Gastro 48 Stomach - Gastric and duodenal ulcer ZES

  1. What is peptic ulcer?
    Erosion of gastric and duodenal mucosa that extend through muscularis mucosa
  2. Pathogenesis of peptic ulcer disease
    Increased aggresive factors - HCL, Pepsin, ethanol, Smoking, Duodenal reflux of bile, NSAIDS, H. pylori infection

    Decreased protective factors - Mucosal bicarbonate secretion, endogenous PG, blood flow
  3. Features of H. pylori
    • Spiral helocobacter
    • Gram negative rod
    • Flagellated (4-6)
    • urease +ve
    • Resides beneath mucous layer
    • Microaerophilic
    • Can live only in gastric epithelium
  4. Sucralphate
    Sucrose Aluminium phosphate

    • Dissociated in acidic mediaum - sucrose polymerise and binds with protein in ulcer
    • crater to produce a protective coating for 6 hours
  5. Most postent H2-antihistaminic
    Famotidine
  6. Difference between gastric and Peptic Ulcer?
    • In gastric ulcer - Food increases pain (food-pain-relief) 
    • In duodenal ulcer - food decreases pain (food-relief-pain). Patient gets pain when the stomach is empty i.e in early morning or before having lunch.
  7. Treatment of complicated peptic duodenal ulcer
    Intractable - acid-reducing operation (truncal vagotomy, selective vagotomy, or highly selective vagotomy, with or without an antrectomy)

    Bleeding - Oversewing of bleeding vessels

    Perforation - Patch closure

    Obstruction - GJ, rule out malignancy

    All cases need treatment of H. pylori
  8. Scoring system to predict rebleeding
    • Blatchford score - doesnot require endoscopic informatin 
    • Rockall score - takes account of endoscopic findings 
    • Forrest Classification
  9. Ulcers that have high risk of rebleeding?
    • Size >2cm 
    • Posterior duodenal ulcer 
    • Gastric ulcers
  10. Forrest Classification
    • I - Active bleeding
    • Ia - Active Spurting
    • Ib - Active oozing

    • II - Recent Hemorrhage
    • IIa - Non Bleeding vessels
    • IIb - Adherent clot
    • IIc - Flat pigmented spot

    III - No signs of hemorrhage, Clean based ulcer
  11. Management of bleeding based on Forrest classification
    • I-IIa -Endoscopic therapy
    • IIb - Adherent clot is removed and base is evaluated. Ulcer with clear base or black spot secondary to hematin deposition do not require endoscopic treatment
  12. Sarins Classification of Gastric Varices?
    • GOV I - Extension of esophageal varices along lesser curvature, 74% [@ 1 is less]
    • GOV II - Extension of esophageal varices along greater curvature [@ 2 is greater]
    • IGV I - Type I isolated gastric varices - in fundus 
    • IGV II - Type 2 Isolated gastric varices - anywhere in stomach
  13. Methods to control bleeding
    • Endoscopic
    • Injection of vasoconstrictors
    • Sclerosing Agents
    • Thermocoagulation
    • Argon Plasma Coagulation (APC)
    • Clip placement - for spurting vessels 
    • Banding 
    • Combined approach - combination of thermal coagulation with epinephrine is better than epinephrine alone


    Angiographic endovascular embolization


    • Surgical
    • Duodenal ulcer - a) placed anteriorly - four quadrant suture ligation b) placed posteriorly - Three point U stitch for GDA and pancreatic branch ligation. Cut duodenum longitudinally, close transversely
    • For gastric ulcer - Gastrostomy and suture ligation
  14. Triple tube decompression?
    • Retrograde duodenal drain 
    • Antegrade FJ tube 
    • Gastric decompression -NG
  15. Treatment of DU perforation
    Small performation (<1cm) – MGPR

    1-3 cm perforation - Graham Patch Repair

    • >3cm
    • - Application of healthy tissue like omentum or jejunum serosa (Thal patch). In such cases, a pyloric exclusion is typically performed by oversewing the pylorus using absorbable suture. GJ is performed – Bilroth II or Roux-en-Y fashion,
    • - Distal gastrectomy with truncal vagotomy

    Drain must be kept in the place until the patient has eaten without the change of drain output or quality.
  16. Most common vessel to bleed in DU
    GDA
  17. Difference in ulcer in H. pylori and NSAIDS?
    • NSAIDS – mostly found in stomach, 25% have histological antral gastritis
    • H. pylori – mostly found in duodenum, 95% have antral gastritis
    • This finding first Elucidated by Marshall and Warren – Nobel prize in 2005
  18. Discuss the role H. pylori in gastroduodenal diseases? [TU 2057,60]

    The mechanisms responsible for H. pylori–induced GI injury and ulcer formation?
    1. Production of toxic products that cause local tissue injury - urease activity (e.g., ammonia); cytotoxins; a mucinase that degrades mucus and glycoproteins; phospholipases that damage epithelial cells and mucous cells; and platelet-activating factor, which is known to cause mucosal injury and thrombosis in the microcirculation.

    2. Induction of a local mucosal immune response attracting neutrophils and monocytes, which then produce numerous proinflammatory cytokines and reactive oxygen metabolites.

    3. Increased gastrin levels with a resultant increase in acid secretion Secondary to a reduction in antral D cells because of infection with H. pylori. A decrease in serum levels of Somatostatin as a result of H. pylori infection, which increases gastrin and acid secretion, could be the underlying causative mechanism behind the gastric hyperacidity.

    4. Gastric metaplasia occurring in the duodenum – H. pylori proliferation - causes duodenitis and likely predisposes to duodenal ulcer formation.
  19. Discuss the role of H. Pylori in the pathogenesis of gastric cancer [TU 2060,70]
    • Long-term infection with the bacteria leads to chronic inflammation that progresses to intestinal metaplasia, dysplasia, and ultimately intestinal-type adenocarcinoma.
    • Host inflammatory responses play an important role in this process. Specifically, individuals with high levels of interleukin-1 expression are at increased risk of gastric cancer development.
    • The presence of the cytoxan-associated gene A (cagA) is associated with increased virulence and risk of gastric cancer.

    It promotes growth of bacteria that generate N-nitroso-compound

    It  inhibits the secretion of ascorbic acid
  20. Diseases associated with H. pylori

    Describe the role of helicobacter pylori in various upper gastroinstestinal diseases. Describe strategies to eradicate it. [TU 67/2]
    • Chronic antral gastritis
    • Intestinal metaplasia
    • Gastric Cancer
    • Mucosal Associated Lymphoid Tissue (MALT)
  21. Detection of  H. pylori?
    • A. Invasive 
    • - Rapid urease test
    • - Histology
    • - Culture – requires 3-5 days

    • B. Non invasive –
    • - Serology – ELISA – IgG Ab of H. pylori, remains positive for 1 year, cannot be used to assess eradication of H.pylori after therapy
    • - Stool Ag and
    • - Urea breath test – Preferred modality for diagnosis
  22. Principle of Urea breath test
    Carbon labeled urea breath – ability of H. pylori to hydrolyze urea due to production of urease. Sensitivity of the test is decreased by antisecretory medication and antibody. Discontinue Antibiotic 4 weeks prior and PPI 2 weeks prior to do this test
  23. Eradication of H. pylori?
    ●For initial therapy - Triple therapy with PPI, amoxicillin (1 g twice daily), and clarithromycin (500 mg twice daily) for 14 days. If the prevalence of clarithromycin resistance < 15%, substitution of amoxicillin with metronidazole (500 mg twice daily) can be done in penicillin-allergic individuals since metronidazole resistance is common and can reduce the efficacy of treatment.

    ● Retreatment, initial treatment in areas where clarithromycin resistance is high (≥15 percent) or in patients with recent or repeated exposure to clarithromycin or metronidazole - Quadruple therapy. Quadruple therapy consists of a PPI twice daily combined with bismuth subsalicylate (524 mg four times daily) and two antibiotics (metronidazole 250 QID and tetracycline 500 mg QID) for 14 days.

    ●For patients failing two attempts at treatment, compliance with medications should be reinforced. Culture with antibiotic sensitivity testing can be done to guide subsequent treatments.

    ●For rescue therapy - levofloxacin (250 mg), amoxicillin (1 g), and a PPI each given twice daily for two weeks.

    Sequential therapy - 5 days of PPI and amoxicillin followed by 5 days of PPI, clarithromycin, and metronidazole. Studies have shown the similar results of sequential therapy as triple therapy.
  24. Intractable peptic ulcer disease?
    • Failure of an ulcer to heal after an initial trial of 8-12 weeks of therapy or if patient relapse after therapy has been discontinued
    • - Confirm H. pylori eradication of NSAIDS
    • - Serum gastrin level – to rule out gastrinoma
    • - Rule out malignancy
    • - T/t – acid reducing operations (to remove vagal stimulation – Vagotomy and to remove Gastrin driven secretion – Antrectomy)
  25. Surgical procedures for peptic ulcers?
    Truncal vagotomy– division of left and right vagus above the hepatic and celiac branches just above GE junction with pyloric drainage. Pyloric relaxation is mediated by vagal stimulation. As it denervates the whole stomacha drainage procedure is required to avoid gastric retention. The drainage procedure is either a gastrojejunostomy or pyloroplasty. Vagotomy without drainage procedure can cause DGE.

    Selective vagotomy  – Division of left and right vagus, distal to celiac and hepatic branches, with pyloric drainage. 

    • Highly selective (Parietal cell vagotomy) –  HSV severs the vagal nerve supply to the proximal two thirds of the stomach, where essentially all the parietal cells are located, and preserves the vagal innervation to the antrum and pylorus, and the remaining abdominal viscera.  Nerve of Laterjet are identified and crow feet innervation cut. No need of pylorus drainage procedure. 
    • The main advantage of highly selective vagotomy is that a drainage procedure is not required as the nerve supply to the pyloric antrum part of the stomach is retained, which is mainly responsible for the propulsion of the food material from stomach to the duodenum.
    • Extent of HSV - Proximal 5cm proximal to GE junction, Distal 7cm proximal to pylorus. Avoid missing criminal nerve of Grassi.

    • Truncal vagotomy and antrectomy
    • Antrectomy is more commonly performed for gastric ulcers. 
    • -  Removal of the antrum allows pathologic examination of antral/prepyloric ulcers to rule out carcinoma, and it decreases the rate of ulcer recurrence by removing the gastrin-secreting G cells
    • - In view of increased mortality and morbidity due to antrectomy this is not a very effective procedure for chronic duodenal ulcer.
    • - When done in combination with truncal vagotomy, it is more effective at reducing acid secretion and recurrence than truncal vagotomy in combination with a drainage procedure or highly selective vagotomy
  26. Indications of antrectomy?
    • (a) refractory to medical therapy;
    • (b) complicated by perforation, bleeding, or obstruction; or
    • (c) recurrent after adequate treatment of H pylori.
  27. What is Taylor procedure?
    Anterior seromyotomy and posterior truncal vagotomy (Taylor procedure), interrupting the branches of the anterior nerve of Latarjet within the wall of the stomach
  28. Complications of Truncal vagotomy?
    Truncal vagotomy reduces the motility of gall bladder and increases gall stone formation.
  29. What are the problems with highly selective vagotomy?
    It is a technically difficult operation. The chance of recurrent ulceration is 2–10%, little higher as compared to truncal vagotomy and drainage where chance of recurrent ulceration is 2–7%.However, slight epigastric fullness and mild dumping may occur following highly selective vagotomy.
  30. Contraindicatios of antrectomy?
    • Cirrhosis
    • Extensive scarring of the proximal duodenum that leaves a difficult or tenuous duodenal closure
    • Previous operations on the proximal duodenum, such as choledochoduodenostomy.

    When done in combination with truncal vagotomy, it is more effective at reducing acid secretion and recurrence than truncal vagotomy in combination with a drainage procedure or highly selective vagotomy.
  31. Types of Pylorus drainage procedures?
    Heineke Mikulicz pyeloplasty – longitudinal incision, transverse closure

    Finney pyeloplasty – Incision in stomach, pylorus and duodenum, closure of inferior stomach with inferior duodenum and superior stomach wth superior duodenum 

    Jaboulay Gastroduodenostomy - Anastomosis of distal stomach and pylorus with first or second part of duodenum, doesnot transect the pyloric muscle.
  32. Reconstruction after Antrectomy?
    • Gastroduodenostomy – Bilroth I - Favored for benign
    • Gastrojejunostomy – Bilroth II, Roux-en-Y reconstruction
  33. What is an ideal gastrojejunostomy?
    A posterior (Retrocolic), short or no loop, isoperistaltic gastrojejunostomy. 

    • Benifits of retrocolic GJ
    • - Minimize length of afferent loop limb – decrease likelihood of twisting that could lead to afferent loop obstruction (may lead to duodenal stump leak). 
    • - Low chance of reflux disease due to dependent drainage
  34. Modified Johnson anatomical classification of Gastric Ulcer?
    Type //  Location //  Incidence //  Acid level

    Type I // In the antrum, near the lesser curvature //  55% //  Normal

    Type II // Combined gastric ulcer (in the Body) with Duodenal ulcer // 25% //  High [@ BD]  

    Type III // Prepyloric ulcer // 15% // High

    Type IV // Gastric ulcer in the proximal stomach or cardia // 5%//  Normal 

    Type V // any site in the stomach // Associated with chronic NSAID intake


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  35. Treatment of Gastric Ulcer?
    Type I – Lesser curvature and incisura – Malignancy is concern – Treatment is wedge resection, even if biopsy is negative, the risk of malignancy is still high after perforated gastric ulcer. Malignancy should be ruled out by repeat endoscopy, to document ulcer has been healed and with repeated biopsy.

    Type II /III – Hyperproducers, Distal gastrectomy with truncal vagotomy

    IV – wedge resection, gastrectomy with Roux-en-y Eosophagojejunostomy, Csendes procedure
  36. What is Giant gastric Ulcer?
    • >2cm diameter , usually in lesser curvature, high chance of malignancy (10%)
    • Medical therapy heals 80% of cases, failed or complicated cases – gastrectomy. Vagotomy for type II and III
  37. What is ZES?
    Triad of gastric acid hypersection, sever PUD and non-beta islet cell tumor of pancreas
  38. Stress Ulcer?
    Multiple superficial (non-ulcerating) erosions that begin in proximal or acid producing portion of stomach and progress distally. E.g – cushing, curling ulcers. Stress ulcer is due to hypoxia, sepsis or organ failure. Major risk of stress ulcer is massive GI bleeding
  39. Type of Gastritis?
    • Type A – Autoimmune
    • Type B – Bacterial (H.Pylori)
  40. Post-gastrectomy syndromes?
    • 1. Dumping syndrome (postcibal syndrome)
    • 2. Metabolic disturbances
    • 3. Afferent loop syndrome
    • 4. Efferent loop syndrome
    • 5. Alkaline reflux gastritis
    • 6. Gastric atony
  41. Types of Dumping syndrome?
    • Early dumping syndrome
    • - Occurs almost immediately
    • - More GI symptoms – Nausea, vomiting, epigastric discomfort, cramping, explosive diarrhoea
    • - Occurs due to hypertonic content in small intestine

    • Late dumping syndrome
    • – after around 2 hrs of food intake
    • - More cardiovascular symptoms
    • - Carbohydrate quickly absorbed results in hyperglycemia, insulin release leads to rebound  hypoglycemia  and sympathetic activation

    Prevention of dumping syndrome - Frequent feeding, avoid food containing high sugar, separate liquid from solid diet
  42. Diagnosis of afferent loop syndrome?
    Failure to visualize afferent loop on upper endoscopy, radionucleotide imaging the hepatobiliary tree – normally, the radionucleotide should pass into the stomach
  43. Treatment of afferent loop syndrome?
    Conversion of Bilroth II to Bilroth I, entero-enterostomy below the stoma, creation of Roux-en-Y procedure
  44. Treatment of afferent loop syndrome?
    Operative intervention is almost always necessary and consists of reducing the retroanastomotic hernia if this is the cause of the obstruction and closing the retroanastomotic space to prevent recurrence of this condition
  45. What are the nutritional problems following gastrectomy?
    • „ Weight loss due to less food intake and less absorption.
    • „ Steatorrhea due to poor pancreatic function or inactivation of pancreatic enzyme in the afferent loop.
    • „ Diarrhea: due to intestinal hurry or steatorrhea.
    • „ Iron deficiency anemia due to reduced absorption or blood loss from the gastric mucosa. Iron deficiency is more pronounced when the duodenum is bypassed.
    • „ Megaloblastic anemia is due to gastric mucosal atrophy or following total gastrectomy. This may be due to a combination of reduced intrinsic factor or bacterial colonization of gut which results in destruction of the B12 in the gut.
    • „ Calcium deficiency: Due to reduced absorption of calcium in the small intestine or due to reduced acidity in the proximal small intestine. This may lead to osteoporosis.
  46. Treatment of Gastric Atony?
    Metochlopramide, Erythromycin
  47. What is the pathology of zollinger elision’s syndrome? How do you diagnose it? Outline the treatment plan. [TU 2057] 


    Gastrinoma triangle boundry
    The triangle is formed by joining the following three points:

    • Superiorly: confluence of the cystic and common bile ducts
    • Inferiorly: junction of the second and third portions of the duodenum
    • Medially: junction of the neck and body of the pancreas
  48. What are the clinical features of ZES?
    • Triad consisting of gastric acid hypersecretion, severe PUD, and non–β-islet cell tumors of the pancreas.
    • Abdominal pain and PUD are the hallmarks of the syndrome and typically occur in more than 80% of patients
    • Patients may also exhibit diarrhea, weight loss, steatorrhea, and esophagitis.

    ZES should be suspected in patients with multiple or refractory peptic ulcers; ulcers distal to the duodenum; peptic ulcer disease and diarrhea, enlarged gastric folds, an endocrinopathy or multiple endocrine neoplasia type 1
  49. Endocopic finding of ZES?
    Prominent gastric rugal folds, reflecting the trophic effect of hypergastrinemia on the gastric fundus in addition to evidence of PUD.
  50. Diagnosis of ZES?
    • Elevated fasting serum gastrin levels (>200 pg/mL), and values higher than 1000 pg/mL are diagnostic.
    • In patients with gastrin levels in this equivocal range, - secretin-stimulated gastrin level. Serum gastrin samples are measured before and after intravenous secretin (2 U/kg) administration at 5-minute intervals for 30 minutes. An increase in the serum gastrin level of greater than 200 pg/mL above basal levels is specific for gastrinoma versus other causes of hypergastrinemia, which do not demonstrate this response.
    • CT or MRI of the abdomen - to localize the gastrin secreting tumor.
    • If initial imaging is nondiagnostic, localization can sometimes be achieved using somatostatin receptor scintigraphy or endoscopic ultrasound (EUS).

    All patients with ZES should be screened for MEN1 syndrome with serum parathormone levels, ionized calcium levels, and prolactin levels at diagnosi
  51. Conditions when fasting gastrin level are elevated?
    • PPI use
    • H. pylori infection
    • Renal failure
  52. Treatment of ZES?
    • Acid suppression therapy is initiated, preferably with a high-dose PPI.
    • Once the tumor is located intraoperatively, a resection according to oncologic principles should be performed (rather than a tumor enucleation) because lymph node metastases are present in 43% to 82% of cases;
    • Localized gastrinoma should be resected
    • Metastatic gastrinoma is the most common cause of morbidity and mortality in patients with ZES. Patients with tumor recurrence or metastatic disease are treated with chemotherapy (streptozotocin with 5-fluorouracil or doxorubicin or both)
  53. Types of enteral access
    • Gastrostomy 
    • Witzel jejunostomy 
    • Stamm gastrostomy 
    • PEG
  54. • Portal gastropathy 72/6
    • • Tumour markers in GIO malignancy 57, 60/12
    • • Paradoxical aciduria 62
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prem77
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327401
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Gastro 48 Stomach - Gastric and duodenal ulcer ZES
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Stomach
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