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Viral hepatitis Carcinomas of the Alimentary tract Esophageal Carcinoma (EC) Gastric Carcinoma (GC) Colorectal Carcinoma (CRC) 1.

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Presentation on theme: "Viral hepatitis Carcinomas of the Alimentary tract Esophageal Carcinoma (EC) Gastric Carcinoma (GC) Colorectal Carcinoma (CRC) 1."— Presentation transcript:

1 Viral hepatitis Carcinomas of the Alimentary tract Esophageal Carcinoma (EC) Gastric Carcinoma (GC) Colorectal Carcinoma (CRC) 1

2 Barrett esophagus (precursor of E-adenocarcinoma ) Preneoplastic disorders of these three tumors: EC: >90%-squamous cell carcinomas, <10%-adenocarcinomas. preceded by chronic esophagitis ---Squamous epithelial dysplasia --- intraepithelial neoplasia (carcinoma in situ)---- preneoplastic disorder 2 chronic esophagitiscarcinoma in situ

3 chronic esophagitis 3 Mild esophagitis: simple hyperemia, with no histologic abnormality. Uremia, prolonged gastric intubation, ingestion of corrosive or irritant substances, radiation, and so on Many causes may induce chronic esophagitis Morphologic change- on gross: Severe esophagitis: epithelial erosion, or ulceration into the submucosa.

4 chronic esophagitis ( on microscope) 4 chronic esophagitis three histologic features: ① eosinophils, with or without neutrophils, in the epithelial layer; ② basal zone hyperplasia, ③ elongation of lamina propria papillae. intraepithelial neutrophils occur in more severe injury.

5 Barrett esophagus: Replacement of esophageal squamous- epithelium with gastric epithelium (in book page 218) distal esophagus (pale pink) stomach (more lush light brown) Gastroesophageal junction 5 (salmon-pink) metaplastic columnar gastric epithelium Normal condition Barrett esophagus

6 Preneoplastic disorders (precursor lesions) GC 1. Atrophic chronic gastritis with mucosal dysplasia 6 2. Adenoma : true neoplasm containing dysplastic epithelium

7 Preneoplastic disorders CRC 1. Adenoma (villous adenoma ) 7 (in book page 236) (in book page ) 3. FAP ( familial adenomatous polyposis) Ulcerative colitis (in book p237 )

8 Adenomas of colon 8 (in book page 236) villous adenoma Basis on the epithelial architecture, adenomas of colon is divided into three sub-types. tubular adenomas (most common) tubulovillous adenoma (5-10%), villous adenomas (only 1%) villous adenoma On gross: sessile, velvety or cauliflower-like masses; On microscope: frondlike villiform extension of the mucosa is covered by dysplastic epithelium. Invasive carcinoma is found in up to 40% of these lesions.

9 9 (in book page ) Ulcerative colitis (ulceroinflammatory disease) affect the colon limite to the mucosa and submucosa (except in the most severe cases) a systemic disorder On gross, mucosa hyperemia, edema, and granularity. (with easy bleeding) In severely active cases, broad-based ulceration. Morphologic features: Histologic features: mucosal inflammation, ulceration of the mucosa, chronic mucosal damage.

10 Morphology 1.Favored Location: EC three natural narrow areas 20% of ~ arise in upper third esophagus (5cm) 50% in the middle third esophagus (18cm) 30% in the lower third esophagus (1-2cm) GC Pylorus and antrum 50~60%; Cardia 25%; remainder in body/fundus Lesser curvature (about 40%) > greater curvature (12%) So, favored location of ~ : lesser curvature of the antropyloric region CRC 50% arise in rectum, and 25% in ascending colon. 10 Three natural narrow of esophagus

11 2. Three gross pattern –take one of three forms EC ● Exophytic polypoid or fungating form: mass protrude into the lumen ● Endophytic ulcerative form : ulcerative cancer mass extend deeply ● Diffuse infiltrative form: cancer mass impart thickening and rigidity to the wall and lead to narrowing of the lumen. 11

12 2. Gross appearance: base on invasive depth-early and advanced ~ GC (1) Early Gastric Carcinoma (E-GC) : confined to the mucosa and submucosa, regardless of presence or absence of perigastric lymph node metastases. ( basis on clinical data: 10 % of E-GC: lymph node metastases ) Elevated form of E-GC Depressed form of E-GC Two gross patterns: elevated form depressed form Both have no obvious tumor mass in the mucosa (---) 12

13 2. Gross appearance GC (2) Advanced Gastric Carcinoma (A-GC) : tumor mass has extended below the submucosa into the muscular wall. In some cases, perhaps has spread more widely. A-GC have three gross forms: (2.1) Exophytic polypoid or fungating mass (form) 13

14 (2.2 ) Endophytic ulcerative form (2.3 )Diffuse infiltrative mass. This rigid and thickened stomach is called a “leather bottle” stomach— 革囊胃 (cancer mass imparts thickening and rigidity to the wall, and lead to narrowing of the lumen) 14

15 (2.2 ) Endophytic ulcerative mass larger, more surface , significant elevated edges 15 Gastric ulcerative carcinoma gastric peptic ulcer

16 gastric peptic ulcer gastric cancer ulcer Location the lesser curvature the lesser and greater ~ Size / shape 1-2cm, round >2 cm, irregular Basis of depth deeper more surface Margins sharply elevation or beading Surrounding mucosal folds radiate absent Base of crater clean necrotic gray Cut section an eroded artery absent Histologic appearance four zones invasion by malignancy Obvious differences between peptic ulcer and cancer ulcer: (list) 16 peptic ulcer Cancer ulcer

17 2. Gross appearance CRC (1)Exophytic Polypoid or fungating form (2)Endophytic ulcerative form (3)Diffuse infiltrative form (4) Mucinous mass with a gel-colloid appearance. (mucinous adenocarcinoma) 17

18 Microscopic appearance : carcinomas arise from superficial epithelium of mucosa or gland EC Squamous cell carcinoma constitute > 90% Adenocarcinomas: (<10%), arise from dysplastic mucosa in Barrett esophagus. Well- moderately- poorly-differentiated (Mucin-producing adenocarcinoma) 18

19 GC Adenocarcinoma > 90% Squamous cell carcinoma (<10%): locate in cardia. Histologic: gastric adenocarcinoma --- two major types: intestinal- type diffuse-type Microscopic appearance There are some differences between these two types (in book page ) WHO Classification Method: well-, moderately-, poorly-differentiated. 19 Malignant calls form neoplastic glands do not form glands Like glands of colonic-- permeate the gastric wall

20 Microscopic appearance GC signet-ring cell carcinoma Nucleous of tumor cell is squeezed to cell margin, like diamond in married-ring. 20

21 Microscopic appearance CRC Adenocarcinoma > 90% Signet-ring cell carcinoma: Mucin present in tumor cells Mucinous adenocarcinoam: Mucin is secreted into gland lumina 21 Squamous cell carcinoma (arising anal zone ) Special type: produce mucin

22 EC ( 食道癌 ) CPC (clinico-pathological correlation) GC ( 胃癌 ) CRC ( 大肠癌 ) In onset: insidious In late stage - dysphagia and obstruction gradually Bleeding-hematemesis or melena Other: weight loss, anorexia, fatigue, weakness and pain (relate with swallowing) 22 E-GC: asymptomatic A-GC: abdominal discomfort or weight loss Locate in cardia: dysphagia Locate in the pyloric canal: obstructive symptoms Other: melena, fatigue, weekness-- Most cases: remain asymptomatic for years To see doctor: Faeces with bright red blood, change in bowel habit, and abdominal discomfort Significant clinical features: Faeces with bright red blood Faeces like writing brush Alternation of obstruction and diarrhea

23 Bleeding: in these three tumors As blood quickly congeals and turns brown in the acid environment of the stomach lumen Vomited blood: coffee grounds in patients with GC bright red blood in EC Faeces: melena (black- faeces) in patients with EC or GC bright red blood in patients with CRC 23

24 Invasion and metastasis ( 浸润和转移 ) Spread by direct extension into adjacent structures For EC: Upper third larynx, trachea, thyroid (occurred) Middle third bronchus Lower third cardia 贲门 into 24

25 Invasion and metastasis Spread by direct extension For GC : spread into greater omentum and pancreas For CRC: spread into urinary bladder or uterus 25

26 Invasion and Metastasis 2. Metastasis ( for EC) Lymphatic pathway: Spread to regional LN late stage terminal LN - left supraclavicular L ( last region )胸导管-左锁骨上 LN ( Virchow LN) Hematogenous pathway : to distant sites favored organs: Lung, liver and bone. Seeding within body cavities: In females, tumor cells of GC seed to both the ovaries, krukenberg tumor ( 克氏瘤 ) 26

27 1. Endoscopy biopsy 2. Digital rectal examination : for rectal cancer. Digital rectal examination Diagnosis 27

28 Prognosis: for all tumors The most important prognostic indicator is the tumor stage at the time of resection. at Early stage: 5-y survival rate 90 ~ 95% , removed at Late stage: 5-y survival rate 10 ~ 15% , removed So the only hope for cure of tumor is early detection and surgical remove. 28

29 Related to gene alterations Many studies indicate: genesis and development of tumor relate to some genes. EC - p53, p16 GC - c-met, K-sam, erb CRC - APC DNA repair gene DCC ( deleted in colon cancer) p53 K-ras 30

30 Colorectal carcinogenesis: two pathogenetically distinct pathways for the development of colon cancer. APC/β-catenin pathway (adenoma-carcinoma sequence, or chromosome instability) Mismatch repair pathway (microsatellite instability) 30

31 Colorectal carcinogenesis: both of these pathways involve the stepwise accumulation of multiple gene’mutations. but the genes involved and the mechanisms are different. 31

32 Mismatch repair pathway (p239, Fig.10-23) APC/β-catenin pathway (p.239,Fig ) Normal colon Adenomas Carcinoma Mucosal at risk APC at 5 APC/β-catenin K-RAS at 12p12 Telomerase Many other genes P-53 at 17p13 LOH at 18q21 Normal colon Carcinoma Sessile serrated adenoma MLH1, MSH2 Alteration of second allele by LOH, mutation, or promoter methylation Microsatellite instability Mutations of BAX,TCF-4, et al 32

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