Contenu connexe


Diseases of stomuch 1.pptx

  1. Al-Hayat Medical University Gastroenterology Batch III Medical Students Lecturer : Dr Abdulfatah Abdullahi Jama Diseases of the Stomuch Date: 26/03/2023
  2. Most dilated part of GIT occupies in the epigastric, umbilical and left hypochondral areas, occupying a recess bounded by upper abdominal viscera, completed above& anterolateraly by anterior abdominal wall &diaphragm
  3. Roughly J Shaped at rest Size and Shape varies with a) Volume of food or fluid it contains b) Position of body c) Phase of respiration High and transverse in obese and short persons Elongated in thin persons
  4. Cardiac orifices Situated to the left of midline behind 7th costal cartilage 2.5cm from its sternal junction at the level of T11 10 cm from ant abdominal wall.
  5. Can be identified by prepyloric vein crossing its anterior surface vertically.
  6. Lesser curvature Extends b/w cardiac & pyloric orifice forming right border Incisura angularis is a notch in the most dependent part ,its position varies with gastric distension Gives attachment to lesser omentum
  7. 4 to 5 times longer than lesser curvature Starts at cardiac incisure Arches upwards & postero laterally & to Lt Highest convexity is fundus Lt 5th Finally turns right to end at the pylorus Attachments
  8.  A large globular Lt part & a narrow tubular Rt part
  9. Mucosa Sub mucosa Muscularis externa Serosa Mucosa Thick, smooth surface Reddish brown to pink in colour
  10. In contracted state mucosa is folded to form RUGAE. They are Longitudinal & more marked towards pyloric & greater curvature Actually they are large folds in sub mucosal connective tissue Obliterated when stomach is distended
  11. Epithelium Lamina propria Muscularis mucosa
  12.  Epithelium Appears as honey combed due to small gastric pits (foveola). Base of gastric pits (foveola) receives gastric glands which extend deep into lamina propria  Epithelium is simple columnar mucous cells
  13. Principal  Found In body & fundus Cardiac glands  Situated near the cardia Pyloric glands numerous mucous & entero endocrine cells predominate
  14.  Highly differentiated  Found In body & fundus Are made of different types of cells Chief Parietal Mucous Entero endocrine
  15. Cardiac glands  Situated near the cardia  Mucous secreting cells predominate Pyloric glands  numerous mucous & entero endocrine cells predominate
  16.  Muscularis mucosa  Inner circular  Outer longitudinal  Ext circular in some places  Sub mucosa  Loose connective tissue  Collagen, elastin,sub mucosal plexus of stomach
  17. Oblique fibres  Limited to gastric body  Most developed near the cardiac orifice Circular fibres  Form a uniform layer external to oblique fibres  At the pylorus form annular pyloric sphincter
  18.  Parasympathetic sympathetic  [ vagus] Anterior br Posterior br (frm rt vagus) ( frm Lt vagus)
  19. o Functions of stomach o Gastric secretion  Mechanism of HCl formation  Gastric digestive enzymes  Neural & hormonal control of gastric secretion  Phases of gastric secretion o Motor functions of the stomach o Stomach Emptying
  20.  Stores food  Digestion ◦ Mechanical – mix ◦ Chemical – protein digestion  Gastric juice: converts meal to acidic chyme ◦ HCl: kills bacteria, denatures proteins ◦ Pepsin: enzyme breaks down proteins  Rugae = large folds  Mucus = protects lining of stomach
  21. oxyntic (gastric) glands Pyloric glands  Secrete: ◦ Hydrochloric acid ◦ Pepsinogen ◦ Intrinsic factor ◦ Mucus  Located in body & fundus  In proximal 80%of stomach  Secrete: ◦ Mucus- protection ◦ Gastrin ◦ Pepsinogen  Located in the antrum  In the distal 20% of stomach  In addition to mucus secreting cells that line the stomach and secrete alkaline mucus there is two important types of tubular glands:
  22.  Vagus nerve (neural effector) either by releasing Ach (direct activation of parietal cells) or by releasing Gastrin releasing peptide, GRP (indirect activation).  Gastrin (hormonal effector)  Enterochromaffin-like cells release Histamine activates H2 receptor (parietal cells)  increases acid secretion  Cimetidine (H2 receptor blocker) peptic ulcer and gastroesophageal reflux
  23.  3 motor functions of the stomach: ◦ Storage of large quantities of food ◦ Mixing of food with gastric secretions to produce chyme ◦ Slow emptying of chyme into the small intestine at a suitable rate for proper digestion & absorption
  24.  Digestion of carbohydrate in mouth & stomach ◦ Food mixed with saliva that contain ptyalin (an α amylase) secreted by parotid gland ◦ It hydrolysis starch to maltose ◦ It continues in stomach for 1 hr ◦ Gastric acid deactivate it
  25.  Digestion of proteins in the stomach ◦ Pepsin  secreted by chief (peptic) cells  It is active at pH 2-3 and inactive at pH 5  Initiate protein digestion (10-20% of protein digestion)  Can digest collagen ◦ Hydrochloric acid  secreted by parital (oxyntic) cells
  26.  Stomach is a poor absorptive area of GIT ◦ It lacks the villous type of absorptive membrane ◦ It has tight junctions between epithelial cells ◦ Only a few highly-lipid soluble substances can be absorbed such as:  Alcohol  Aspirin
  27. 2500 ml/day Contents cations Na,K,Mg,H+ anions Cl,HPO2,so4 pepsin lipase Mucus IF
  28. Gastric mucosal protection: Intraluminal concentration of H+ is 3 million times greater than blood and tissue. “Mucosal barrier” 1] Mucous secretion. 2] Bicarbonate secretion. 3] Epithelial barrier (rapid regeneration). 4] Mucosal blood flow (to sweep away hydrogen ions). 5] Prostaglandin protection (help maintain blood flow).
  29. 1983-discovered by Warren and Marshall in Australia Discovery revolutionised the treatment of duodenal and gastric ulcers. Earned them the Nobel Prize for Medicine in 2005. Formerly known as Campylobacter pyloridis.
  30. • Nearly 20 species of Helicobacter are now recognised • The gastric helicobacters colonise the stomachs of animals. The monkey, cat, dog, all harbour their own species • H. cinaedi and H. fennelliae are associated with proctitis in homosexual men. • H. pylori are found in the human stomach. Molecular studies suggest transmission from an animal source.
  31. Gram-negative spiral bacillus Fastidious in terms of growth requirements :strictly micro-aerophilic :require C02 for growth Has a tuft of sheathed unipolar flagella; specially adapted to colonise mucous membranes
  32. Hallmark of the species is production of urease enzyme -urease breaks urea down to C02+NH3 -amonia is a strong base -process helps H. pylori survive strongly acidic stomach conditions Very fragile (a point of importance when referring samples to the lab)
  33. • H. pylori infection occurs worldwide • Prevalence varies greatly among countries and population groups • 20 – 50% prevalence in middle age adults in industrialised countries • >80% prevalence in middle age adults in developing countries  :may reflect poorer living conditions
  34. • Oral ingestion of bacterium  within families (esp children)  person-person contact  faecal-oral transmission 
  35. Highly adapted organism that lives only on gastric mucosa Gastric antrum is the most favoured site Present in the mucus that overlies the mucosa
  36. After several days incubation period, patients suffer mild attack of acute gastritis -abdominal pain -nausea -flatulence -bad breath Symptoms can last but hypochlorhydria can last up to one year
  37. Despite a substantial antibiotic response, infection and chronic gastritis persist After decades there may be progression to atrophic gastritis (conditions which are inhospitable for the bacteria) and numbers reduce.
  38. Strain virulence Host genotype Environmental factors
  39. PUD -lifetime risk 3% in US, 25% Japan -eradication provides long-term cure Gastric carcinoma -strong evidence of increased risk 0.1-3% -unclear whether eradication reduces the risk of gastric cancer MALT lymphoma -72%→ 98% of MALT lymphoma infected with H. pylori
  40. Aim: to understand the pathogenesis of gastritis, peptic ulcer disease and cancer of stomach.
  41. Definition of Gastritis: Inflammation of the gastric mucosa. group of disorders with inflammatory changes in the gastric mucosa (G.M.) that have different clinical features, histological characteristics and pathogenesis. A. Acute Gastritis B. Chronic Gastritis
  42. ACUTE GASTRITIS + HELICOBACTER PYLORI - short spiral – shaped, microaerophitic gram - bacillus - in gastric samples by histological examination, culture, increase activity, by endonuclease analysis. - UBT 13C, 14C - antibodies (Ig G, Ig A) to H.P. 90 – 100 % Hp + antral biopsy specimens of DU patients 70 % - G.U. 80 % - chronic gastritis involving the antral mucosa
  43. CHRONIC GASTRITIS Definition: Chronic inflammatory cells, predominately lymphocytes and plasma cells. HISTOLOGIC CLASSIFICATION I. SUPERFICIAL GASTRITIS - Inflammatory changes in the lamina propia of the superficial mucosa of the upper half of G.M. and the glands are preserved II. ATROPHIC GASTRITIS - the inflammatory infiltrate extends to the deep positions of the mucosa - profound loss of the glandular structures which are separated widely by connective tissue, with a greatly reduced / absent inflammatory infiltrate. Gastritis progresses – changes in the morphology of the gastric glandular elements. Intestinal metaplasia – conversion of gastric glands to the small-intestinal mucosal glands with goblet cells.
  44. CHRONIC GASTRITIS – TYPES A & B Type A – involves the body and fundus of the stomach – from that may lead to pernicious anemia Antibodies to parietal cells, intrinsec factor in serum  immuno / autoimmuno pathogenesis Parietal cell Antibodies 20% of patients over age 60  20% of patients with – hypoparathyroidism – Addison’s disease – vitiligo Antibodies to intrinsec factor 40 % of those with pernicious anemia. The risk of stomach cancer in patients with type A gastritis and pernicious anemia is three times than the general population Type B: In younger patients  involves the antrum In elderly patients  involves entire stomach The incidence increases with age - Strong associations of H. pylori with type B gastrities
  45. DIAGNOSIS - Biopsy of the G.M. provides the most reliable means of identifying and classifying gastritis. -Several biopsies of suspected areas, when safe and possible, are recommended. TREATMENT In type A.G. + pernicious anemia Vit. B12 – indefinite regular parental administration
  46. CORROSIVE GASTRITIS - corrosive chemicals  antrum injury (HCl, H2SO4, NaOH) Symtoms: burning of the mouth, throat, retrosternal area epigastric pain vomiting hemorrhage / perforation Treatment: supportive therapy
  47. INFECTIOUS GASTRITIS Phlegmonous G – necrosis, sepsis - streptococci, staphylococci, Proteus, Escherichia coli TREATMENT i.v. antibiotics fluids + electrolyte replacement gastrectomy – in lack of response It can occur in immuno-compromised patients  cytomegalovirus
  48. EOSINOPHILIC GASTRITIS extensive eosinophilic infiltration (e.i) of the wall of the stomach -biopsy reveals . - antrum is more frequently involved than gastric body and fundus. SYMPTOMS: epigastric pain nausea, vomiting TREATMENT: glucocorticoids
  49. GRANULOMATOUS GASTRITIS Chron’s disease produce: ulceration granulomatous infiltration stricture formation Other’s: histoplasmosis candidosis syphilis tuberculoses Diagnostic: biopsies + cytology to exclude malignancy surgical exploration if the diagnostic is not established by biopsy at endoscopy.

Notes de l'éditeur

  1. 3
  2. 38
  3. Later reclassified as HP
  4. 43
  5. 44
  7. 50
  8. 1