The Digestive System Flashcards
Boundaries of the Abdominal Cavity
Superior: Diraphragm, reaching up to the inferior apex of the sternum.
Inferior: Iliac crest and the pelvic inlet.
Layers of the abdominal fascia from superficial to deep
Skin, superficial fascia, external oblique (inferomedial), internal oblique (superomedial), transversus abdominis, transversalis fascia, extraperitoneal fascia, parietal peritoneum.
Rectus abdominis
Connects the pubic tubercle and the costal cartilage of the middle ribs.
Vertically oriented fibres separated into horizontal divisions by intertendinous bands.
F: Flexion of trunk. Compression of the abdominal wall.
N: Anterior rami of thoracic nerves.
External oblique
O: Posterolateral aspects of the middle and lower ribs.
I: Iliac crest, linea alba via anterior rectus sheath, Inferior free edge forms the inguinal ligament.
F: Bilateral contraction causes trunk flexion. Unilateral contraction leads to rotation to the contralateral direction.
N: Anterior rami of thoracic nerves
Internal oblique
O: Iliac crest and the thoracolumbar fascia.
I: Lower ribs, linea alba via the anterior and posterior rectus sheaths.
F: Bilateral contraction flexes trunk. Unilateral contraction leads to ipsilateral rotation and flexion.
N: Anterior rami of thoracic nerves and L1.
Transversus abdominis
Longitudinal origin from lateral ribs to the iliac crest.
Longitudinal insertion from the linea alba to the pubic crest.
F: Bilateral contraction tenses abdominal wall.
N: Anterior rami of thoracic nerves and L1.
Distribution of the rectus sheath
Anterior and posterior to the rectus abdominis muscle, but the posterior section is missing for the inferior 1/4. Allows the inferior epigastric artery to pierce through the sheath and move anteriorly to anastomose with the superior epigastric arteries, which descend from the suclavian artery along the plane of the transversalis fascia.
Venous and lymphatic drainage of the abdominal cavity.
Superior venous: Thoracoepigastric into the axillary vein. Inferior venous: Superficial epigastric into femoral vein. Superior lymphatic (above umbilicus): Drains into axillary nodes. Inferior lymphatic (below umbilicus): Drains in inguinal nodes.
Innervation of the abdominal wall
Anterior rami of the thoracic (and L1) nerves. Wraps around the lateral side of the thoracic wall as it moves anteriorly. Pierces the superficial fascia adjacent to the linea alba to provide cutaneous innervation to the anterior abdominal wall.
Inferior regions of IO and TA are supplied by the iliohypogastric and the ilioinguinal nerves.
Peritoneal structures
Foregut, jejunum and terminal ileum: The mesentery.
Transverse colon: transverse mesocolon.
Sigmoid colon: Sidmoid mesocolon.
Omental bursa/ Lesser sac
Positioned posterior to the stomach and separates the intraperitoneal and retroperitoneal structures of the abdominal cavity. Roof is formed from the hepatogastric and hepatoduodenal ligaments.
Opens to the right at the omental foramen.
Paracolic gutters and associated pathology
Sulci lateral to the ascending and descending colon to allow mass movement of pathologically accumulated fluids in the abdominal cavity.
Upright: Conducts fluid down to the appendix region of the abdominal cavity. Presents with appendicitis-like symptoms.
Supine: Fluid moves superiorly into the hepatorenal recess and into the lesser sac. Pain in the epigastric region.
Embryonic Formation of the Oesophagus and pathology
Formed from the mesoderm and endoderm layers into a cylindrical shape during embryonic folding. Rapidly proliferates to the connect the gut to the oral membrane.
Respiratory diverticulum buds off at the tracheoesophageal ridge.
Congenital tracheoesophageal atresia: Failure for the respiratory diverticulum to bud off correctly, resulting in a blind-ended oesophagus that does not connect properly to the gut, or is connected to the trachea.
Congenital hiatal hernia: Failure of rapid oesophageal elongation means the stomach and the rest of the gut is pulled anteriorly.
Embryonic formation of the stomach and pathology
Initially a narrow structure suspended by anterior and dorsal mesogastrium. Expands asymmetrically- faster rate on the posterior side.
Rotates 90 degrees clockwise in the transverse plane so the greater curvature faces left. Dorsal mesogastrium is pulled to the left to form an invagination that would become the omental bursa. Spleen is pushed against the dorsal abdominal wall.
Rotates 90 degrees clockwise in the coronal plane and the sac formed in the previous step is rotated inferiorly so it will proliferate downwards to become the omentum as the four layers of peritoneum fuse.
Congenital hypertrophic pyloric stenosis: Excess thickening of the pyloric sphincter muscles
Embryonic liver, biliary tree and pancreatic development.
Originates as the hepatic diverticulum which buds off just caudal to the midgut, which separates into the liver, gallbladder and the ventral pancreatic bud, A dorsal pancreatic bud is also formed on the dorsal side of the pylorus of the stomach precursor.
Clockwise rotation of the stomach in the coronal plane will bring the two pancreatic buds together to form the pancreas, while the liver will be positioned to the right and anterior to the stomach. It will also position the liver up against the posterior abdominal wall to make it a retroperitoneal structure.
Ligaments associated with the liver
The liver is formed within the anterior mesogastrium of your stomach. The anterior section holds the umbilical vein in its free inferior border which becomes the hepatic ligamentum teres. It becomes the falciform ligament between the lobes of the liver.
The mesentery between the liver and the stomach will become the hepatoduodenal and the hepatogastric ligaments, which form the lesser omentum.
Midgut Twisting
1) Physiological herniation of the midgut precusor into the umbilical cord. Cranial limb is the small intestine precursor while caudal limb is the colon precursor.
2) Midgut spins anticlockwise 270 degrees as it is retracted back into the abdominal cavity.
3) The colon rotates clockwise so the caecum is positioned at the right groin region.
(Refer to notes for diagram to reinforce mechanism)
Congenital Malformations of the Midgut
- Nonrotation: Failure of anticlockwise rotation of the midgut leads to separation of the small intestine and colon.
- Mixed rotation: Leads to volvulsus, where the twisting of the midgut severs itself from the stomach or occludes itself.
- Reverse rotation: Clockwise rotation of the midgut, resulting in the colon being trapped under the superior mesenteric artery.
- Umbilical herniation: Failure of the umbilical cord to close, which allows the herniation of the small intestine.
Meckel’s Diverticulum
Remnant of the yolk stalk does not regress, so a stalk is formed from the ileum at the umbilicus, which sometimes joins to the umbilicus and opens up to the outside world via the omphaloenteric fistula.
The diverticulum usually acts like a tube that can be inflammed.
False diverticulum are formed when the protrusion is not due to malformation during development, but rather the herniation of a region of ileum through weakened smooth muscle.
Hindgut development and congenital malformations.
Initially formed as the cloaca, which is the combined membrane-sealed orifice. The urorectal sphincter forms by week 4 to split the digestive and genitourinary systems.
Imperforate anus: Condition where the cloacal membrane fails to rupture during development.
Rectal atresia and fistula: Failure for the anal canal to form a continuous channel with the rectum. Fistula can intrude into the genitourinary tract.
Division of the Anal canal `
Section above the pectinate line: Endoderm and part of digestive system.
Venous drainage to hepatic portal vein.
Poor somatic sensation as it is primarily innervated by the autonomous nervous system.
Section below pectinate line: Ectoderm and part of the integumentary system.
Good somatic sensation as there are cutaneous somatic sensory receptors.
Venous drainage to inferior vena cava.
Role of the Upper Oesophageal Sphincter
Tonally contracted to keep the sphincter closed. Significant barrier function so high pressure needed to open.
Superior regions of the oesophagus contains skeletal muscle to confer somatic control over the swallowing process.
- Reduces airflow into stomach to prevent overextension and pain.
- Prevents gastric reflux into the oral cavity and lungs.
- Prevents reflux of oesophageal contents.
- Transient aperture during swallowing via relaxation of the inner smooth msucle sphincter.
Primary and Secondary Peristalsis
Primary: Initiated by the pharyngeal phase of swallowing, where the peristaltic contraction of the pharynx pushes the the bolus into the oesophagus. Peristaltic contraction involves the generation of a pressure gradient by increasing pressure behind the bolus while relaxing of the oesophagus before the bolus to drive its movement.
Secondary peristalsis: Stretch receptors detect distension of the oesophagus which indicates remnants of the bolus is present in the oesophagus. Initiates peristaltic movement.
Peristalsis involves both layers of muscularis externa- OL: shortens oesophagus, IC: contracts lumen.
Regulated by the myenteric plexus of the enteric nervous system but activity is influenced by factors from the autonomous nervous system.
Lower oesophageal sphincter function
Entirely consisting of smooth muscle- entirely autonomous control.
Contracts less strongly and aperture is less transient.
Demarcates the interface between the protective stratified squamous epithelium of the oesophagus and the secretory simple columnar epithelium of the stomach.
Relaxation of the sphincter results in relaxation of the fundus, which allows accomodation of more food.
Phases of Swallowing
Voluntary oral phase:
Preparatory–> Formation of bolus via mastication of food and lubrication with saliva.
Transfer/Involuntary Pharyngeal phase–> Tongue presses against the hard palate to shut off anterior oral cavity Nasopharynx and larynx closed off. Sound-making apparatus in the trachea are adducted.
Pharynx contracts peristaltically to push the bolus through the UOS. The involuntary phases are initiated by pressure receptors at the back of the oral cavity, which detect distension and sends the signal to the swallowing centre of the brainstem
Involuntary oesophageal phase: Relaxation of the UOS and initiation of oesophageal peristaltic movement following peristaltic ejection from the pharynx.
Causes of GORD
- Excessive acid in the fundic region of the stomach.
- Hiatus hernia: Weakness of the diaphragm allows herniation of the stomach into the thoracic cavity. This forms a pocket where stomach acid can be ‘stored’ and refluxed into the oesophagus.
- Hypotensive LOS: Failure of barrier function leaves the sphincter patent. Free movement of gastric acid into the oesophagus.
- Impaired secondary peristalsis mechanism–> Failure to detect oesophageal distension due to refluxed food material.
Symptoms of GORD
- Painful burning sensation (heartburn)– > Due to disruption of the stratified squamous epithelium, which allows the acid to reach the submucosa where the nociceptors are.
- Oesophagitis due to excess damage to the oesophageal lining causing inflammation. Formation of ulcers close to the LOS due to epithelium damage.
- Submucosal damage can lead to damage of the submucosal blood vessels, which causes bleeding and presents as haematemesis.
- Oesophageal stricture: Excess, repeated oesophageal damage leads to formation of hypertrophic scar tissue, which will protrude into the oesophageal lumen and reduce its diameter. Disrupts passage of food-dysphagia.
Barrett’s Oesophagus and oesophageal adenocarcinoma.
Repeated oesophageal mucosa damage leads to metaplasia of the oesopageal lining into columnar epithelium (which appears dark red instead of light pink). Metaplasia can lead to adenocarcinoma, where some cells become malignant due to interference with growth factors during the metaplasia process. Reversible process (reversed by stopping metaplasia) but can progress irreversibly to become a carcinoma.
Zenker’s Diverticulum
Failure for the UOS to relax during swallowing means the pharynx peristaltic contraction will push food into the wall. Causes a pocket to form at the weakest point at the region cranial to the UOS.
Motility Disorders of the Oesophagus
Diffuse oesophageal spasm: Failured of coordinated smooth muscle contraction in the oesophageal wall. Leads to contortion of the oesophagus into a corkscrew. Dysphagia and chest pain.
Achalasia: Degeneration of the myenteric plexus prevents signals which signal relaxation of the LOS sphincter muscles and peristalsis of the smooth muscles of the oesophageal wall. Results in accumulation of food in the oesophagus just before the sphincter. Manifests in enlarged oesophagus, dysphagia and chest pain.
Scleroderma: Fibrosis of submucosa and muscularis leading to rigidity of the oesophagus. Poor peristaltic movement generated and loss of LOS tone. Severe acid reflux and weak peristaltic contractions.
Anatomy and Vasculature of the Stomach
- Located at the Epigastric region.
- Lesser curvature supplied by the right gastric artery inferiorly and the left gastric superiorly The right gastric is a branch of the hepatic artery while the left gastric forms directly from the coeliac trunk and moves cranially to pass along the oesophagus, but also forming a recurrent branch along the superior half of the lesser curvature.
- Inferior greater curvature supplied by the left gastro-omental artery, which is formed from the SMA. The splenic artery forms the short gastric artery which supplies the superior half of the greater curvature.
- Drained by the hepatic portal vein venously and the thoracic duct via the coeliac nodes.
