GIT Block 2023-2024 Minia University PDF

Faculty of Medicine Minia University GIT BLOCK For 2nd year students GIT Block (207) 2023-2024 Lecture(1): ANTERIOR ABDOMINAL WALL AND PERITONEUM Layers of the anterior abdominal wall 1- Skin 2- Superficial fascia: consist of; - Camper's fascia - fatty superficial layer - Scarpa's fascia - deep fibrous layer 3- Deep fascia: no deep fascia 4- Muscle - External oblique abdominal - Internal oblique abdominal - Rectus abdominis - Transverse abdominal muscle - Pyramidalis muscle 5- Fascia transversalis 6- Peritoneum External oblique muscle Origin: Lower 8 ribs. Direction of fibers: downward, foreword and medially. Insertion: - Fleshy fibers: into anterior ½ of the outer lip of iliac crest. - By an aponeurosis: into xiphoid process, linea alba, pubic crest, pubic tubercle and anterior superior iliac spine(ASIS) Ligaments derived from the external oblique - Inguinal ligament : runs from the ASIS to the pubic tubercle. It formed by the free edge of the external oblique. - Lacunar ligament: a crescent-shaped extension of the inguinal ligament, attached to the superior ramus of the pubic bone. - Pectineal ligament: extends from the lacunar ligament along the pelvic brim. 2 GIT Block (207) 2023-2024 Internal oblique muscle Origin: 1- Ilioinguinal origin: from - Lateral ⅔ of upper surface of inguinal ligament. - Anterior ⅔ of intermediate line of iliac crest. 2- Lumbar origin: from thoracolumbar fascia. Direction of fibers: upwards & medially. Insertion: -Fleshy fibers: lower 3 or 4 ribs and their costal cartilages. - By an aponeurosis: attached to 7th, 8th and 9th costal cartilages. xiphoid process, linea alba, pubic crest and pubic tubercle. Transversus abdominis muscle Origin: 1- Costal: from the inner aspects of lower 6 costal cartilages. 2- Lumbar: from thoracolumbar fascia. 3- Ilioinguinal: from the anterior ⅔ of the inner lip of iliac crest and lateral ⅓ of inguinal ligament. # Direction of fibers: transversely Insertion: xiphoid process, linea alba, symphysis pubis 3 GIT Block (207) 2023-2024 NB: The lowermost aponeurotic fibers fuse with corresponding part of the aponeurosis of transversus abdominis, and attach to pubic crest forming the conjoint tendon. Rectus abdominus muscle Origin: - From pubic crest (lateral head). - From symphysis pubis (medial head). Insertion: To the 5th, 6th and 7th costal cartilages and xiphoid process. NB: (The pyramidalis is a small muscle sometimes found overlying the inferior end of rectus abdominis, running from the lineal alba to the pubis.) Rectus sheath Definition: it's an apponeurotic sheath surrounding rectus abdominis and pyramidalis muscles and their associated nerves and vessels. Formed mainly by aponeurosis of three lateral abdominal muscles Contents of the rectus sheath - 2 muscles (rectus abdominins and pramidalis). - 4 vessels (superior epigastric artery and vein+ inferior epigastric artery and vein). - 6 nerves (terminal parts of the lower 5 intercostal nerves and subcostal nerve) For description it is considered at 3 levels: 1- Above the costal margin: - Anterior wall: ext. oblique apponeurosis. - Posterior wall: costal cartilages. 2- from costal margin to midway between umbilicus and pubis (arcuate line). - Anterior wall: ext. oblique apponeurosis+ anterior ½ of internal oblique ms. 4 GIT Block (207) 2023-2024 - Posterior wall: transversus apponeurosis + posterior ½ of internal oblique ms. 3- from previous line to pubis. - Anterior wall: apponeurosis of the 3 abdominal ms. - Posterior wall: deficient( formed by fascia tranversalis) Nerves of the anterior wall - supply the skin, muscles and the parietal peritoneum. - They are derived from the anterior rami of lower 6 thoracic and the 1stlumbar nerves (iliohypogastric and ilioinguinal nerves) Vascular supply of anterior abdominal wall. Arterial supply Venous driange - Superior and Inferior epigastric - above level of umbilicus: artery drained into, - musculo-phrenic artery. 1- Superior epigastric vein. - 10th and 11th Posterior intercostal 2- Lateral thoracic vein. arteries - below level of umbilicus: - Subcostal and lumbar arteries drained into, - Superficial epigastric artery. 1- Inferior epigastric vein. - Deep and Superficial circumflex 2- Superficial epigastric vein. iliac artery. The Inguinal canal The path of descent of testis carries it obliquely through anterior abdominal wall, creating a passageway oriented in an inferomedial direction. Inguinal canal has 2 opening: - Superficial inguinal ring: defect in the aponeurosis of the external oblique muscle, lies immediately above and medial to the pubic tubercle. - Deep inguinal ring: oval opening in fascia transversalis, lies 1cm above the mid-inguinal point. NB: Cremaster muscle 5 GIT Block (207) 2023-2024 origin: From the lower arching fibers of internal oblique ms at middle of inguinal ligament. insertion: U shaped around the spermatic cord, inserted into pubic tubercle. nerve supply: by genitofemoral nerve PERITONEUM - Thin, serous, continuous glistening membrane lining the abdominal & pelvic walls and clothing the abdominal and pelvic viscera. - Parietal layer lines the wall & visceral layer covers the organs. - The potential space between the two layers is filled with very thin film of serous fluid to facilitate the movement of the abdominal organs. - Peritoneal cavity is the largest cavity in the body. - The surface area of parietal & visceral layers is enormous. The relationship between viscera and peritoneum - Intraperitoneal viscera: viscera completely surrounded by peritoneum, example, stomach, superior part of duodenum, jejunum, ileum, cecum, vermiform appendix, transverse and sigmoid colons, spleen and ovary - Interperitoneal viscera: most part of viscera surrounded by peritoneum, example, liver, gallbladder, ascending and descending colon, upper part of rectum, urinary bladder and uterus - Retroperitoneal viscera: some organs lie on the posterior abdominal wall and are covered by peritoneum on their anterior surfaces only, example, kidney, suprarenal gland, pancreas, descending and horizontal parts of duodenum, middle and lower parts of rectum, and ureter 6 GIT Block (207) 2023-2024 The peritoneal cavity It is divided into two main sacs: 1- Greater sac. 2- Lesser sac or omental bursa. These two sacs are interconnected by a single oval opening called the epiploic foramen or opening into lesser sac or foramen of Winslow Lesser sac Definition: large peritoneal sac situated behind lesser omentum and stomach Walls: - Superior: peritoneum which covers caudate lobe of liver and diaphragm. - Anterior: formed by lesser omentum, peritoneum of posterior wall of stomach and anterior 2 layers of greater omentum. - Inferior: closed by folding of greater omentum on itself - Posterior: formed by posterior 2 layers of greater omentum, transverse colon and transverse mesocolon, peritoneum covering pancreas. - Left: formed by spleen, gastrosplenic ligament and splenorenal ligament. - Right: formed by omental foramen. Greater sac The transverse colon and transverse mesocolon divides the greater sac into supracolic and infracolic compartments Supracolic compartments Infracolic compartments - Site: - lies between diaphragm and －lies below transverse transverse colon and transverse colon and transverse mesocolon. mesocolon - Parts: - The falciform ligament divides - The mesentry of small it into right and left parts. intestine divide it into upper RT region and lower LT region. 7 GIT Block (207) 2023-2024 Contents: - Its contents are: (subphrenic spaces) Left subphrenic spaces: - its contents are: - left anterior subphrenic space. (paracolic gutters) - left posterior subphrenic space Right paracolic gutter (lesser sac). - Right lateral paracolic Right subphrenic spaces gutter. - Right anterior subphrenic - Right medial paracolic space(bare area of liver) gutter. - Right posterior subphrenic left paracolic gutter space. - Left lateral paracolic Extraperitoneal spaces: gutter. - Right extraperitoneal space. - Left medial paracolic - left extraperitoneal space. gutter Epiploic Foramen Boundaries Anterior: free margin of lesser omentum, containing (hepatic artery, bile duct and portal vein) Posterior: peritoneum covering IVC. Superior: Caudate process of the caudate lobe of the liver. Inferior: 1st inch of the1st part of duodenum. Peritoneal folds Definition: Double layers of peritoneum that connect organ to organ or organ to abdominal wall, they are of 3types: 1- Omenta: connect the stomach to other organs, they are: A- Greater omentum. B- Lesser omentum. 8 GIT Block (207) 2023-2024 2- Mesenteries: connect intestine to post. Abdominal wall, they are: A- Mesentery of small intestine. B- Transverse mesocolon. C- Sigmoid mesocolon. D- mesoappendix. 3- Ligaments: connect organ to organ or organ to abdominal wall, they are: A- gastrosplenic ligament. B- lienorenal ligament. C- falciform ligament. Greater Omentum Definition: largest peritoneal fold connecting stomach to transverse colon. - It formed of 4 layers 2 anterior and 2 posterior. - It hangs down like an apron in front of coils of small intestine Attachments: -The anterior 2 layers: attach to greater curvature of stomach and descends a variable distance into the peritoneal cavity and then turns sharply on itself to ascend as the posterior 2 layers. -The posterior 2 layers: passes anterior to transverse colon and transverse mesocolon. It end by attachment to anterior border of body of pancreas. Contents: - Right and left gastroepiploic vessels. - Right gastroepiploic LN and lymphatics. Lessor omentum (gastrohepatic ligament) Definition: 2 layers of peritoneum, runs from inferior visceral surface of the liver to the abdominal oesophagus, stomach, and first part of duodenum. Attachment: - Superiorly (hepatic attachment): forms an L-shape, the vertical component of the L is formed by the fissure for ligamentum venosum and the horizontal limb to the lips of porta hepatis. 9 GIT Block (207) 2023-2024 - Inferiorly (gastric attachment): attached to lesser curvatures of stomach and 1st inch of the duodenum. To form gastrohepatic and hepatoduodenal ligaments, respectively. - RT free border: from porta hepatis to 1st inch of the duodenum and form the anterior boundary of lesser omentum. - Upper border (diaphragmatic): attached to the under surface of diaphragm. Contents: 1- in the right lateral border: it forms the anterior wall of the epiploic foramen. It contains the portal vein, common bile duct, and hepatic artery. 2- along the gastric border: it contains RT and LT gastric vessels, branches of the vagus nerves, and gastrohepatic lymph nodes 3- between the 2 layers: it contains LN and lymphatics and the hepatic plexus of nerves. 10 GIT Block (207) 2023-2024 Lecture(2): DEVELOPMENT OF GIT - Lateral embryonic folding forms the gut but head to tail fold form 3 parts of the gut, foregut in head fold, hindgut in tail fold and midgut in between - each part of the gut receives a branch of the aorta: ♥ Celiac trunk supplies the foregut & its derivatives ♥ Superior mesenteric artery supplies the midgut & its derivatives ♥ Inferior mesenteric artery supplies the hindgut & its derivatives - The endoderm of the primordial gut gives rise to most of the epithelium and glands of the digestive tract but muscles, connective tissue and other layers of the wall of the tract are derived from the splanchnic mesoderm The foregut derivatives - Primordial pharynx and its derivatives - Lower respiratory tract (larynx, trachea, bronchi & lungs) - Derivatives of foregut proper: esophagus+ stomach+ proximal half of duodenum+ liver & biliary apparatus+ pancreas Development of the stomach in the 4th week, begin as a fusiform dilatation in the caudal part of foregut - - During next 2 weeks, the dorsal border grows much faster and forms the greater curvature and the ventral border forms the lesser curvature - stomach rotate due to enlarged liver, so the ventral border moves to the right and the dorsal border to the left→ the right side becomes the dorsal surface and the left side becomes the ventral surface - Fate of dorsal mesogastrium→ lienorenal ligament+ gastrosplenic ligament+ gastrophrenic+ greater omentum - Fate of ventral mesogastrium→ lesser omentum +falciform ligament 11 GIT Block (207) 2023-2024 Anomalies of the stomach 1- Congenital hypertrophic pyloric stenosis: most common 2- Variations in stomach shape 3- Malrotation of stomach 4- Thoracic stomach. 5- Transposition to right side. Development of the liver Sources of the liver development: 1- Endoderm of the foregut form→ the hepatic cords and the epithelial lining of the intrahepatic portion of the biliary system. 2- Mesoderm of the septum transversum→ forms the fibrous tissue, hematopoeitic tissue and Kupffer cells 3- Vitelline veins form→ hepatic sinusoids. Stages of development: - it appears as a hepatic diverticulum, from ventral caudal part of foregut - The bud grows into the septum transversum and divides into 2 parts - The larger cranial part is primordium of liver (pars hepatica), the smaller caudal part gives rise to the gall bladder and cystic duct(pars cystica) - The liver grows rapidly and in 5-10th weeks fills a large part of abdominal cavity. By 9th week, the liver forms about 10% of total body weight - Initially RT and LT lobes are of same size, later right lobe grows larger Development of the biliary apparatus - The stalk of the hepatic diverticulum becomes→ the common bile duct which opens on the duodenum. - The stalk of the pars cystica diverticulum forms the cystic duct but the stalk of pars hepatica form the common hepatic duct. - The ducts become occluded initially, but are later canalized 12 GIT Block (207) 2023-2024 Anomalies of the liver & gall Bladder 1- Anomalies of liver are rare, as increase lobes of the liver. 2- Variations in hepatic ducts, cystic and bile ducts are common and clinically significant 3- Extrahepatic biliary atresia is the most common serious anomaly 4- Absent gall bladder. 5- Double gall bladder. Development of the pancreas - Pancreas begins to appears as 2 buds from the endoderm of foregut, dorsal (larger, appears first and lies cranial) and ventral(arise with hepatic bud) both grow within the dorsal and ventral mesenteries respectively - Rotation of stomach and duodenum carry the ventral bud dorsally→ comes to lie posterior to the dorsal bud and later fuses with it. - The dorsal bud forms most of the pancreas but the ventral bud gives rise to the uncinate process and part of the head of the pancreas. - Insulin secretion begins by 10 weeks Ducts of the pancreas: - Main pancreatic duct: formed from the duct of ventral bud and distal part of the duct of the dorsal bud, it opens on the major duodenal papilla - Accessory pancreatic duct: formed from the proximal part of the duct of the dorsal bud, it opens separately on the minor duodenal papilla Anomalies of the Pancreas: 1- Accessory pancreatic tissue 2- Annular pancreas 3- Accessory pancreatic ducts Development of the spleen - Spleen develops from the mesoderm within the dorsal mesogastrium - initially lobulated but lobules normally disappear before birth 13 GIT Block (207) 2023-2024 Congenital anomalies of spleen 1- Accessory splenic tissue: may be in gastrosplenic or greater omentum. 2- retension of fetal lobulation. 3- the spleen may be divided or consist of multiple masses. Development of midgut The derivatives of the midgut are: lower ½ of duodenum, jejunum, ileum, cecum, appendix, ascending colon and right ⅔ of transverse colon. - Midgut derivatives are supplied by the superior mesenteric artery - The midgut loop is suspended from the dorsal abdominal wall by an elongated mesentery and connected to yolk sac by vitello-intestinal duct. Stages of midgut development: 1- Formation of U-shaped loop: - As midgut elongates, it forms a ventral U-shaped midgut loop, this loop has a cranial and a caudal limb, at its apex vitello- intestinal duct attach. - Cranial limb gives→ lower ½ of duodenum, jejunum, ileum. The caudal limb gives→ cecum, appendix, ascending colon and right ⅔ of the transverse colon. 2- Rotation of the midgut loop: - The midgut loop rotates 90º anticlockwise around the superior mesentric artery → cranial limb now to the RT while the caudal limb to the LT. 3- Herniation of the midgut loop: - It is a physiological umbilical herniation, that occur normally at 5 th -10th. - midgut loop projects into the proximal part of the umbilical cord - herniation occurs due to relatively massive liver and kidneys at this time. 14 GIT Block (207) 2023-2024 4- Reduction of midgut loop: - During the 10th week the intestines return to the abdomen. - As the large intestine returns, it undergoes further 180º counterclockwise rotation (total 270º), the small intestine formed from cranial limb returns first and occupies the central & LT part of the abdomen. - The cecum is the last part to return to abdomen, where it lies under the RT lobe of the liver, then descend to RT iliac fossa. Anomalies of midgut 1- Abnormal rotation A- Non rotation: non rotation after reduction→ LT sided colon. B- Reversed rotation: the duodenum superficial to transverse colon. C- incomplete rotation: situs inversus. 2- Omphalocele: failure of bowel to return from its physiological herniation→ herniation of abdominal viscera through the umbilical ring, the viscera are covered by amnion. 3- Gastroschisis: is a herniation of abdominal contents through the body wall directly into the amniotic cavity. It occurs lateral to the umbilicus. 4- Vitellointestinal duct anomalies: - Persistence →ileal (Meckel’s) diverticulum - Fistula. - Cyst. - Fibrous cord. 5- intestinal duplication: failure of normal recanalization→ two lumina 6- Subhepatic cecum: failure of descend of the cecum. 7- Retention of fetal shape of appendix: appendix arise from apex of caecum. 15 GIT Block (207) 2023-2024 8- Umbilical hernia: intestines return back to the abdominal cavity then herniate through an imperfectly closed umbilicus. HINDGUT - Derivatives of the hindgut are: left ⅓ of the transverse colon+ descending + sigmoid colon+ rectum and the superior part of the anal canal+ epithelium of the urinary bladder and most of the urethra. - derivatives of hindgut are supplied by the inferior mesenteric artery Cloaca Definition: terminal dilated part of the hindgut. - It is an endoderm-lined chamber that is in contact with the surface ectoderm at the membrane. It receives the allantois opening. - cloacal membrane is composed of endoderm of the cloaca and ectoderm of the proctodeum or anal pit Partitioning of cloaca - The cloaca is divided into dorsal and ventral parts by the urorectal septum - As the septum grows toward the cloacal membrane and divides the cloaca into two parts; 1- ano-rectal canal (dorsally): gives rectum and cranial ½ of anal canal. 2- primitive urogenital sinus: ventrally. - at 7th week, the urorectal septum has fused with the cloacal membrane, dividing it into a dorsal anal membrane and a ventral urogenital membrane - The anal membrane usually ruptures at the end of the eighth week Anal canal - its superior ⅔ of the adult anal canal is derived from cloaca(endoderm), but its inferior ⅓ develops from the proctodeum (ectoderm) 16 GIT Block (207) 2023-2024 - The junction between the two sources is indicated by the pectinate line, it indicates the former site of anal membrane - Because of its different origin, there is a differences in blood supply, nerve supply, venous and lymphatic drainage of anal canal between upper and lower parts of anal canal. Congenital anomalies of the hindgut 1- Anal agenesis with or without a fistula: due to incomplete separation of the cloaca→ a temporary communication between rectum dorsally, and the vagina(in females) or urethra (in males). 2- Imperforated anus: failure of rupture of anal membrane. 3- Rectal atresia: due to abnormal recanalization of the rectum→ the rectum replaced by mass of connective tissue. 4- Anorectal agenesis with or without fistula. 5- Persistant cloaca. 6- Congenital megacolon: failure of neural crest cells to migrate into the colon wall→ part of the colon is dilated due of the absence of autonomic ganglion cells in the myenteric plexus distal to the dilated segment of colon→ failure of peristalsis in the aganglionic segment. 17 GIT Block (207) 2023-2024 Lecture(3):ANATOMY OF ORAL CAVITY, PHARYNX, ESOPHAGUS AND STOMACH Boundaries of the mouth - Lips (labia): protect the anterior opening - Cheeks: form the lateral walls - Hard palate: forms the anterior roof - Soft palate: forms the posterior roof - Uvula: fleshy projection of the soft palate Parts of oral cavity and teeth internally 1- Vestibule: space between lips externally and gums 2- Oral cavity proper: area contained by the teeth Salivary glands - Parotid gland: In the parotid fossa, three main structures transverse this gland – facial nerve, external carotid artery, and retromandibular vein. The parotid duct opens opposite to the upper 2nd molar tooth. The gland is completely serous - Submandibular gland: Sitting most posteriorly in the submandibular triangle, it is supplied by the facial artery and vein Submandibular ducts, which cross the lingual nerves, open on both sides of the tongue frenulum. It is mostly serous but partially mucus, - Sublingual gland: The smallest salivary gland sits beneath the oral mucosa in the floor of the mouth. It has multiple small openings. It is almost completely mucus- secreting. Pharynx Parts - Nasopharynx : not part of the digestive system 18 GIT Block (207) 2023-2024 - Oropharynx : posterior to oral cavity - Laryngopharynx : below the oropharynx and connected to the esophagus It: Oropharynx is the middle part of the pharynx situated behind the oral cavity Boundaries of oropharynx - Above: communicates with nasopharynx through nasopharyngeal isthmus Below: opens into laryngopharynx- Anterior wall- - upper part, deficient, oropharynx communicates with oral cavity through oropharyngeal isthmus/ isthmus of fauces - lower part, related to - base of tongue - lingual tonsils - valleculae - Posterior wall: 3rd cervical vertebrae - Lateral wall: ♦ Palatine/faucial tonsil ♦ Anterior pillar (Palatoglossus muscle) ♦ Posterior pillar (Palatopharyngeus muscle) ESOPHAGUS - It is a tubular structure about 25 cm long. Beginning: it begins as the continuation of the pharynx at the level of the 6th cervical vertebra. End: it pierces the diaphragm at the level of the 10th thoracic vertebra to join the stomach. It is divided into 3 parts: 1- Cervical. 2- Thoracic. 3- Abdominal. - In the thorax, it passes downward and to the left through superior then to posterior mediastinum 19 GIT Block (207) 2023-2024 - At level of sternal angle, aortic arch pushes esophagus again to midline. Esophageal constrictions The esophagus has 4 anatomic constrictions. 1- at the junction with the pharynx(pharyngeoesophageal junction). 2- where it crossed by aortic arch at superior mediastinum 3- where it crossed by left main bronchus at posterior mediastinum. 3- at the junction with the stomach where it piercing the diaphragm. They have a considerable clinical importance. 1- They may cause difficulties in passing an esophagoscope. 2- In case of swallowing of caustic liquids strictures develop in these sites. 3- The esophageal strictures are a common sites of the development of esophageal carcinoma. Arterial supply: from; - thoracic part: from descending aorta, bronchial arteries, and right intercostal arteries. - abdominal part: by left gastric artery, short gastric arteries Venous drainage - The upper third drains in into the inferior thyroid veins. - The middle third into the azygos veins. - The lower third into the left gastric vein, which is a tributary of the portal vein. Lymphatic drainage - The upper third is drained into the deep cervical nodes. - The middle third is drained into the superior and inferior mediastinal nodes. - The lower third is drained in the celiac lymph nodes in the abdomen. The stomach Definition: it is the widest part of the alimentary tract 20 GIT Block (207) 2023-2024 and lies between the esophagus and the duodenum. Site: located in the hypochondriac, epigastric and umbilical areas. Shape: J-shaped has 2 surfaces, 2 borders, 2 ends and 3 parts: Gastric surfaces: Anterior (superior) Posterior (inferior) surface surface The entire anterior The posterior surface is covered by peritoneum of (superior) surface is the lesser sac, which separate stomach from the covered by peritoneum of stomach bedstructures (4 horizontal, 4 vertical). the greater sac. - Transverse colon. -mesocolon. - Related to ant. Abd. Wall, - Body of pancreas. -splenic artery. diaphragm and Lt lobe of - Spleen. - LT crus of the liver. diaphragm. - LT suprarenal gland. - LT kidney. Gastric borders: Lesser curvature (RT border) Greater curvature (LT border) - It shows a notch, the angular notch, - It is four or five times longer than the whose position and appearance vary lesser. with gastric distension. -it gives attachment to: - The lesser omentum is attached to - gastrophrenic ligament. the lesser curvature and contains the - gastrosplenic ligament. right and left gastric vessels and LT - greateromentum, which contains the gastric LN. gastroepiploic vessels and gastroepiploic LN. 21 GIT Block (207) 2023-2024 Parts of the stomach: Fundus Body pylorus It is dome shaped, Extends from fundus to Include the following: projects above and to the the angular notch, A line a-pyloricantrum: left of cardiac orifice, It drawn from the angular dilated part below the lies above a line drawn notch to an indentation on body. horizontally from the greater curvature defines b- pyloric canal: distal cardiac notch to the lower boundary of body. narrow 2.5 cm of greater curvature. stomach. c- pyloric sphincter: distal end of stomach. Gastric orifices (surface anatomy): Cardiac orifice Pyloric orifice - The opening of oesophagus into the -It is the opening of stomach. stomach into duodenum. - It is situated to LT of the midline behind 7th - It lies 1–2 cm to the right costal cartilage at the level of T11 vertebra. It of the midline in the is10 cm from anterior abdominal wall and 40 transpyloric plane L1. cm from incisor teeth. Relations - Quadrate lobe the liver. -anteriory: LT lobe of liver & anterior gastric - Neck of pancreas. nerve. - posteriory: Diaphragm and posterior gastric - There is specific nerve. anatomical pyloric Sphincter: sphincter - There is no specific anatomical cardiac - It is often marked by: sphincter related to this orifice but - A prepyloric vein which physiological sphincter depends on: crosses the anterior surface 22 GIT Block (207) 2023-2024 - acute angle between stomach and vertically downwards. esophagus. - feeling thickness of - Lower end of esophagus is surrounded by pyloric sphincter. RT crus of diaphragm (has sphincteric - circular groove(pyloric action). constriction). - Lower end of esophagus has thick mucosal folds. Vascular supply and lymphatics: Arteries Veins Lymphatic drainage arteries of the stomach arise - has the same - Lymphatic drainage of mainly from the coeliac trunk names and stomach is of great 1- Left gastric artery: arises accompany importance during directly from celiac trunk. the resection of the 2- Right gastric artery: arise from corresponding stomach, particularly gastroduodenal artery, from arteries. for malignancy. hepatic art. - They end in - lymphatics of the 3- Right gastroepiploic artery: portal vein. stomach end on: arise from gastroduodenal artery, - They may 1- superior gastric L.N. from hepatic artery. end in splenic 2-Inferior gastric L.N. 4- leftgastroepiploic artery: : arise or superior 3- pancreatico-dudenal from splenic artery. mesenteric L.N. 5- Short gastric arteries: arise veins. These lymphatics end from splenic artery. finally in celiac L.N.→ preaortic L.N. Peritoneal attachment of the stomach: - gastrophrenic ligament. - gastrosplenic ligament. - greater omentum. -lesser omentum. 23 GIT Block (207) 2023-2024 Lecture 4 (Histology) Histology of oral cavity and general plan of GIT and Stomach Digestive system consists of the digestive tract (extending from oral cavity to anal canal) and its associated glands (salivary gland, liver and pancreas). Oral Cavity The entire oral cavity is lined by oral mucosa (mucous membrane) that is formed of: Stratified squamous epithelium. Underlying connective tissue. There are 3 types of mucosa according to function. 1. Masticatory epithelium In contact with food during mastication. Form 25% of surface area. Gingiva, hard palate Keratinized stratified squamous epithelium, tough, tightly bound to underlying connective tissue. 2. Lining epithelium, Not contact with food during masticating. Form 60% of surface area Flour of mouth, ventral (underside) tongue, cheeks, lips, soft palate Non keratinized, soft, loosely bound to underlying connective tissue 3. Specialized epithelium Form 15% of surface area Dorsal surface of tongue with its tongue papillae Partially Keratinized Tongue The tongue situated in the floor of the mouth It is important in taste, mastication, swallowing, and speech. 24 GIT Block (207) 2023-2024 It is composed chiefly of skeletal muscle, is covered by mucous membrane, and presents a tip and margin, dorsum, ventral (inferior) surface, and root. The dorsal surface of the tongue is divided by the sulcus terminalis into an oral part, the anterior two-thirds, and a pharyngeal part, the posterior one- third. On the basis of their appearance four types of papillae can be distinguished: filiform, fungiform, circumvallate and foliate papillae. Taste bud: Intraepithelial sensory organ responsible for taste sensation Present in dorsum of tongue, soft palate, cheeks, upper esophagus and epiglottis. Taste bud consists of: ❑ Receptor (taste) cells: each has microvilli in the taste pore at its apical end. These allow contact with the external medium. At the basal end, each sensory 25 GIT Block (207) 2023-2024 cell makes synaptic contact with fibers of the facial nerve (VII) or glossopharyngeal nerve (IX). ❑ Sustentacular (supporting) cells: Those surround a tiny taste pore. ❑ Basal cells: renew both of these types of cells. Chemicals stimulate the receptors, and initiate impulses in the afferent nerve fibers Lips the lip is formed of a core of skeletal muscle (orbicularis oris) which covered externally by skin and lined internally with oral mucosa. In addition, we find labial vessels, nerves, and labial salivary glands. The vermilion border (red margin) is the area of transition from the skin to the oral mucosa. It is covered with partially keratinized epithelium. Numerous connective tissue papilla extend deep into the epithelium, are rich in sensory nerve ending and are heavily vascularized. The proximity of these vessels to the surface of the epithelium gives the vermilion its red appearance. It contains few sebaceous glands. It has no hair follicles or sweet glands. Salivary glands Types of salivary glands:- Major salivary glands: - parotid, sublingual, and submandibular salivary glands. Minor salivary glands: - they are scattered under oral mucosa. Saliva is produced by secretory units and is conducted to the 26 GIT Block (207) 2023-2024 oral cavity by short ducts. They include buccal, labial, palatal and lingual glands General Histology of the digestive (Alimentary) Canal The wall of the alimentary canal has the same basic structure throughout its length. It consists of four basic layers. 1) the mucosa, 2) submucosa, 3) musculosa and 4) the serosa or adventitia. 1. Mucosa (tunica mucosa): innermost 3 layers surrounding lumen ▪ Epithelium: may be a wet surface epithelium stratified squamous epithelium or simple columnar epithelium. ▪ Lamina propria: loose CT that may contain glands as in fundus, pylorus, and intestinal crypts. ▪ Muscularis mucosa: thin layer smooth muscle → movement in mucosa. Formed of inner circular and outer longitudinal 2. Submucosa: loose CT, may contain glands (as esophagus & duodenum) and Meissner's nervous plexuses. 3. Musculosa: two or more muscle layers: inner circular may be modified in sphincters & Auerbach's plexus outer longitudinal, Auerbach's plexus between muscle layers → independent peristaltic action. Meissner's 4. Serosa (Adventitia): irregular dense CT nervous surrounded by mesothelium (serosa) or bound to body wall (adventitia). Esophagus It extends from the cricoid cartilage through diaphragm to opening of stomach. The wall is formed of: 1. Mucosa: ▪ Epithelium: stratified squamous non keratinized epithelium for protection. 27 GIT Block (207) 2023-2024 ▪ Lamina propria: esophageal cardiac glands (mucus), two clusters. one near pharynx, other near junction with stomach ▪ Muscularis mucosa: unusual formed of single longitudinal layer thickened near stomach 2. Submucosa: CT containing esophageal mucous glands. 3. Musculosa: 1. In the upper third, muculosa is formed of skeletal muscle 2. In the middle third → mixed. 3. In the lower third → smooth muscle 4. Adventitia: CT, becomes serosa after esophagus passes through diaphragm. Clinical application Oral thrush (oral candidiasis) Fungal infection caused by Candida species, primarily Candida albicans that can asymptomatically colonize the oral mucosa in healthy individuals. If an immune defect occur, Candida overgrowth may lead to an opportunistic infection. It is common but usually cause no serious problem. The main symptom is a white colored deposits in mouth Treatment: Antifungal, rinse mouth with salt water 28 GIT Block (207) 2023-2024 Esophageal structure Symptoms ❑ Difficulty swallowing (dysphagia). ❑ Feeling of food getting stuck in your throat. ❑ Frequent episodes of choking Complication: hyperplasia Reflux esophagitis, due to defect in lower esophageal sphincter leading to reflux of acidic gastric content into esophagus. Symptoms: ❑ Dysphagia ❑ chest and abdominal pain ❑ untreatable heartburn Complication: Hyperplasia and metaplasia Histology of the Stomach The stomach is an expanded organ in the upper left region of the abdominal cavity. It is continuous with the esophagus superiorly and empties into the duodenum of the small intestine inferiorly. It continues the mechanical and chemical digestion of the bolus. After the bolus has been completely processed in the stomach, the product is called chyme. It is lined with mucosa which has longitudinal folds called rugae. 29 GIT Block (207) 2023-2024 Fundus and body Mucosa (tunica mucosa) ❑ Epithelium: simple columnar epithelium ❑ Lamina propria: contains fundic glands. ❑ Muscularis mucosa Submucosa Musculosa: thick, arranged as: inner oblique, middle circular, outer longitudinal. Serosa: CT cover by squamous mesothelium Gastro-esophageal junction: Changes from esophagus to stomach: Mucosa: Epithelium abruptly changes from stratified squamous to simple columnar. L.P.: appearance fundic gland in stomach Submucosa: esophageal mucous glands end abruptly. Musculosa: thickened in stomach Fundic glands It is branched tubular glands Extend from bottom of gastric pit to muscularismucosa 2-3 fundic gland open in one gastric pit Glands are straight, crowded and perpendicular tosurface Each gland formed of isthmus, nick and base 30 GIT Block (207) 2023-2024 Comparison between fundus and pylorus Fundus and body Pylorus Mucosa (tunica mucosa) Mucosa (tunica mucosa) ❑ Epithelium: simple ❑ Epithelium: simple columnar columnarepithelium epithelium ❑ Lamina propria: ❑ Lamina propria: containspyloric containsfundic glands. glands. ❑ Muscularis mucosa ❑ Muscularis mucosa Submucosa Submucosa Musculosa: thick, arranged as: Musculosa: thick inner circular → to inner oblique, middle circular, form pyloric sphincter and outer outerlongitudinal. longitudinal Serosa: loose CT cover by Serosa: loose CT cover by squamous mesothelium squamous mesothelium Cells of the fundic gland: Mucous cells Peptic cells Parietal APUD Stem cells EX: Glycoprotein cells Protein Mineral Cell → Protein cells formingcell metaboliccells short peptides Site: Mucous surface Base only, Mainly in Base of gland Neck, up cell,mucous neck cell mostnumerous upperhalf in anddown gland LM: Vacuolated Basal ∆ Cell, Infranuclear Pale basophilic basophiliccytoplasm basopilia, Parietal granules, cytoplasm, apical position, never stainedwith vesicular acidophilia and reach lumen, silver nucleus vesicular strongly nucleus acidophilic cytoplasm EM: Apical ↑↑rER, Golgi, Intracellular presence of ↑↑free mucinogengranules, mitochondria, canaliculi, with abundant dense ribosomes, rER, Golgi apical microvilli, secretory Golgi, zymogen SER, granules,mostly at mitochondria, granules mitochondria basal cytoplasm, mitotic infranuclear Golgi figures Function: Gastric HCL, intrinsic secrete hormones Renew all enzyme factor that is gastrin, cellsof fundic surface → s essential for serotonin, gland neutralmucous vit.B12 somatostatin and Mucous neck→ absorption enteroglucagon. acidicmucous 31 GIT Block (207) 2023-2024 Comparison between cardiac, fundic and pyloric glands: Cardiac gland Fundic gland Pyloric gland Other Zymogenic gland Mucoparietal gland name Gastric Medium sized pits Short and narrow Deep and wide pit (Smallest gastric pits) Type, Tubular coiled Long (most thickness of Short (1∕ 2 thickness of shape mucosa) mucosa) of Branched tubular, Branched tubular gland straight, crowded and coiled widely spaced perpendicular to surface and oblique Cells All types of cells All types All types except chief cells Parietal cells more Parietal cell few Absent of few parietal cells Clinical application Pernicious anemia: Gastritis (Inflammation ofthe lining of the stomach): It is believed to affect about half of people worldwide. The most common symptom is upper abdominal pain. Complications may include stomach bleeding, stomach ulcers,and stomach tumors. 32 GIT Block (207) 2023-2024 Causes: infection with Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs (NSAIDs). Treatment: avoiding the cause and medications such as antacids Gastric peptic ulcer: It is a mucosal perforation that penetrates the lamina propriaand muscularis mucosae Most common in lesser curvature Pain may worsen with eating, burning sensation, vomiting Complications may include bleeding (Bleeding occurs in as many as 15% of cases) and perforation Common causes include the bacteria Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). 33 GIT Block (207) 2023-2024 Lecture 5 (Physiology) Functions of Digestive System & Control of GIT function, Chewing and Swallowing The Digestive System is formed of: I. Alimentary Canal: It is a muscular tube (about 5-7 meters) that runs from the mouth to the anus. It includes; the mouth, pharynx, esophagus, stomach, small intestine and large intestine. II. Digestive glands: These glands include salivary, gastric, and intestinal glands. It releases their secretions containing digestive enzymes into GIT. III. Accessory digestive organs: liver, gall bladder, and pancreas GIT Morphology: - Wall formed of 4 layers: Mucosa, Submucosa, Muscles, and Serosa. - Muscle formed of 2 layers: Inner circular & Outer longitudinal. - The 2 muscle layers are connected. - Muscle arranged in bundle of 1000 muscle fibers & connected by Gap - Junction, allowing action potential to pass from one fiber to the other fiber. - So, it functions as Syncytium. 34 GIT-207 2021-2022 Electrical Activity of Gastrointestinal Smooth Muscle: - RMP = - 50 - 60 mv, unstable. - Slow waves (i.e. Basic Electrical Rhythm): it is NOT an action potential. - Electrical because it is formed of depolarization due to Ca++ influx & repolarization due to K+ efflux. - Rhythmic because it is at regular rate; 3/minute in the stomach, and 12/minute in the small intestine. - Not all slow waves (gradual depolarization & gradual repolarization) reach to the firing level (- 40 mv); ONLY the one reach to it can form action (spike) potentials that cause contractions. - Depolarization is stimulated by: stretch, parasympathetic. - Hyperpolarization is stimulated by: Sympathetic. Functions of the Digestive System: 1. Motility. 2. Absorption 3. Secretion of digestive juice. 4. Digestion 5. Excretion of undigested food in feces. 35 GIT-207 2021-2022 36 GIT-207 2021-2022 Control System of Gastrointestinal Function I. Intrinsic Control System: 1. Nervous control by Enteric Nervous System (Local Nerve Plexuses) that present in the wall of the gut and includes 2 plexuses: Auerbach's (Myenteric) Plexus Meissner's (Submucosal) Plexus Site Between longitudinal and In the submucosal layer circular smooth muscle layers Function Controls the GIT motility Control the GIT secretions 2. Hormonal control by the Gut Hormones: Gut hormones are group of hormones secreted by certain cells in the GIT mucosa. These hormones are released into circulation and carried by blood to be returned back to the GIT to exert its actions (i.e. local hormones). The secretion of these hormones is regulated by neuronal impulses along either the external autonomic nerves or from local nerve plexuses, as well as directly by changes in composition of the luminal contents. It includes: Gastrin hormone, Gastric Inhibitory Peptide (GIP) hormone, Secretin hormone, Cholecystokinin hormone (CCK), and Motilin hormone. II. Extrinsic Control System: 1. Nervous control by the Autonomic Nervous System (ANS): 37 GIT-207 2021-2022 A. Parasympathetic nervous supply (i.e. excitatory) via; Vagus nerve: supplying esophagus, stomach, small intestine and upper part of large intestine. Facial nerve supplying submandibular and sublingual salivary glands, nasal, palatine and pharyngeal mucous glands. Glossopharyngeal nerve supplying larynx, pharynx, tongue, tonsil, parotid gland. Pelvic nerve supplying the lower part of large intestine, rectum and anus. Functions: a. Increase of motility of GIT. b. Increase all GIT secretions. c. Increase blood flow. d. Relaxation of sphincters and enhances emptying of GIT. B. Sympathetic nervous supply (i.e. inhibitory) via; Greater splanchnic nerve (to the abdomen). Lesser splanchnic nerve (to the pelvis). Functions: a. Decrease of motility. b. Decrease of secretions. c. Decrease blood flow. d. Contraction of sphincters and delay empty of GIT. Mechanism of Nervous Regulation: Via Gastrointestinal Reflexes; the reflexes that regulate the GIT functions are of two types: 1. Short reflexes; mediated by local nerve plexuses and its receptors in gut wall so it is concerned with self-regulation of GIT. 2. Long reflexes; initiated in response to impulse conducted to CNS and they 38 GIT-207 2021-2022 include the following types: Conditioned reflexes Unconditioned reflexes Receptors outside gut including Receptors in the gut wall either olfactory, visual and auditory receptors. mechanoreceptors or chemoreceptors. Acquired training. Inborn reflex. Need cerebral cortex. No need for cerebral cortex. III. Hormonal control by the aldosterone Hormones. Functions: stimulates sodium and water reabsorption from the gut and salivary glands in exchange. GIT Hormones 1. Gastrin Hormone Site of release: Gastrin-secretory cells (G cells) in the duodenum & upper jejunum as well stomach antrum & pylorus. Chemical nature: Polypeptide act rapidly within minutes. Stimuli: a) Distension of stomach antrum. 39 GIT-207 2021-2022 b) Chemical stimuli as soup extract & peptones (product of protein digestion). Rise of gastric pH above 2 (that occurs after meal intake). c) Vagal stimulation by gastrin releasing peptide (GRP), not acetylcholine; so NOT blocked by atropine. Actions: a) Stimulation of gastric HCl & Pepsin secretion. b) Trophic to GIT mucosa. c) Contraction of Lower Esophageal Sphincter. d) Stimulation of gastric motility. e) Stimulation of insulin secretion. Notes: Gastrin hormone has 2 types: G17 (small gastrin): formed of 17 amino acid. G34 (big gastrin): formed of 34 amino acid. Zollinger Ellison Syndrome: Pancreatic tumor, with excessive gastrin production that induce marked increase in gastric HCl leading to duodenal ulcer. 40 GIT-207 2021-2022 2. Secretin Hormone: Site of release: Duodenum & upper jejunum. Chemical nature: Polypeptide act rapidly within minutes. Stimuli: Decline pH of intestinal fluid below 4.5 due to gastric acid, bile acid, protein, or fat in the intestine. Actions: a) On the stomach: Inhibit HCl secretion (natural antacid). b) On the pancreas: Stimulate aqueous pancreatic secretion; large in volume, rich in NaHCo3, poor in enzymes. c) On the liver: bile large in volume, rich in NaHCo3. Notes: Smoking inhibits secretin hormone secretion, increasing liability to duodenal ulcer. 3. Gastric Inhibitory Peptide (GIP) Hormone: Site of release: Duodenum & upper jejunum Chemical nature: Polypeptide act rapidly within minutes. Stimuli: a) Decrease pH of intestinal fluid. b) Carbohydrate & fat. Actions: a) On the stomach: Inhibit gastric HCl. 41 GIT-207 2021-2022 b) Delayed gastric emptying. c) On the pancreas: Stimulate insulin secretion. 4. Cholecystokinin Pancreozymin (CCK) Hormone: Site of release: Duodenum & upper jejunum Chemical nature: Polypeptide act rapidly within minutes Stimuli: Contact of amino acids, small peptides, fatty acids to intestinal mucosa. Actions: a) Evacuation of stored bile from gall bladder. b) Stimulation of pancreatic secretion; small in volume, poor in NaHCo3 & rich in enzymes. c) Trophic to pancreas. 5. Motilin Hormone: Site of release: Duodenum & upper jejunum Chemical nature: Polypeptide act rapidly within minutes Stimuli: Act in between meals & interrupted by feeding. Actions: 42 GIT-207 2021-2022 a) Stimulate small intestine motility, to move undigested substance to large intestine to prevent bacterial growth and multiplication. b) Stimulate gastric emptying. 6. Somatostatin: Site of release: D cells of GIT mucosa & D cells of pancreas. Stimuli: HCl in the lumen of all GIT. Actions: Inhibits; GIT motility & GIT secretion & GIT hormones. Types of GIT motility Digestion and absorption depend on a variety of mechanisms that soften the food, propel it through the length of the gastrointestinal tract, and mix it with bile and digestive enzymes. Two fundamental patterns of motility are conducted by the digestive tube 1. Propulsive (i.e. Peristalsis) Movement: Peristalsis is a reflex response that is initiated when the gut wall is stretched, and occurs in all parts of the gastrointestinal tract. The stretch initiates a circular contraction behind the stimulus and an area of relaxation in front of it. The wave of contraction then moves in a mouth-to-anus direction, propelling the contents forward. Peristalsis can be increased or decreased by autonomic input, but its occurrence is independent of extrinsic innervation. It is an excellent example of the integrated activity of the enteric nervous system. 43 GIT-207 2021-2022 2. Segmentation (i.e. Mixing) movement: Ring like contractions appear at regular interval along the digestive tube dividing it into nearly equal segments. A few seconds later, contractions appear in the middle of each segment, while the previous constrictions disappear and the process is repeated in that manner. Function: a) It is a mixing motility seen mainly in the small intestine (mixing the gut solid contents with the gut secretion), thus helping digestion. b) Press the gut contents to come in contact with mucosa (help absorption). 44 GIT-207 2021-2022 Lecture 6 (Physiology) Physiology of the Mouth & Esophagus Mastication (Chewing) The chewing movements break the food into small pieces and stimulate the secretion of saliva to make a suitable food bolus ready for swallowing. Chewing reflex: The act of chewing is partly voluntary and partly reflex in nature (i.e. semi reflex). The contact of food on the palate and tongue causes inhibition (relaxation) of muscles of mastication that results in reflex opening of the mouth. Drop of the lower jaw causes stretch of the muscles of mastication that results in its reflex contraction with closure of the mouth. Functions of mastication: 1. Break down of food into small particles to increase the surface area of food exposed to the action of enzymes. 2. It stimulates salivary secretions which help swallowing. 3. Reduce mechanical damage of GIT. 4. Development of satiety through stimulation of smell and taste receptors. 45 GIT-207 2021-2022 Salivary glands: The mouth has three pairs of salivary glands: parotid, sub-maxillary (i.e. sub- mandibular) and sublingual glands. Each gland is formed of groups of acini, the secretion of which is carried by a duct which opens into the buccal cavity. Composition of Saliva: Saliva is a viscid colorless fluid with neutral pH 7. Bacteria act on sugar remaining in the mouth producing lactic acid which may destroy the teeth because the calcium (of the teeth) dissolve in acidic media. It’s about 1.5 liters in volume/day. It is composed of 99.5% water, while the other 0.5% consists of electrolytes (mainly Na+, Cl-, HCO3- and K+), mucus, enzymes (α amylase), antibacterial compounds such as secretory immunoglobulin A (IgA) and lysozyme. Each salivary gland is formed of acini, which secrete a primary secretion that flows through the salivary ducts, which open into the oral cavity. 46 GIT-207 2021-2022 Stages of Salivary Secretion: 1. Primary secretion (in the acini): Filtration from the plasma with similar ionic concentration, isotonic, and α amylase & mucin are added by acini. 2. Secondary secretion (in the duct): As the primary secretion passes through the ducts of the salivary glands, it is modified by aldosterone hormone as follows: a) Sodium is actively reabsorbed & Potassium is actively secreted in exchange with the sodium (Na+-K+ pump). Saliva become hypotonic; each time 3 Na+ reabsorbed in exchange with only 2 K+. b) Chloride is passively reabsorbed. c) HCO3- is actively secreted. So the secondary secretion contains more potassium, bicarbonate and less sodium chloride compared to primary secretion. Functions of saliva: 1. Articulation; helps in speech by moistening the mouth. 2. Buffering action to keep mouth pH at about 7 by mucin which is protein in nature & by bicarbonate that buffer acids. 47 GIT-207 2021-2022 3. Cooling & Cleaning action (continuous wash to the mouth & antibacterial action by the IgA and lysozymes in it). 4. Digestion. Through action of salivary amylase on the starch. 5. Deglutition; soft the food and prepare it for swallowing. 6. Excretory function: as excretion of heavy metals as lead. 7. Facilitates stimulation of taste buds by its solvent function. 8. Growth hormone in it help recovery of any buccal wound rapidly. 9. H2O balance regulation through thirst sensation. 10. Heat regulation especially in panting animals. Control of Salivary Secretion The control of salivary secretion is ONLY Nervous control, NO hormonal control, by both the sympathetic and the parasympathetic nervous system. A. Parasympathetic (7&9) cranial nerve: - Facial (7) nerve: supplying sublingual & submandibular gland. - Glossopharyngeal (9) cranial nerve: supplying parotid gland: Effect: 1. Produce vasodilatation. 2. Saliva is watery, large in volume (i.e. true secretion), high electrolytes, low in organic. B. Sympathetic (T1, T2): Effect: 1. Produce vasoconstriction. 2. Saliva is viscid, rich in organic, and small in volume (i.e. trophic secretion). 48 GIT-207 2021-2022 Mechanism (Control) of Salivary Secretion: Secretion of saliva can occur in response to conditioned or unconditioned reflex. Unconditioned reflexes Conditioned reflexes (Inborn reflex) (Acquired reflex) Seeing, smelling, hearing or Stimulus Taste of food in the mouth. thinking in food Taste buds in the mouth (i.e. Receptors inside the gut In eye, nose and ear Receptors wall) (i.e. Receptors outside the gut wall) Cranial nerves (optic, olfactory & Afferent Cranial nerves 7, 9, 10 auditory) Medulla oblongata (salivary Cerebral cortex → medulla Center center). oblongata (salivary center). Autonomic supply to salivary Autonomic supply to salivary Efferent glands glands Response Increase salivary secretion. Increase salivary secretion. Deglutition (Swallowing) It is the passage of food from mouth to stomach. It is subdivided into three stages or phases: 1. Buccal stage 2. Pharyngeal stage 3. Esophageal stage 49 GIT-207 2021-2022 1. Buccal Stage of Swallowing: In which food passes from mouth to pharynx by elevation of the anterior part of the tongue pushing food bolus backwards which is then forced into pharynx by contraction of mylohyoid muscles. It is the voluntary phase. 2. Pharyngeal Stage of Swallowing: In which food passes from the pharynx to the esophagus. It is involuntary (i.e. deglutition reflex): Stimulus: touching the pharynx (swallowing receptors) by food. Afferent: trigeminal nerve (5th cranial nerve). Center: swallowing center in medulla oblongata & lower pons. Efferent: glossopharyngeal and vagus nerve (9th and 10th cranial nerves). Responses: A. Protective reflexes: - Nose closure by elevation of soft palate to close posterior nasal opening to prevent regurgitation of food to nose. 50 GIT-207 2021-2022 - Mouth closure by elevation of tongue and contraction of mylohyoid muscle. - Larynx closure by elevation of the larynx to be covered by epiglottis to prevent entry of food to the trachea, with approximation of the vocal cords, and temporary apnea as swallowing center inhibits respiratory center few seconds. B. Pharyngeal peristalsis: Contraction of pharyngeal muscles and relaxation of upper part of esophagus (upper esophageal sphincter) to push the food bolus to the esophagus. 3. Esophageal stage of swallowing: In which food passes from esophagus to stomach. It is involuntary. Mechanism: Primary peristalsis: They start at upper end of esophagus as a continuation of the pharyngeal peristalsis. 51 GIT-207 2021-2022 Secondary peristalsis: If the primary wave fails to propel the food down in the esophagus, a secondary wave starts at the site of bolus and propagates down. Secondary waves are repeated until the bolus is driven down into the stomach. Esophagus: Esophagus is a muscular tube with two sphincters: Upper esophageal sphincter (UES): It is closed to prevent entry of air except during swallowing. Lower esophageal sphincter (LES), or Gastro-esophageal sphincter: - It is tonically contracted in between meals to prevent reflux of gastric contents in esophagus. - This sphincter relaxes in front of esophageal peristaltic wave to allow easy entrance of food bolus into the stomach. The tone of LES is under neuronal control: 1. Acetylcholine from Vagus causes contraction of LES. 2. Nitric oxide (NO) and vasoactive intestinal peptide (VIP) from Neurons of theenteric plexus 52 GIT-207 2021-2022 causes relaxation of LES. Achalasia: Definition: It means incomplete relaxation of the LES that lead to accumulation of food in the esophagus with massive dilatation of the segment above the sphincter. Caused by absence of NO and VIP released by inhibitory neurons of myenteric plexus. Symptoms: dysphagia, discomfort in the chest, weight loss, heartburn and regurgitation of undigested food. Diagnosis: X-ray with barium (i.e. rat-tail appearance) or by endoscopy. It is treated by: 1. Drugs: e.g. nitrates, or calcium channel blockers. 2. Botulinum Injection in the LES to inhibit Acetyl choline release to relax the sphincter. 3. Dilatation of the sphincter. 4. Surgery; esophageal muscle incision. 53 GIT-207 2021-2022 Lecture 7 (Physiology) Physiology of the Stomach The Stomach: Gastric Mucosa: 54 GIT-207 2021-2022 Gastric mucosa contains different types of cells: 1. Parietal or oxyntic cells: Secrete hydrochloric acid (HCl) and intrinsic factor. 2. Chief (peptic) cells: secrete pepsinogen that is activated to pepsin (protein- digesting enzyme) by HCl. 3. Neck cells & surface epithelial cells: Secrete mucous. 4. Gastrin (G) cells: secret gastrin, one of the important hormones of GI tract. Gastric Secretion: The stomach secrets 2.5 liters/day of gastric juice. The gastric juice is highly acidic secretion; pH approximately 1. Composed of: - Water: about 99%. - HCl - Intrinsic factor. - Mucus. - Enzymes: as pepsinogen, gastric lipase, gelatinase. - Electrolytes: Na+, K+, H+, Cl- Mechanisms and Phases of Gastric Secretion: Phases of Gastric Secretion 1. Cephalic phase. 55 GIT-207 2021-2022 2. Gastric phase. 3. Intestinal phase. 1. Cephalic phase: 1/3 of gastric secretion, starts before the entering of the food to the stomach or even before taking the food. Mechanism: Nervous mechanism (conditioned & unconditioned) Unconditioned reflexes Conditioned reflexes Seeing, smelling, hearing or thinking Stimulus Taste of food in the mouth. in food In eye, nose and ear Receptors Taste buds in the mouth (Receptors in the gut wall). (Receptors outside the gut wall). Cranial nerves Afferent Cranial nerves 7, 9, and 10. (optic, olfactory & auditory) Cerebral cortex → medulla oblongata Center Medulla oblongata (vagal nucleus). (vagal nucleus). Efferent Vagus nerve to the stomach Vagus nerve to the stomach Response Increase gastric secretion. Increase gastric secretion. 2. Gastric phase: 2/3 of gastric secretion, starts when the food reaches the stomach. Mechanism: Nervous & Hormonal mechanism. A. Nervous mechanism: - Long reflex: Vago-vagal reflex. 56 GIT-207 2021-2022 - Short (local) reflex: Sub-mucosal plexus. Stimulus: Mechanically by distension of stomach by gastric contents, chemically by the effect of food, especially amino acids, in the stomach. Receptors: Gastric mucosa & stomach wall. Response: Stimulation of parietal and chief cells to excrete HCl & pepsinogen. B. Hormonal mechanism: Through gastrin hormone, mainly secreted by G-cells in the antrum & pyloric mucosa beside the upper part of small intestine. 3. Intestinal phase: Starts when the food reaches the duodenum. Inhibitory to Gastric secretion. Mechanism: Nervous & Hormonal mechanism. A. Nervous mechanism: Enterogastric reflex: Vago-vagal reflex. Stimulus: Mechanically by distension of duodenum by food & chemically by the increase acidity in the duodenum. Receptors: intestinal mucosa & duodenal wall. Response: Inhibition of gastric secretion. B. Hormonal mechanism: Through enterogastrone hormones (Secretin, GIP, CCK). Stimulus: chemical stimulation of the duodenum by the effect of food products, mainly the fat & hypertonic solution as sugar. Site of release: from in the intestinal mucosa. Functions: Act on the stomach to inhibit gastric secretion. 57 GIT-207 2021-2022 Mechanism of Inhibition of Gastric Secretion: 1. Depression and fear: via impulse from cerebral cortex, inhibit the dorsal vagal nucleus (cephalic phase of gastric secretion). 2. Drop of the pyloric & duodenal pH below 2, inhibits gastrin secretion i.e. HCl inhibits its own secretion (gastric phase of gastric secretion). 3. Somatostatin hormone (gastric phase of gastric secretion). 4. Enterogastric reflex (intestinal phase of gastric secretion). 5. Enterogastrone hormones (intestinal phase of gastric secretion). Component of Gastric Secretion 1. Pepsinogen: Pepsinogen secreted by the chief (peptic) cells, is activated by gastric HCl to active pepsin. Function: digestion (incomplete) of proteins to various peptides. 2. Intrinsic factor: Secreted by parietal cells of the stomach. It combines with vitamin B12 → intrinsic factor-vitamin B12 complex which is absorbed in the lower ileum. 58 GIT-207 2021-2022 Its absence leads to vitamin B12 deficiency (pernicious anemia). 3. Gastric lipase: Weak lipolytic enzyme. 4. Mucus: Soluble mucus secreted by mucus neck cells of gastric glands to lubricates the gastric chyme. Insoluble mucus secreted by surface epithelium. It forms a layer to protect the gastric mucosa against the mechanical friction with food, and to neutralize the corrosive effect of the acid. 5. Gastric hydrochloric acid (HCl): Produced by oxyntic (parietal) cells. It is an active secretion needs high energy coming from the large number of mitochondria in the parietal cells. Functions of HCl: 1. HCl activates pepsinogen into the active pepsin & provide optimum pH for the action of pepsin. 2. Food sterility by killing ingested bacteria. 3. Dissolve food particles and changes food into “chyme”. 4. Helps in the absorption of Ca++ and iron. 5. Helps milk clotting. 6. Stimulate the flow of bile. HCl formation (Mechanism of Acid Secretion): 1. Cl– is actively transported from the cytoplasm of parietal cells to the lumen & Na + is actively pumped from the lumen to the parietal cells. This create negative 59 GIT-207 2021-2022 potential of - 40 to -70 mv inside lumen, leading to passive diffusion of K+ from the cell to the lumen. 2. H2O dissociated into H+ and OH- in the parietal cells, then H+ is actively secreted to lumen in exchange for K+ by H+/K+ ATPase pump (proton pump). Thus, most of the K+ that had diffused into the lumen in step 1 is reabsorbed by the cell and H+ takes their place in the lumen. 3. CO2 (formed during cell metabolism or entering by blood) combines with H 2O under the effect of carbonic anhydrase enzyme to form carbonic acid (H2CO3), that is dissociates into HCO3- and H+. H+ combine with OH- to give H2O, and HCO3- diffuses out of the cell to extracellular fluid in exchange for Cl- then step 1 is repeated. HCO3- combine with Na+ in the extracellular fluid to form NaHCO3. HCO3- combine with Na + in the extracellular fluid to form NaHCO3. 4. H2O that passes through the cell to the lumen by osmosis. Alkaline tide: as HCl is secreted by the parietal cells HCO3- is added to the gastric venous blood so the PH of the blood increases. 60 GIT-207 2021-2022 Types of receptors on the parietal cells: There are three types of receptors on the parietal cells: 1. Acetylcholine: acts via M3 muscarinic receptors, M3 receptor stimulation increases intracellular Ca++. 2. Histamine: act via H2 receptors, H2 receptor stimulation increase intracellular cAMP. 3. Gastrin: act either directly on oxyntic cells by increasing intracellular Ca++, or indirectly through stimulating the secretion of histamine. N.B. Binding of the stimuli with their receptors in the parietal cells release 2nd messengers which increase gastric HCl secretion by activation of H+/K+ ATPase. Mechanisms of protection of the gastric mucosa: 1. The insoluble mucous secreted by the gastric surface mucous cells, that form gel layer which coats gastric mucosa. 2. Impermeability of gastric mucosal cells to H+ ions, with the presence of active H+ pump, pumping it from the mucosal cells into the gastric lumen. 3. Prostaglandins: they stimulate mucus & bicarbonate secretion, stimulate mucosal blood flow, and inhibit acid secretion. Peptic ulcers is caused by: 1. Breakdown of gastric mucosal barrier by: - Alcohol or Aspirin which inhibit prostaglandin production. - Helicobacter pylori bacteria which disrupts the mucosal barrier. 2. Excess secretion of HCl as in Zollinger-Ellison syndrome. 61 GIT-207 2021-2022 Gastric Motility The stomach is divided into 2 parts: 1. Proximal motor unit: It includes the fundus and body. Has thin wall. It functions mainly as a reservoir for food. Type of movement: Receptive relaxation. Stimulus: gastric distension & swallowing (pharyngeal & esophageal movement). Response: stomach distension, from 50ml (when empty) to 1-1.5 L; without marked increase in intragastric pressure. Mediated by Vagus nerve by the Vago-vagal reflex, Vagus has inhibitory effect here through the ATP (NOT acetyl choline) from purinergic inhibitory fiber. 2. Distal motor unit: It includes the antrum and pylorus. Has a thick wall Its function is mixing the food, and then emptying into duodenum. Type of movement: peristalsis. 62 GIT-207 2021-2022 Mechanism: Gastric contraction usually begins in the middle of the body of the stomach and travel toward the pylorus. The contraction increases in force and velocity as they travel towards the intestine and as digestion proceeds. Waves initiated by Gastric Slow Wave (Basic Electrical Rhythm (BER)), start at the midpoint of the greater curvature of the stomach (pace maker of the stomach), at a rate of 3-5 cycles/min. Some waves lead to spike bursts, which lead to peristaltic waves. At rest, rate of spike bursts is 3/minute, increase by vagal stimulation (excitatory cholinergic) or gastrin hormone to reach 5/minute, but can never exceed the BER. Regulation of Gastric Evacuation 1. Gastric factors: (Nervous & hormonal): Distention of the stomach wall, increases stomach emptying by increasing the pyloric pumping force, through both nervous reflexes (short and long vagal reflex) and gastrin hormone release. 2. Intestinal factors: (Nervous & hormonal): A. Nervous: (Enterogastric Reflex mediated by Purinergic vagal fibers) Presence of the following factors in the intestine inhibits gastric emptying: - Increased acidity - Hypertonicity - Fats - Protein - Irritation - Distension B. Hormonal: Presence of fat in duodenum releases some GIT hormones [Enterogastrone hormones (CCK, GIP and secretin)] from duodenal mucosa. They result in inhibition of pyloric pump and emptying, with closure of pyloric sphincter. 3. Consistency of food: 63 GIT-207 2021-2022 Liquid food evacuated more rapidly than solids. 4. Reflex from outside the GIT: - Pain produces reflex inhibition of gastric motility. - Emotions can either increase or decrease gastric motility. Hunger Contractions (Hunger pains) It is a strong & painful peristaltic contraction that occur in the body of the stomach when it is empty for long time. The feeding center in hypothalamus is normally active, unless it is inhibited by impulses from satiety center. Several hours after fasting, hypoglycemia increases the activity of the feeding center which in turn activates vagal nucleus in medulla oblongata, leading to hunger contraction. Vomiting: Definition: It is a reflex evacuation of gastric (mainly) and upper intestinal contents through the esophagus, pharynx and mouth. Center: In the medulla oblongata. Causes of vomiting: 1. Reflex vomiting: a. Visual or olfactory stimuli. b. Chemical or mechanical irritation of posterior part of tongue, soft palate, pharynx. c. Irritation of the gastric mucosa. d. Intestinal obstruction or irritation. e. Visceral; renal colic and appendicitis. f. Motion thickness; sea and air sickness, due to labyrinthine stimulation. 2. Central vomiting: a. Drugs as apomorphine. b. Acidosis. 64 GIT-207 2021-2022 c. Early pregnancy due to metabolic disturbances. d. Hypoxia of vomiting center in medulla oblongata as in high altitude. e. Trauma of vomiting center as in head injury. f. Meningitis or ↑ intracranial tension as in brain tumors. Mechanism of Vomiting: It is preceded by salivation and sensation of nausea. 1. A strong contraction of the incisura separating stomach body from pylorus. 2. The lower esophageal sphincter relaxes and stomach wall completely relaxed (stomach is passive). 3. A powerful contraction of diaphragm, abdominal wall, and pelvic floor muscles → ↑ intra-abdominal pressure → squeezing of relaxed stomach and expulsion of its contents to the mouth with contraction of the pyloric sphincter to close pyloric opening. 4. Protective reflexes to prevent entrance of vomitus to respiratory passages: Closure of nose by reflex elevation of soft palate. Larynx closure by closure of the glottis. Temporary apnea. 65 GIT-207 2021-2022 Complications of Persistent Vomiting: 1. Dehydration due to loss of water 2. Alkalosis due to HCl loss. 3. Potassium depletion. Treatment of Vomiting: 1. Treat the cause. 2. Anti-emetic drugs. 3. Correct the complications by supplying fluids, electrolytes (K+) and acidifying salts. 66 GIT-207 2021-2022 Lecture 8 (Pathology) Pathology of the oral cavity, oropharynx, esophagus, and salivaryglands Inflammatory Conditions of the oral cavity -Aphthous ulcers -The commonest cause of oral ulceration. -Those are small ulcerations of oral squamous mucosa, can be caused by different causes including various types of food , viral infection, stress, allergy, hormonal imbalance, nutritional deficiencies, and GIT disturbances. -They are typically painful self-limited but may be an indication of underlying systemic disease. -They are typically small, shallow, round ulcers with gray bases & heal in 7-14 days -Lichen planus It is a chronic inflammatory process that can involve skin or squamous mucosa of the oral cavity with a characteristic linear (band-like) chronic inflammatory cell infiltrate. -Oral candidiasis (thrush) -It is a fungal infection in the mouth. -it is commonly seen in breast-feeding infants or immunocompromised hosts. -White plaques that can be scraped off. -HSV-1 herpetic stomatitis Caused by herpes simplex virus. It is formed of Vesicular lesions with erythematous bases 67 GIT-207 2021-2022 Tongue ulcers 1-Traumatic (Dental) Caused by a sharp tooth. It is usually single with moderate size. It occurs on sides of tongue, oval in shape with shallow edge, hyperemic margin. 2-Aphthous ulcer It occurrs on the tip and sides of tongue 3-Infectious ulcers a- Tuberculous ulcer: Usually multiple, small in size. It is oval in shape with undermined edge, bluish margin, with caseous floor Microscopically : central caseation surrounded by epithelioid and giant cells, enclosed in a wide zone of lymphocytes and fibroblasts. b- Syphilitic ulcer: Oral lesions may occur in primary, secondary, and tertiary syphilis. It is single, large in size, circular or serpiginous margin with deep punched out edge, indurated base, and slough discharge. Microscopically: granulation tissue, fibrosis, endarteritis and accumulation of chronic inflammatory cells mainly plasma cells (important) and lymphocytes around the blood vessels 4-Malignant ulcer: It is Squamous cell carcinoma Etiology: Various risk factors such as: i) Tobacco smoking. ii) Chronic alcohol consumption. iii) Chronic irritation from ill-fitting denture or jagged teeth. 68 GIT-207 2021-2022 v) Human papilloma virus infection.. Gross: single, large in size, irregular in shape with raised everted edge, irregular margin, necrotic floor, indurated base and bloody or necrotic tissue discharge. Microscopically: Squamous cell carcinoma ranges from well-differentiated keratinizing carcinoma to undifferentiated neoplasm. Precancerous lesions of the tongue Leukoplakia: It is a clinical term referring to white patches in the oral squamous mucosa. These white patches or plaques cannot be scraped off. It is associated with smoking and alcohol Leukoplakia can result from inflammatory or reactive conditions The presence of epithelial dysplasia is the most important risk factor for transformation into squamous cell carcinoma. Microscopically: Acanthosis (thickening of the squamous mucosa) and hyperkeratosis (increased thickening of stratum corneum ) and parakeratosis (abnormal retention of nuclei in stratum corneum). Dysplastic changes may be seen with characteristic cytology and architecture. Tumors of the oral cavity The predominant tumor of the oral cavity is squamous cell carcinoma, which is strongly associated with tobacco use, and high alcohol consumption. Invasive squamous cell carcinomas could be keratinizing or non-keratinizing Different lymph nodes are at risk for metastasis depending on the location of the primary tumor. Squamous cell carcinoma of the oropharynx can present with metastatic disease in 69 GIT-207 2021-2022 cervical lymph nodes before the primary tumor is identified. Salivary glands enlargement Etiology: 1-Sialadenitis It is inflammation of salivary gland due to infectious Causes (Viral , Bacterial) and Autoimmune disease (Sjogren’s Syndrome) Sjogren’s Syndrome An autoimmune disease that results in a chronic inflammatory reaction in the salivary and lacrimal glands. It can result in atrophy and loss of function of these glands, causing xerostomia (dry mouth) and xerophthalmia (dry eyes). The inflammatory cell infiltrate is composed mainly of CD4+ T cells, but B cells are also present and may be prominent. B cells frequently infiltrate the salivary gland epithelium to form lymphoepithelial lesions. This lymphoproliferative process usually remains localized to the salivary gland, but at risk for transformation to a high-grade B-cell lymphoma. 2-Sialolithiasis Stones can develop in the ducts of major and minor salivary glands. It is caused by dehydration or trauma It results in obstruction and inflammation. Prolonged obstruction results in atrophy, fibrosis, and destruction of the parenchyma 3-Tumors of the salivary gland Multiple benign and malignant tumors can arise in the major and minor salivary glands. Pleomorphic adenoma is the commonest tumor 70 GIT-207 2021-2022 Classification of salivary gland tumors 1- Benign (Adenoma) I) Pleomorphic adenoma (Mixed tumour) (65-80%). II) Monomorphic adenoma (a) Warthin's tumour (5-10%) (b) Oncocytoma (< 1%) (c) Other types (Myoepithelioma, Basal cell adenoma) 2-Malignant 1-Mucoepidermoid carcinoma (most common, 5-10%) 2-Malignant mixed tumor (2%) 3-Adenoid cystic carcinoma (3-10%) 4-Acinic cell carcinoma (2-3%) 5- Undifferenliated carcinoma Pleomorphic adenoma Is the most common tumor of salivary glands. It is benign, although can recur if ruptured during surgical excision. Rarely, recurrent tumors may undergo malignant transformation (called carcinoma ex pleomorphic adenoma). microscopic appearance: It is a tumor of myoepithelial cells and chondromyxoid stroma Warthin tumor It is a benign cystic tumor typically found in smokers. microscopic: composed of oncocytic epithelium with dense lymphoid stroma. Mucoepidermoid carcinoma: The most common malignant tumor of salivary glands. It has mucinous and squamous components. 71 GIT-207 2021-2022 Diseases of the Esophagus The esophagus is lined by nonkeratinizing squamous mucosa and Its wall contains well-developed muscle layers The lower esophageal sphincter normally prevents reflux of gastric contents into the esophagus. Disorders of esophageal motility or strictures within the esophagus can result in difficulty in swallowing (dysphagia). Achalasia It is a condition in which there is incomplete relaxation of the lower esophageal sphincter that results in functional esophageal obstruction. Gastroesophageal Reflux Disease (GERD) GERD results from the reflux of gastric contents into the tubular esophagus. Etiology: GERD can occur as a result of: -abnormal function of the lower esophageal sphincter -in association with a hiatal hernia when a portion of the stomach is herniated through the diaphragm. Presentation Symptoms of GERD may include heartburn, dysphagia, hoarseness of voice (laryngopharyngeal reflux)), chronic cough, and regurgitation Pathological features and effects: The presence of acidic gastric contents in the esophagus results in a marked inflammatory reaction. This is initially manifested by intramucosal eosinophils and may progress to ulceration. Prolonged reflux can result in metaplasia of the gastric mucosa (Barrett’s Esophagus). 72 GIT-207 2021-2022 Barrett’s Esophagus This is a type of metaplasia of the gastric mucosa from squamous to glandular similar to that in the small intestine and is characterized by the presence of intestinal type goblet cells. It usually persists throughout life and may extend to involve the proximal esophagus. This metaplastic epithelium is at increased risk for transformation into adenocarcinoma, usually preceded by dysplasia. Tumors of the Esophagous Esophageal cancer typically presents with progressive dysphagia and weight loss. Aggressive course due to lack of serosa in esophageal wall, allowing rapid extension. Poor prognosis due to advanced disease at presentation and lymph node metastases are frequently present at diagnosis. There are two major types: Squamous cell carcinoma: Linked to smoking, alcohol consumption, nitrites, radiation, very hot drinks, and achalasia. It appears in the upper and middle (upper 2/3) of the esophagus. Adenocarcinoma: A result of GERD leading to Barrett esophagus, which leads to dysplastic changes and adenocarcinoma. Dysplasia usually precedes the development of invasive adenocarcinoma by months or years so monitoring of Barrett’s esophagous by serial endoscopic biopsy is usually employed to identify patients at highest risk for invasive adenocarcinoma. It appears in the lower 1/3 of the esophagus. 73 GIT-207 2021-2022 Leture 9 Pathology of stomach I-Gastritis 1-Acute Gastritis It is acute inflammatory reaction in the gastric mucosa which is usually transient and self-limited. Causes:.NSAIDs lead to decrease PGE2 and this depletes gastric mucosa protection.. Burns (Curling ulcer): hypovolemia leads to mucosal ischemia. Brain injury (Cushing ulcer): are associated with head trauma. -Stress as in Systemic diseases (e.g., increased corticosteroid secretion) -Heavy Smoking and alcohol consumption - Spicy food and malnutrition -Radiation Pathogenesis: If the protective mucous layer is injured, the gastric acid reaches the gastric epithelial cells causing direct injury and initiates a superficial acute inflammatory reaction. Gross: Superficial small erosions. Microscopic: Shallow (does not invade the muscular layer). 2-Chronic gastritis It is a chronic inflammatory reaction in the gastric mucosa usually leads to mucosal atrophy and epithelial metaplasia Causes and pathogenesis: 1-Helicobacter pylori gastritis -This is the commonest cause. 74 GIT-207 2021-2022 -It can adapt to live in the acidic pH of the gastric lumen. Most of organisms remain extracellular in the mucous layer adherent to gastric mucosa, this result in persistent acute and chronic inflammation with injury to the epithelium. -Infection can result in small intestinal epithelium metaplasia, dysplasia, atrophy, peptic ulcer, adenocarcinoma and extranodal marginal zone lymphoma of mucosa- associated lymphoid tissue (MALT lymphoma). -H. Pylori initiates a chronic inflammatory reaction that results in the formation of germinal centers in the mucosa. The organism could be detected in microscopic section of superficial gastric mucosa stained with a modified Giemsa stain. 2- Autoimmune gastritis It is due to Autoantibodies to the H+/K+ ATPase on parietal cells and to intrinsic factor. There is risk of pernicious anemia. 3- Granulomatous gastritis a) non-infectious: Crohn's disease, sarcoidosis. b) Infectious: such as Tuberculosis, syphilis. 4- Other cause: Chemical (Reflux), Toxins (Alcohol0, Tobacco), Radiation. -Classification of chronic gastritis: *.Chronic superficial gastritis: inflammatory infiltrate consisting of plasma cells and lymphocytes in the superficial layer of the gastric mucosa *.Chronic atrophic gastritis (atrophic gastropathy): inflammatory infiltrate in the deeper layer of the mucosa and atrophy of the epithelium with destruction of the glands. *.Gastric atrophy :There is both loss (disappearance) and metaplasia of the native glands. but no inflammation though lymphoid aggregates may be present. 75 GIT-207 2021-2022 II-Peptic Ulcer Definition: These are defects occurring in any portion of the gastrointestinal mucosa exposed to acid-pepsin secretions. Sites: -Stomach: about 18% -First portion of the Duodenum: about 80% -Lower 1/3 of the esophagus -Meckel diverticulum -Margins of the gastrojejunostomy: stomal ulcer Pathogenesis: Peptic ulcers are produced by an imbalance between the mucosal defense mechanisms and damaging forces of gastric acid-pepsin. H. pylori secretes urease (generates ammonia) and protease (breaks down glycoprotein in the gastric mucus). -Also, bacterial lipopolysaccharide attracts inflammatory cells to the mucosa → inflammation of the gastric mucosa. -Damage of the protective mucosal layer and the chronically inflamed epithelial cells are more susceptible to the damaging effect of acid-pepsin and prone to peptic ulceration. 1-Gastric peptic ulcer -Epigastric pain is greater with meals leading to weight loss (Food pain pattern). -Vomiting is common. - Haematemesis is more common than melena -No seasonal variations -No night pain 76 GIT-207 2021-2022 Etiology: ** Usually normal to low acid level. 1-Depletion of mucosal protection against gastric acid due to : -Local irritant as alcohol, spicy food, drugs and smoking. -Chemical irritation by bile and pancreatic juice with duodenal-gastric reflux -Psychological effect due to Stress & anxiety 2- H. pylori infection in about ~ 70% of cases 2-Duodenal peptic ulcer -Pain decreases with meals leading to weight gain (Pain-food relief pattern) -Deep tenderness in the right hypochondrium. -Night pain common -No vomiting -Melena is more common than haematemesis. -Marked seasonal variations Etiology: 1-Hyperacidity: -due to Zollinger Ellison syndrome→ ↑ 𝑔𝑎𝑠𝑡𝑟𝑖𝑛 2- H. pylori infection in about ~ 90% of cases 3-Genetic: Depletion of mucosal protection against gastric acid due to low Mucus & PGs Pathologic Changes of peptic ulcer Location: -Gastric Ulcer: more common along lesser curvature in the region of pyloric antrum at the incusira angularis. -Duodenal Ulcer: more common in the first part of the duodenum, more commonly on the anterior than the posterior wall. 77 GIT-207 2021-2022 Gross : Usually solitary, oval or round, with punched out edge. Sharp edge is seen in active disease. Microscopic: 1- Surface purulent exudate & necrotic debris 2- Fibrinoid necrosis 3- Granulation tissue 4- Fibrosis replacing muscle layer Complications: 1-Haemorrhage by erosions of small vessels in the base of an ulcer 2-Perforation leads to acute peritonitis, Pneumoperitoneum, pancreatitis. 3-Malignant transformation occurs in < 1% of gastric ulcer. 4-Fibrosis leads to: a- Duodenal stenosis b- Pyloric stenosis c- Hour glass deformatiy of stomach due to saddle ulcer III- Tumors of the stomach According to the WHO classification: I-Epithelial i) Benign tumors: Intestinal-type Adenoma Foveolar Adenoma Pyloric gland Adenoma Oxyntic gland Adenoma. ii)Malignant tumors: - Adenocarcinoma 78 GIT-207 2021-2022 -Squamous cell carcinoma -Adenosquamous -Undifferentiated carcinoma II- Mesenchymal: i) Benign tumors: Gangilioneuroma Glomus tumor Hemangioma Leiomyoma Lipoma

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