadirHasan
 
Lec 2 gastritis, gastric neoplasm
byimrana tanvir
 
Benign diseases of stomach and management
byMehmood Rehman
 
Stomach.pptx pathology of stomach lecture notes by wachemo university.every o...
bymekahussen90
 
Lect 4- gastric disord
byMohanad Mohanad
 
Lect 4- gastric disorder
byMohanad Mohanad
 
PEPTIC ULCER DISEASE medical management.pptx
byMayankrajkarn
 
3 gastritis.pptx
bycolmanny
 
Diseases of stomuch 1.pptx
byAbdirahmaan6
 
24. GASTRITIS gastritis gastritis gastritis.pptx
bymuhammadbarakatalata
 
Gastritis
byKofiNtiBaffourAboagy
 
non neoplastic disease of stomach
byamiliannisa
 
5_Stomach_Gastro¬intestinal_bleeding,_bezoars_and_foreign_body_in.pdf
byAnsaraMariam
 
2.stomach
byPNK SINGH
 

Recently uploaded

PDF
Antibiotics: Cephalosporins & Monobactams.pdf
byPrerana Jadhav
 
PPTX
FACIAL NERVE AND ITS APPLIED ANATOMY BY Dr. AASTHA DUBEY
byAASTHA DUBEY
 
PPTX
composition, functions of Extra cellular matrix. ECM Proteins, glycoproteins ...
byDr. Santhosh Kumar. N
 
PPTX
Human Reproductive System (RIT BRANCH): Physiology, Hormonal Control & Clinic...
byBALAJI SOMA
 
PPTX
blood banking and blood component. New onepptx
byRayAdhikariRatnesh
 
PPTX
Sahil Srivastava ppt on Moringa Oleifera.pptx
bySahil Srivastava
 
PDF
Ibrutinib 140 mg Capsule Treatment Guide
byLetsMeds
 
PDF
Lenvatinib Tablets: Uses, Benefits, Diseases Treated & Availability in the Ph...
byLetsMeds
 
PPTX
Pharmacovigilance in Rare Diseases by Sahil Srivastava.pptx
bySahil Srivastava
 
PPTX
CELL PHYSIOLOGY: STRUCTURE AND FUNCTIONS
byDR.P.S SUDHAKAR
 
PPTX
Differentiation between benign and malignant tumors.pptx
byalialiali20052016
 
PPTX
Apporach to lung biopsy [Auto-saved].pptx latest
byRayAdhikariRatnesh
 
PPTX
Speech language Pathology-1 (lecture 1).pptx
byDr Zonera Khalid PT
 
PPTX
Full Endoscopic Interlaminar Lumbar Discectomy
byNtambi Rogers
 
PPTX
HD catheters, what do we need to know 2025 updated.pptx
byJAFAR ALSAID
 
PDF
Unit II 02.2 Non-Aqueous Titration, Acidimetry and Alkalimetry
bysanjayudps2016
 
PPTX
Holistic Oral Care- Danta Davana and Jihwa nilekhana in Ayurveda: Classical ...
bySudha Sumathy
 
PDF
ICL Implantation: A Lifetime of Clear, Sharp Vision
byDr Chameen Samarawickrama
 
PPTX
Surgery instruments for MBBS Students, pptx
bycbmesurgery
 
PDF
Microencapsulation and their Application in Novel Drug Delivery
byGOKULAKRISHNAN S
 
Antibiotics: Cephalosporins & Monobactams.pdf
byPrerana Jadhav
 
FACIAL NERVE AND ITS APPLIED ANATOMY BY Dr. AASTHA DUBEY
byAASTHA DUBEY
 
composition, functions of Extra cellular matrix. ECM Proteins, glycoproteins ...
byDr. Santhosh Kumar. N
 
Human Reproductive System (RIT BRANCH): Physiology, Hormonal Control & Clinic...
byBALAJI SOMA
 
blood banking and blood component. New onepptx
byRayAdhikariRatnesh
 
Sahil Srivastava ppt on Moringa Oleifera.pptx
bySahil Srivastava
 
Ibrutinib 140 mg Capsule Treatment Guide
byLetsMeds
 
Lenvatinib Tablets: Uses, Benefits, Diseases Treated & Availability in the Ph...
byLetsMeds
 
Pharmacovigilance in Rare Diseases by Sahil Srivastava.pptx
bySahil Srivastava
 
CELL PHYSIOLOGY: STRUCTURE AND FUNCTIONS
byDR.P.S SUDHAKAR
 
Differentiation between benign and malignant tumors.pptx
byalialiali20052016
 
Apporach to lung biopsy [Auto-saved].pptx latest
byRayAdhikariRatnesh
 
Speech language Pathology-1 (lecture 1).pptx
byDr Zonera Khalid PT
 
Full Endoscopic Interlaminar Lumbar Discectomy
byNtambi Rogers
 
HD catheters, what do we need to know 2025 updated.pptx
byJAFAR ALSAID
 
Unit II 02.2 Non-Aqueous Titration, Acidimetry and Alkalimetry
bysanjayudps2016
 
Holistic Oral Care- Danta Davana and Jihwa nilekhana in Ayurveda: Classical ...
bySudha Sumathy
 
ICL Implantation: A Lifetime of Clear, Sharp Vision
byDr Chameen Samarawickrama
 
Surgery instruments for MBBS Students, pptx
bycbmesurgery
 
Microencapsulation and their Application in Novel Drug Delivery
byGOKULAKRISHNAN S
 

Stomach pathology lecture

  • 1.
  • 2.
  • 3.
  • 4.
    The normal gastricmucosa  Cardia – mainly mucus-secreting cells  Fundus (body) – acid producing parietal cells, pepsin producing chief cells  Pylorus – hormone (gastrin) production 4
  • 5.
  • 6.
  • 7.
  • 8.
    Stomach  Functions ◦ Mixfood ◦ Reservoir ◦ Start digestion of  Protein  Nucleic acids  Fats ◦ Activates some enzymes ◦ Destroy some bacteria ◦ Makes intrinsic factor – B 12 absorption ◦ Destroys some bacteria ◦ Absorbs  Alcohol  Water  Lipophilic acid  B 12 8
  • 9.
    Bezoar  A bezoaris a mass found trapped in the gastrointestinal system (usually the stomach), though it can occur in other locations.  A pseudobezoar is an indigestible object introduced intentionally into the digestive system.  There are several varieties of bezoar, some of which have inorganic constituents and others organic.
  • 10.
    Stomach pathology  Congenitalanomaly – pyloric stenosis  Inflammatory conditions – gastritis, peptic ulcers  Tumors 10
  • 11.
    Pyloric stenosis  In95% of infants with pyloric stenosis the age at presentation is between 3 and 12 weeks of life, typically between 3 and 8 weeks.  Pyloric stenosis has been reported in neonates within the first day of life. 11
  • 12.
  • 13.
    etiology  3 in1,000 live births  more commonly in males  30 percent of cases occur in firstborn  genetic predisposition  Sibling has 5 times more incidence  environmental factors  Neonatal hypergastrinemia and gastric hyperacidity may have a role 13
  • 14.
    CLINICAL MANIFESTATIONS  Theclassic presentation of IHPS is the three- to six-week-old baby who develops immediate postprandial, non-bilious, often projectile VOMITING and demands to be re-fed soon afterwards  (a "hungry vomiter"). 14
  • 15.
    Palpable mass  Themass is most easily felt immediately after emesis because it may otherwise be obscured by a distended antrum and/or tensed abdominal muscles 15
  • 16.
    Pancreatic heterotopia  Pancreatictissue outside boundaries of pancreas without anatomic or vascular connections to pancreas ● Also called ectopic pancreas ● Present in 0.5% to 14% of autopsies ● Due to displacement of pancreatic tissue during embryonic development 16
  • 17.
  • 18.
  • 19.
    Definition  The termgastritis is used to denote inflammation associated with mucosal injury.  . 19
  • 20.
  • 21.
    Pathophysiology The mechanisms ofmucosal injury in gastritis is thought to be an imbalance of aggressive factors  acid production or pepsin and defensive factors  mucus production  bicarbonate  and blood flow 21
  • 22.
    Protective factors vs.hostile factors 22
  • 23.
  • 24.
    Classification of gastritis AcuteChronic •H pylori gastritis •Other infective gastritis – bacteria, virus, fungi, parasite •Acute non infective gastritis •Type A- autoimmune •Type B- h pylori related •Type AB- environmental •Chemical – reflux gastritis •Uncommon forms 24
  • 25.
    Acute & ChronicDifference ◦ Acute refers to short term inflammation ◦ Acute refering to neurophilic infiltrate ◦ Chronic referring to long standing forms ◦ Chronic referring to mononuclear cell infiltrate especially lymphocyte and macrophages 25
  • 26.
    Acute Gastritis  Definition ◦An acute mucosal inflammatory process, with neutrophilic infiltrate, that is usually transient. ◦ There may be hemorrhage into the mucosa or sloughing of the mucosa. ◦ Severe erosive form is an important cause of severe GI bleeding 26
  • 27.
    Etiology ◦ Frequently associatedwith, among others:  heavy use of NSAIDS, especially aspirin  excessive alcohol consumption  heavy smoking  severe stress e.g. trauma, burns, surgery  Ischemia  Systemic infection ◦ Often, idiopathic 27
  • 28.
    NSAIDs NSAIDs and aspirinalso interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins 28
  • 29.
    Smoking  Promotes gastritis& ulcer occurrence  Increases the likelihood of ulcer complications  Mechanisms ◦ Stimulate gastric acid secretion ◦ Stimulate bile salt reflux ◦ Causes alteration in mucosal blood flow ◦ Decrease mucus secretion ◦ Reduces prostaglandin synthesis ◦ Decrease pancreatic bicarbonate secretion 29
  • 30.
    Acute Gastritis -Pathogenesis 30 All above Factor Acid secretion + back diffusion + Bicarbonate buffer + Blood flow Disruption of Mucus layer + Direct Mucosal Injury Acute Gastritis
  • 31.
    Stages of AcuteGastritis  Acute superficial gastritis Inflammation of superficial gastric mucosa.  Acute erosive gastritis Destruction of multiple small zones of superficial mucosa.  Acute Gastric Ulceration Destruction of full thickness of mucosa 31
  • 32.
    Mucosal congestion ,edema inflammation& ulceration ACUTE GASTRITIS - MORPHOLOGY 32
  • 33.
    Acute Gastritis -Morphology Ranges from edema with neutrophil infiltration, vascular congestion,& an intact epithelium, to erosion (mucosal defect that does not cross the muscularis mucosa) and hemorrhage. 33
  • 34.
    Acute Gastritis  Gastricmucosa demonstrates infiltration by Neutrophils 34
  • 35.
  • 36.
    Acute Gastritis  diffuselyhyperemic gastric mucosa  causes for acute gastritis ◦ alcoholism ◦ drugs ◦ infections, etc. 36
  • 37.
  • 38.
    Chronic Gastritis  Definition ◦Chronic mucosal inflammatory changes leading to atrophy and metaplasia (usually without erosions)  Dysplasia and ultimate neoplasia are complications. 38
  • 39.
  • 40.
  • 41.
    Type B (AntralGastritis) ◦ 90% of patients with antral chronic gastritis: Helicobacter pylori infected  Motile, gram negative curvilinear rods that elaborate urease (buffers gastric acid) & toxins and have adhesins to bind to the epithelium.  Pathogenesis ◦ H. pylori (urease  NH4 + + toxins) + Host (acid + peptic enzymes)  Chronic Inflammation ◦ Antibodies  Gland destruction + Mucosal atrophy   acid   intrinsic factor (which can lead to pernicious anemia) 41
  • 42.
  • 43.
    H. pylori –silver stain 43
  • 44.
    H. pylori –giemsa stain 44
  • 45.
    H. pylori –H & E stain 45
  • 46.
    Pathogenetic qualities ofH.pylori; Adheres to gastric epithelium Lives within mucous gel layer overlying gastric epithelium Penetrates intercellular junctions Invades gastric glands and canaliculi of parietal cells Secretes urease to produce ammonia, which protects it from gastric acid Produces cytotoxins that may play role in pathogenicity Induces epithelial cytolysis and disrupts intercellular junctions Increases permeability of mucous layer to hydrogen ions and pepsin Enables gastric acid and pepsin to create ulcer craters Evades host immune defenses Damages tissue. 46
  • 47.
  • 48.
    Noninvasive Urea Breath Test(UBT) Blood test Invasive Biopsy Urease TestHistology
  • 49.
    Culture Stool antigen test Uppergastrointestinal (upper GI) X-ray Other tests Endoscopy
  • 50.
    Helicobacter gastritis  2patterns of infection ◦ Diffuse involvement of body and antrum (“pan gastritis” associated with diminishing acid output) ◦ Infection confined to antrum (antral gastritis, associate with increased acid output) 50
  • 51.
    Type A (Autoimmune) Etiology ◦ Autoimmune - antibodies to parietal cells, gastrin receptor, intrinsic factor, and H+,K+ ATPase  <10% of cases of chronic gastritis  Possible autosomal dominant inheritance 51
  • 52.
    Morphology of chronicgastritis  Chronic inflammatory cell infiltration  Mucosal atrophy  Intestinal (goblet cell) metaplasia Seen in Helicobacter and autoimmune gastritis (not chemical) 52
  • 53.
    Autoimmune gastritis  Autoimmunegastritis - pernicious anemia  Chronic atrophic gastritis is associated with Ab’s - intrinsic factor - patietal cell  bright green IF- in the parietal cells of the gastric mucosa. 53
  • 54.
    Autoimmune Gastritis -Morphology PJGoldblatt, MD Diffuse mucosal damage of the body and fundic mucosa. Antrum less involved. 54
  • 55.
    Chronic Gastritis  ClinicalFeatures ◦ Usually only a few symptoms: nausea, vomiting, upper abdominal discomfort ◦ Autoimmune  Hypo to achlorhydria (severe loss of parietal glands)  Hypergastrinemia  10% have pernicious anemia 55
  • 56.
    Clinical Complications ◦ Autoimmune: Often seen in association with other autoimmune disorders (Hashimoto thyroiditis, Addison disease, and type I diabetes)  Significant risk for the development of gastric carcinoma (2-4%) and endocrine tumors (carcinoid tumor) 56
  • 57.
    Chronic Gastritis Morphology ◦ Varyingdegrees of mucosal damage possible ◦ Mucosal lesions are reddened, with thickened rugae ◦ Atrophied rugae in long-standing cases ◦ Lymphocytes and plasma cell infiltrate; neutrophils indicate “active” inflammation (may or may not be present) 57
  • 58.
    ◦ Regeneration -constant feature ◦ Metaplasia - mucosa of antral and body-fundic regions converts to columnar absorptive cells and goblet cells (intestinal metaplasia) ◦ Atrophy - marked loss of glands ◦ Dysplasia – precursor lesion to gastric cancer in atrophic gastritis 58
  • 59.
    Sydney System of GradingChronic Gastritis 1. Site: Antral, Corporal mucosa 2. Grading of: (Mild, Moderate, Marked)  H-Pylori  Chronic inflammation  Activity  Atrophy  Intestinal metaplasia *Normal lymphocytes & plasma cells in lamina propria = up to 5/HPF *No Neutrophils in lamina propria
  • 60.
  • 61.
    Peptic Ulcer Disease Condition characterized by ◦ Erosion of GI mucosa resulting from digestive action of HCl and pepsin
  • 62.
    Peptic Ulcer Disease Ulcer development ◦ Lower esophagus ◦ Stomach ◦ Duodenum ◦ 10% of men, 4% of women
  • 63.
    Types  Acute ◦ Superficialerosion ◦ Minimal erosion  Chronic ◦ Muscular wall erosion with formation of fibrous tissue ◦ Present continuously for many months or intermittently
  • 64.
    Peptic Ulcer Disease Etiologyand Pathophysiology  Develop only in presence of acid environment  Excess of gastric acid not necessary for ulcer development  Person with a gastric ulcer has normal to less than normal gastric acidity compared with person with a duodenal ulcer
  • 65.
    Peptic Ulcer Size –variable; 0.3 – 4 cm in diameter Shape - round to oval Sharply demarcated, clean-cut, punched-out area with clean base Margins are usually level with surrounding mucosa or slightly elevated due to edema; the mucosa is undermined at the edges Radiating mucosal rugae 80% are solitary, 80% occur in the duodenum, of which 90% in the first part of the duodenum on the anterior wall’ within a few centimeter of the pyloric ring. 19% occur in the stomach(usually at the lesser curvature at the border of the body and antrum. 65
  • 66.
  • 67.
    Gastric Ulcer- GrossAppearance Sharply punched-out Large, mucosal defect or ulcer Radiating mucosal folds 67
  • 68.
  • 69.
  • 70.
  • 71.
    Microscopy:  Overhanging gastric mucosalmargins (A)  Necrotic fibrinoid debris (B)  Acute inflammatory infiltrate (C)  Granulation tissue (D)  Fibrotic scarred base (E) 71 A B C, D E
  • 72.
    Ulcer Base  Superficialthin layer of necrotic fibrinoid debris  Zone of inflammatory infiltrate with neutrophils  Zone of granulation tissue with dilated blood vessels and lymphocytes  Zone of fibrous scarring 72
  • 73.
  • 74.
    Gastric ulcerDuodenal Ulcer middleage 50-60Any age specially 30-40Age More in maleMore in maleSex SameStress job eg. ManagerOccupation Epi. Can radiate to back Epigastric , discomfortPain Immediately after eating 2-3 hours after eating & midnight Onset EatingHungerAgg.by
  • 75.
    Gastric ulcerDuodenal Ulcer Lyingdown or vomitingEatingRelived by Few weeks1-2 monthsDuration Common(to relieve the pain) UncommonVomiting Pt. afraid to eatGoodAppetite Avoid fried foodGood , eat to relieve the painDiet wt. LossNo wt. lossWeight 60%40%Hematemesis 40%60%Melena
  • 76.
    GASTRIC TUMORS  BENIGN: POLYPS (HYPERPLASTIC vs. ADENOMATOUS)  LEIOMYOMAS (Same gross and micro as sm. muscle)  LIPOMAS (Same gross and micro as adipose tissue)  MALIGNANT  (ADENO)Carcinoma  LYMPHOMA  POTENTIALLY MALIGNANT  G.I.S.T. (Gastro-Intestinal “Stromal” Tumor)  CARCINOID (NEUROENDOCRINE)
  • 77.
    WHO GASTRIC NEOPLASMS Epithelial Tumors:  Adenomatous polyps  Adenocarcinoma (papillary, tubular, mucinous, signet ring, adenosquamous, unclassified),  Small cell, Carcinoid (neuroendocrine)  Nonepithelial Tumors: Leiomyooma, Leimyosarcoma,  Schwannoma, GIST, Granular Cell Tumor, Kaposi sarcoma  Malignant Lymphomas:
  • 78.
  • 79.
    GC is notfar from us…… Napoleon‘s gastric cancer：tumor found on the lesser curvature of the stomach: What cause? How to treat? Ambition is never content, even on the summit of greatness. He conquered the larger part of Europe, but he could not conquer gastric cancer
  • 80.
    How to diagnose Whatis epidemiology and etilogy What is the pathology How to treat Content
  • 81.
    How to diagnose Whatis epidemiology and etilogy What is the pathology How to treat Content
  • 82.
    GC Worldwide incidence Male16.4 Female 8.2 Male 36.3 Female 16.9 Male 77.9 Female 33.3 Male 10.8 Female 4.9 Male 43.6 Female 19.0 Male 5.9 Female 2.6 Male 11.5 Female 4.3 Male 18.6 Female 13.3 Male 8.4 Female 4.0 Eastern Europe Japan Australia/ New Zealand China Northern Africa Southern Africa Central America Western Europe North America In terms of geographic distribution, high rates apply to Japan, China and Eastern Europe and low rates to North America. Almost 40% of cases occur in China . Pazdur R et al. Cancer management: A multidisciplinary approach. edition,2002
  • 83.
  • 84.
    Precancerous changes  precancerousdiseases  chronic atrophic gastritis  gastric ulcer  gastric polyps  gastric remnant  precancerous lesion  atypical hyperplasia
  • 85.
    “The new studysuggest he was chronically infected with the bacteria Helicobacter pylori.” “full of salt-preserved foods but sparse in fruits and vegetables-- common fare for long military” H. pylori Genetic factors “his father had also died of stomach cancer which led to the theory that he had inherited the disease.” Diet Precancerous changes Why Napoleon died of GC chronic atrophic gastritis?
  • 86.
    How to diagnose Whatis epidemiology and etilogy What is the pathology How to treat Content
  • 87.
    Early gastric cancer Defined as a tumor confined to the mucosal or submucosal layer, with or without lymph node metastasis
  • 88.
    Advanced gastric cancer invasion depth beyond submucosal layer
  • 89.
    Morphology SITE - Favouredlocation is the lesser curvature of the antropyloric region Gastric carcinoma is classified on the basis of - depth of invasion - macroscopic growth pattern - histologic subtype
  • 90.
  • 91.
    Gross: Linitis plastica carcinoma diffuselyinfiltrates the entire gastric wall without forming an intraluminal mass. The wall of the stomach is typically thickened to about 2-3 cm. and has a leathery, inelastic consistency.
  • 92.
    Lauren classification Intestinal type ---associated with most environmental risk factors --- carries a better prognosis --- shows no familial history  Diffuse type --- consists of scattered cell clusters with poor prognosis
  • 93.
    Intestinal type gland formationby malignant cells, Gastric carcinoma. Diffuse type demonstrating signet-ring carcinoma cells.
  • 94.
    Bormann classifications  Grossclassification phymatoid type ulcerative type infiltrative ulcerative diffuse infiltrative type
  • 95.
    Histology classification  Adenocarcinomaoccupy 95%  Lymphomas 2%  Carcinoids 1%  Adenocathomas 1%  Squamous cell 1%
  • 96.
    TNM classification ——T Primary tumor: depth of tumor invasion Tx- cannot be assessed T0- no evidence Tis- carcinoma in situ, no invasion of lamina T1- invades lamina propria or submucosa T2- invades muscularis or subserosa T3- penetrates serosa, no adjacent structure T4- invades adjacent structures
  • 97.
    T:Primary tumor  Directextension into omentum, pancreas, diaphragm, transverse colon, and duodenum.  If lesion extends beyond wall to a free peritoneal surface, peritoneal involvement is frequent.
  • 98.
    TNM classification ——N Regional Lymph Nodes NX- cannot be assessed N0- no nodes N1- mets in 1-6 regional nodes N2- mets in 7-15 regional nodes N3- mets in more than 15 regional nodes
  • 99.
    TNM classification ——M Distant metastasis MX- cannot be assessed M0- no distant metastases M1-distant metastases
  • 100.
    Spread Patterns  Directinvasion  Lymph node dissemination  Blood spread  Intraperitoneal colonization
  • 101.
    Special term  Blumershelf A shelf palpable by reactal examination, due to metastatic tumor cells gravitating from an abdominal cancer and growing in the rectovesical or rectouterine pouch  Krukenberg tumor A tumor in the ovary by the spread of stomach cancer
  • 102.
    What is theclassification for Napoleon , GC “The scientists suggest that Napoleon died from a T3N1M0 (stage IIIA) gastric cancer. This means the tumour (T3) had spread to some local lymph nodes (N1) near the stomach, but had not spread or metastased (M0) to other organs. The prognosis for such tumours is known to be very poor. ”
  • 103.
    How to diagnose Whatis epidemiology and etilogy What is the pathology How to treat Content
  • 104.
    Clinical manifestation Early GastricCancer  Asymptomatic or silent 80%  Peptic ulcer symptoms 10%  Nausea or vomiting 8%  Anorexia 8%  Early satiety 5%  Abdominal pain 2%  Gastrointestinal blood loss <2%  Weight loss <2%  Dysphagia <1%
  • 105.
    Clinical manifestation Advanced GastricCancer  Weight loss 60%  Abdominal pain 50%  Nausea or vomiting 30%  Anorexia 30%  Dysphagia 25%  Gastrointestinal blood loss 20%  Early satiety 20%  Peptic ulcer symptoms 20%  Abdominal mass or fullness 5%  Asymptomatic or silent <5%
  • 106.
    Special signs  Linitisplastica: --- diffusely infiltrating with a rigid stomach  Virchow’s node: --- left supraclavicular lymph node  Sister Mary Joseph’s node: --- umbilical lymph node  prerectal pouch mass (Blumer shelf) --- seeding metastasis
  • 107.
  • 108.
    Laboratory tests  Assistsin determining optimal therapy.  CBC identifies anemia, with may be caused by bleeding, liver dysfunction, or poor nutrition.  30% have anemia.  Tumor markers CEA:carcino-embryonic antigen CA19-9:carbohydrate antigen CA724:carbohydrate antigen
  • 109.
    Imaging Studies  Endoscopicdiagnosis --- biopsy needed for definitive diagnosis  Endoscopic screening --- general population or high risk persons
  • 110.
    How to diagnoseNapoleon , GC Endoscopic diagnosis? Endoscopic Ultrasonography? CT scan? Preoperative staging ...... Why?
  • 111.
    How to diagnose Whatis epidemiology and etilogy What is the pathology How to treat Content
  • 112.
    G.I.S.T. TUMORS  Canbehave and/or look benign or malignant  Usually look like smooth muscle, i.e., “stroma”  Are usually POSITIVE for c-KIT (CD117), i.e., express this antigen on immunochemical staining, the tumor cells are derived from the interstitial cells, of Cajal, a “neural” type of cell
  • 113.
    G.I.S.T. TUMORS  c-KIT(receptor for stem cell factor) mutations  platelet-derived growth factor receptor-a. (PDGFRA) mutations  tyrosine kinase inhibitor (STIS71) has been shown to be effective in treatment
  • 114.
  • 115.
    CARCINOID TUMOR  arisefrom the diffuse components of the endocrine system  majority are found in the GI tract, and more than 40% occur in the small intestine  tracheobronchial tree and lungs
  • 116.
    Gastric carcinoids  releasepeptide and nonpeptide hormones to coordinate gut function  carcinoids are intramural or submucosal masses that create small polypoid lesions
  • 117.
  • 119.
  • 120.
    The most importantprognostic factor for GI carcinoid tumors is location Foregut carcinoid tumors  rarely metastasize and are generally cured by resection Midgut carcinoid tumors  Aggressive, greater depth of local invasion, increased size, and presence of necrosis and mitosis are associated with poor outcome Hindgut carcinoids occur in appendix & rectum  in appendix almost uniformly benign < 2cm  Rectal carcinoid rarely metastsize
  • 121.
    GASTRIC LYMPHOMA Primary : Mucosa (gut)-associated lymphoid tissue tumor Previously called MALToma, MALT-type lymphoma, or MALT lymphoma, Now called Extranodal marginal zone B-cell lymphoma of MALT type lymphoepithelial lesion (LEL) is a hallmark Secondary spread from adjacent lymph nodes
  • 122.
     Peptic ulcers Gastric carcinoma 122
  • 123.