G.I. Tract Test II Flashcards
GI System
Consumes, digests, and eliminates food
Made of;
Upper division (Oral cavity, Pharynx, Esophagus, and Stomach)
Lower division (Small intestine, Large intestine, and anus)
Hepatobiliary system (Liver, gallbladder, and pancreas)
GI System tissues
Four Layers - Muscosa, Submucosa, Muscle, Serosa
Peritoneum - Parietal (lines the cavity), Visceral (Lines the organs), Cavity (space between the two).
Mesentary - double layer peritoneum containing blood vessels and nerves that supply the intestinal wall.
GI wall
GI Wall part 2
Epithelium - Most exposed part of the mucosa - composed of simple columnar epithelium or stratified squamous epithelium, also present ar Goblet cells (secrete mucus that protects the epithelium from digestion) and endocrine cells (secrete hormones into the blood).
Under the epithelium is the lamina propria, which contains myofibroblasts, blood vessels, nerves and several different immune cells, and the muscularis mucosa which is a layer of smooth muscle that aids in the action of continued peristalsis along the gut.
The submucosa contains nerves including the submucosal plexus (Meissner’s plexus), blood vessels and elastic fibers with collagen, that stretches with increased capacity but maintains the shape of the intestine.
Surrounding this is the muscular layer, which comprises both longitudinal, and circular smooth muscle that also helps with continued peristalsis and the movement of digested material out of and along the gut. In between the two layers of muscle lies the myenteric plexus (Auerbach’s plexus).
The serosa is a serous membrane that covers the muscularis externa of the digestive tract in the peritoneal cavity.
Upper GI tract
Food enters mouth to begin mechanical/chemical digestion.
Swallowing coordinated by the swallowing center in the medulla and cranial nerves V, IX, X, and XII.
Digestive juices and actions
From the Salivary Glands
Bicarbonate - Moistens food
Salivary Lipase - Digests Fat
From the Stomach
Hydrochloric acid - Kills Bacteria
Pepsin - Digests Protein
Gastric Lipase - Digests Fat
Intrinsic Factor - Aids in B12 absorption
Mucus - Protects stomach lining.
Congenital abnormalities of the GI
Atresia, Fistulae, and Duplications
Atresia - Incomplete development of the Esophagus.
Most commonly occurs at the tracheal bifurcation and is usually associated with a Fistula (Adhesion of the esophagus to the trachea ). Discovered shortly after birth - Regurgitation during feeding. Leads to Aspiration, suffocation, pneumonia, and severe fluid/electrolyte imbalances. (associated with congenital heart defects, genitourinary malformations, and neurologic disease)
Acquired Stenosis - inflammatory scarring eg. GERD, irradiation, systemic sclerosis, or caustic injury.
Congenital abnormalities of the GI
Diaphragmatic Hernia & Omphalocele
Diaphragmatic Hernia - Incomplete formation of the diaphragm allows the abdominal viscera to herniate into the thoracic cavity
Omphalocele - occurs when the closure of the abdominal musculature is incomplete and the abdominal viscera herniate into a ventral membranous sac.
Congenital abnormalities of the GI
Meckel’s Diverticulum
A true diverticulum - blind outpouring of the alimentary tract that communicates with the Lumen.
Failed involution of the Vitelline duct.
Rule of 2
Occurs in 25 of the population present within 2 feet of the ileocecal valve, approx 2 inches long, 2 times as common in males, most often symptomatic by 2 y/o. (only 4% symptomatic)
Ectopic pancreatic or gastric tissue may also be present giving the ability to Secrete acid causing peptic ulceration of adjacent small intestinal mucosa.
May present with occult bleeding (painless BRBPR) or abdominal pain resembling acute appendicitis or obstruction.
Congenital abnormalities of the GI
Pyloric Stenosis
3-5 times more common in males and occurs 1 in 300-900 live births.
Increased risk in monozygotic twins, dizygotic twins, siblings, Turner syndrome, and trisomy 18, erythromycin or Azithromycin exposure.
Presents between 3-6 weeks as new onset Regurgitation, projectile, non-bilious vomiting after feeding, and frequent demands for re-feeding.
Hyperplasia of the pyloric muscularis externa, which obstructs the gastric outflow tract.
Edema and inflammatory changes in the mucosa and submucosa may aggravate the narrowing.
Acquired - antral gastritis or peptic ulcers close to the pylorus, ca. stomach.
Congenital Abnormalities of the GI
Hirschsprung Disease
1 in 5000 live births, ~ 10% in Down Syndrome
Presents with failure to pass meconium in the immediate postnatal period.
Obstruction or constipation follows, often with visible ineffective peristalsis, and may progress to abnormal distension and bilious vomiting (congenital aganglionic megacolon).
Major Threats - enterocolitis, fluid/electrolyte disturbances, perforation, and peritonitis
Congenital Abnormalities of the GI
Achalasia
Increased amounts of Ach at the Lower Esophageal Sphincter (LES) prevents it from opening all the way which then leads to a back-up in the esophagus.
Symptoms - Dysphagia for solids/liquids, difficulty in belching, regurgitation, chest pain, and weight loss.
Primary- ganglion cell degeneration
Secondary- Chagas disease, diabetic neuropathy, infiltrative disorders such as malignancy, amyloidosis, lesions of the dorsal motor nuclei of vagus, polio or surgical ablation, in association with Down syndrome; alacrima and adrenal insufficiency.
Esophageal conditions
Relux Esophagus
Reflux of gastric contents into the lower esophagus.
SSE - sensetive to acid
Submucosal glands - protection by secreting mucin and HCO3.
Alcohol/tobacco, obesity, CNS depressants, pregnancy, hiatal hernia, decreased gastric emptying leads to Less Tone of LES and Inc abdominal pressure.
Most Frequent Clinical Features - Heartburn, dysphagia, regurgitation, sour-tasting gastric contents.
Complications - ulceration, hematemesis, melena, stricture development, and Barret’s esophagus.
Esophageal conditions
Esophageal Varacies
Abnormal dilation of the junction between the portal and systemic venous systems.
Important cause of massive and frequent life-threatening bleeding.
Portal HTN -> Esophageal Varacies -> Bleeding
Portal HTN forces Portal blood into alternate channels.
Presents in nearly half of the PTs with cirrhosis - as many as half the PTs die from the first bleeding episode.
Esophageal conditions
Barrett Esophagus
Complication of the chronic GERD characterized by intestinal metaplasia
Characterized by the replacement of the normal stratified squamous epithelial lining -> simple columnar epithelium with goblet cells (which are mostly found lower in the GI tract)
Most commonly found in white males 40-60 y/o
Increased risk of esophageal adenocarcinoma
Barrett esophagus can only be identified through endoscopy and biopsy, which are usually prompted by GERD symptoms.
Esophageal conditions
Esophageal Tumors
7th leading cause of cancer death.
Incidence increases with age: peak -> 6th -7th decade.
Sq. Cell carcinoma (middle 3rd) / Adenocarcinoma (Lower 3rd)
Worldwide: SCC - most common
Adenocarcinoma >50% in the USA due to its association with GERD, Barrett esophagus and obesity.
Sq. Cell Carcinoma Risk Factors
Alcohol/Tobacco use (90%)
Caustic esophageal injury
Achalasia, Tylosis
Plummer - Vinson syndrome
Diet deficient in fruits or Vegetables
Very hot beverages
Generic Abnormalities - p53, EGFR
Adenocarcinoma Risk Factors
Barret Esophagus, Gerd, hiatal hernia
Obesity
Smoking
Increased acid exposure eg., Zollinger-Ellison Syndrome
Esophageal tumors clinical features
Present with dysphagia (90%), odynophagia (pain on swallowing), or progressively increasing obstruction.
Prominent weight loss and debilitation result from both impaired nutrition and the effects of the tumor itself.
Hemorrhage and sepsis may accompany tumor ulceration, and symptoms of iron deficiency are often present.
Lymph node metastases - poor prognosis
5-year survival rate <25%
Stomach anatomy
4 major regions - Cardia (the neck), Fundus (top of the body) Body (The main portion of the stomach) Antrum (beginning of the Pyloric canal)
Cardia and Antrum lined mainly with mucin-secreting foveolar cells that form small glands.
The Antral glands are similar but also contain endocrine cells, such as G-cells, that release gastrin to stimulate luminal acid secretion by parietal cells within the gastric fundus and body.
The well-developed glands of the body and fundus also contain chief cells that produce and secrete digestive enzymes such as pepsin.
