Benign and malign diseases of Stomach

... konulu sunumlar: "Benign and malign diseases of Stomach"— Sunum transkripti:

1 Benign and malign diseases of Stomach
Prof. Dr. Öge TAŞCILAR

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5 MİDE Mukoza Submukoza Muskularis Propria Seroza İntraepitelyal Mukoza
Bazal Membran Lamina Propria Muskularis Mukoza

6 Fonksiyon: MİDE Alınan gıdaların sindirimi ve emilimi
Reseptif relaksasyon ve gastrik adaptasyon İntragastrik basınç düşer. 100cc cc

7 Mallory-Weiss Sendromu
MİDE Mallory-Weiss Sendromu Kusma ile ÖG bileşke mukoza submukoza yırtık ve kanama Endoskopi Alkol,diyabet,gebelik, üremi, Tam kat olursa Booerhaave sendromu

8 MİDE Bezoarlar Midede oluşan yabancı cisimler. Trikobezoar-fitobezoar
Mide operasyonu sonrası Antrumun öğütücü işlevinin kaybolması HCL azalmasına bağlı Candida Albicans bezoar Tanı: Radyoloji-endoskopi Tedavi:Endoskopik-Cerrahi

9 MİDE Menetrier Hastalığı Hipertrofik mukozal gastropati
Fundus ve korpusta dev rugalar Foveolar hiperplazi Hipoklorhidri ve Hipoalbüminemi 50> erkekler Epigastrik ağrı, kilo kaybı, (özellikle protein) , kanama, diare, ödem Medikal tedavi PPI Destek tedavisi Çok ciddi olgularda rezeksiyon

10 Acute gastritis Drugs (non-steroidal anti-inflammatory drugs NSAID), alcohol cause acute erosion (loss of mucosa superficial to muscularis mucosae). Can result in severe haemorrhage

11 Chronic gastritis ABC A – autoimmune(associated with vitamin B12 malabsorption (pernicious anaemia) B – bacterial (helicobacter) C – chemical(bile reflux, drugs)

12 Autoimmune chronic gastritis
Autoantibodies to gastric parietal cells Hypochlorhydria/achlorhydria Loss of gastric intrinsic factor leads to malabsorption of vitamin B12 with macrocytic,megaloblastic anaemia

13 Helicobacter pylori Adapted to live in association with surface epithelium beneath mucus barrier Causes cell damage and inflammatory cell infiltration In most countries the majority of adults are infected

14 Peptic ulcer disease A surface breach of mucosal lining of GI tract occurring as a result of acid and pepsin attack Sites: Duodenum (DU) Stomach (GU) Oesophagus Gastro-enterostomy stoma Related to ectopic gastric mucosa (e.g. in Meckel’s diverticulum)

15 Pathogenesis In normal acid/pepsin attack is balanced by mucosal defences Increased attack by hyperacidity Weakened mucosal defence – the major factor (H. pylori related)

16 MİDE Duodenal Ülser: Duodenal HCO3 sekresyonu azalmış
Gece asit sekresyonu artmış Duodenal asit yükü artmış Bazal ve postprandial gastrin artmış Tamamına yakın HP gastrit saptanmıştır.

17 Morphology of peptic ulcers
Clean, non-elevated edge Granulation tissue base (floor) Underlying fibrosis

18 MİDE Klinik: Yanıcı, kemirici, açlık ağrısı. Epigastrium
Antiasit ve gıda ile hafifler. Mevsimsel bir ağrı. İlkbahar, sonbahar, stress dönemleri Penetre olursa ağrı özellikleri değişir.

19 MİDE Tedavi: Anamnez, Radyoloji Endoskopi, biyopsi Medikal tedavi
Antiasit Sükralfat H2 blokör PPI Prostoglandin analogları

20 MİDE DÜ Cerrahi Tedavi: BTV-PP BTV-Distal gastrektomi+GJ PGV

21 MİDE Mide Ülseri

22 Complications of peptic ulcer
Perforation leading to peritonitis Haemorrhage by erosion of vessel in base Penetration of surrounding organ (liver/pancreas) Obstruction (by scarring) – pyloric stenosis (Cancer – rare event in true peptic ulcer)

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24 BENIGN__ 10% MALIGNANT__90% BENIGN Polyps Lipomas Leiomyomas
NEOPLASMS OF STOMACH BENIGN__ 10% MALIGNANT__90% BENIGN Polyps Lipomas Leiomyomas 24

25 NEOPLASMS OF STOMACH MALIGNANT Adenocarcinoma 95% Lymphoma % Others % (sq.cell ca, angiosarcoma, carcinosarcoma, Gist)

26 Less common gastric neoplasms
Gastrointestinal stromal tumour (GIST) Lymphoma Neuroendocrine (carcinoid) tumours

27 GIST Risk categories were assigned according to current recommended NIH criteria. Tumors <2 cm and<5 mitosis per 50 high-power fields (HPF) were classified as very low risk. Tumors ranging from 2 to 5 cm and having <5 mitoses/50 HPF were classified as low risk.

28 Tumors <5 cm but having 6 to 10 mitoses/50 HPF were intermediate risk, as were tumors from 5 to 10 cm with <5 mitoses/50 HPF. Tumors >5 cm with >5 mitoses/50 HPF was defined as high risk, as was any tumor >10 cm or any tumor with >10 mitoses/50 HPF.

29 GASTRIC STROMAL TUMOURS
PRESENTATION; Mass abdomen Upper GI bleeding Obstruction PATHOLOGY; Difficult to ascertain benign or malignant nature Size & Histology is the criteria TREATMENT; Surgical resection Lymph node resection not necessary. 29

30 MİDE LENFOMA Non-Hodgkin Lenfoma(NHL) klasik olarak lenf nodlarından gelişir. Ama NHL %30 olguda ekstranodal(Solid organ kaynaklı) olarak gelişebilir. GI sistem tüm NHL %20

31 MİDE LENFOMA GI lenfoma; oral kaviteden rektuma En sık; Mide
Sonra ince barsak Kolon Pankreas

32 MİDE LENFOMA NHL, ekstranodal lenfoma ve GI lenfomanın en sık görülen tipi diffüz B hücre lenfoması. MALT lenfoma Burkitt lenfoma T- hücre lenfoma

33 Gastric lymphoma Malignant neoplasm of mucosa associated lymphoid tissue (MALT) A (usually) low grade B-cell (marginal cell) lymphoma

34 MİDE LENFOMA Antrum ve distal mide Proksimal yerleşebilir.
Karın ağrısı, erken doyma Bulantı, kusma, halsizlik Abdominal dolgunluk Kronik kan kaybı, anemi melena

35 Gastric lymphoma (maltoma)
Neoplastic cells infiltrate the epithelium (lymphoepithelial lesions) Strongly associated with chronic H. pylori and can be cured by eliminating infection.

36 MİDE LENFOMA Tedavi HP tedavi edilmeli. Bir zamanlar cerrahi
Şimdi Konservatif, bazı olgularda cerrahi Low grade lenfoma(MALT) HP eradikasyonu, KRT, High Grade: Antihelikobakter tedaviye cevap vermeyen erken evre PGL, ileri evre lenfoma, diffüz büyük hücreli lenfoma ise cerrahi tedavi KT-RT Residual hastalık: KT-cerrahi

37 Neuroendocrine tumours
Carcinoids are tumours of resident neuroendocrine cells in gastric glands Usually seen in context of chronic atrophic gastritis (driven by gastrin) Clinical behaviour variable

38 GASTRIC CANCER 38

39 ETIOLOGY 1.HELICOBACTER PYLORI CA of body & distal stomach
Gastritis Gastric atrophy Intestinal metaplasia 2.PERNICIOUS ANEMIA 3.GASTRIC POLYPS 4.Pt. with surgery of peptic ulcer disease Billroth II gastrectomy Gastroenterostomy Pyloroplasty 4 times increased risk 39

40 5.Cigarette smoking &dust ingestion
6.Diet Consumption of potatoes,pickled vegetables,dried/salted fish & less milk Alcohol ingestion Excessive salt intake Deficiencies of anti oxidants Exposure to N- Nitrosocompounds 7.Familial predisposition Relatives of CA stomach pt. are 4 times more at risk Genetically H-ras, C-erb B2 & APC gene mutations have some role in pathogenesis of CA stomach Blood group A 8.Gastric ulcer 3-5% of cases?? 9. İntestinal metaplazi Tip1,2 ve 3 En tehlikeli olanı Tip 3 40

41 PATHOLOGY MACROSCOPIC CLASSIFICATION Schirrous (lintis plastica)
Ulcerative Polypoid Superficial spreading HISTOLOGICALLY (W.H.O) Papillary Tubular Mucin secreting Signet ring cell 41

42 Clinical Features GASTRIC CANCER Early feeling of fullness after meal
Bloating , distention Vomiting Pallor – iron deficiency anemia due to tumour bleed Dysphygia –epigastric fullness or vomiting due to obstrution of gastric outlet Epigastric mass – ¼ of cases Non metastatic effects ; thrombophlebitis Deep venous thrombosis ( by affecting thrombotic & haemostatic mechanism) 42

43 Trosier sign(virchows node)
Ascites Jaundice Trosier sign(virchows node) Sister mary joseph nodule krukenberg tumour Blummer Shelf 43

44 INVESTIGATIONS BLOOD COMPLETE EXAM. ------ Anemia
STOOL EXAM. --- for occult blood in ½ of pts. CARCINOEMBRYONIC (CEA) LEVEL--- elevated in 65% of cases GASTRIC JUICE ANALYSIS--- 20% are achlorhydric after maximal stimulation DOUBLE CONTRAST BARIUM MEAL--- mucosal irregularities and to assess the size , shape, margins of lesions GASTROSCOPY & BIOPSY---minimum of 6 biopsies for accuracy --- brush cytology C.T. SCAN ENDOSCOPIC USG LAPAROSCOPY 44

45 Advanced Gastric CA 45

46 Advanced Gastric CA 46

47 Advanced Gastric CA 47

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51 STAGING TNM Staging of Gastric CA
Tis tumour limited to limited to mucosa without penetration through basement memb into lamina propria T1 Tumour limited to mocosa or mucosa and submucosa T2 Tumour extendind into muscularis propia and may extend into but not through the serosa T3 Tumour penetrates serosa without invadind contiguous strutures T4 Tumour invading adjacent strutures N0 No metastasis to regional lymph nodes N1 Involvement of perigastric lymph nodes within 3cm of primary tumour N2 Involvement of regional lymph nodes more than 3cm from the primary tumour including nodes along left gastric,splenic, celiac and common hepatic arteries N3 Involvement of other nodes such as para-aortic, hepatoduodenal, retropancreatic and mesenteric nodes. M0 No distant metastases M1 Distant metastasis present N1—1-6..REGIONAL NODES INVOLVED N NODES INVOLVED N3– MORE THAN 15 NODES INVOLVED 51

52 CT STAGING OF GASTRIC CA
STAGE I Intraluminal mass without wall thickening STAGE II Wall thickening greater than 1 cm STAGE III Direct invasion of adjacent structures STAGE IV Metastatic disease STAGING IA T N MO IB T N M0 II T N M0 III T N M0 IIIB T N M IV AnyT Any N M1 52

53 SPREAD DIRECT : LYMPHATIC : By permeation Emboli Trosier,s sign
BLOOD BORN METASTASIS Liver Lung,bones TRANSPERITONEAL SPREAD Indicates incureability Manifests as ascities Krukenberg tumour Sister joseph nodule Blumer,s shelf 53

54 TREATMENT SURGICAL TREATMENT 1.SURGERY; --curative --palliative
2.RADIOTHERAPY 3.CHEMOTHERAPY SURGICAL TREATMENT Incurable disease is not subjected to radical surgery Evidence of incureability are; --Haematogenous spread --Distant peritoneal involvement --N4 nodal disease & disease beyond N4 nodes --Fixation to structures that can not be removed Cure resection should be considered in remaining pts. 54

55 Total Gastrectomy 55

56 Subtotal Gastrectomy 56

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60 3.PALLIATIVE SURGERY; RADIOTHERAPY; CHEMOTHERAPY;
In symptoms of obstruction & bleeding Only tumour is removed &GIT continuity is restored by ROUX LOOP Gastric exclusion & oesophagojejunostomy Palliative intubation & stenting (for inoperable cardia tumours) RADIOTHERAPY; Results are disappoiting in CA stomach But have benefits in painful bony metastasis CHEMOTHERAPY; Epirubacin + cispltinium+5-FU Mitomycin C– impregnated charcoal in intraperitoneal route ( in Japan) RELAPSE & METASTASIS; Common site of relapse is Gastric bed Metastasis occur in –intra peritoneal & distal LNs -- liver -- lungs & bones 60