Dsa14 Gi Intro

Front 1

Describe and explain the embryonic development of the trachea and the esophagus that leads to tracheoesophageal fistula or atresia

Back 1

Atresia = thin, non-canalized cord replaces a segment of esophagus, causing obstruction

Atresia = Connects upper or lower esophageal pouches to bronchus or trachea. Can be present without atresia. Usually proximal esophageal atresia + distal esophagus rising out of trachea

Front 2

Describe the histology of the esophagus related to the response to reflux of acid and metaplasia.

(Barrett Esophagus)

Back 2

Normal = stratified squamous

Metaplasia to nonciliated columnar epithelium with goblet cells

Looks like intestinal epithelium

Response of lower esophageal stem cells to acidic stress

Front 3

Functions of the upper esophageal sphincter and lower esophageal sphincter

Back 3

Upper esophageal sphincter (UES)

• Excludes air during respiration
• Aspiration of contents into tracheal-bronchial tree is an issue

Lower esophageal sphincter (LES)

• Prevents reflux of gastric contents
• Regurgitation, effortless reflux of gastric contents is an issue
  

Front 4

Locate the neural networks in the wall of the esophagus and describe the control of the upper and lower esophageal sphincters

Back 4

LES is tonically contracted, and can vary to release gastric pressure.

This positive pressure gradient between the stomach and the esophagus can be considered the driving force for gastroesophageal reflux, with the high pressure zone at the gastroesophageal junction considered a barrier to the prevention of reflux of gastric contents.

A significant component of LES pressure is contributed by the diaphragm and that augmentation of the LES pressure.

Front 5

What is a hiatal hernia?

Back 5

Elements of the abdominal cavity, most commonly the stomach, herniate through the esophageal hiatus into the mediastinum.

Front 6

What is the pathophysiology of a sliding hiatal hernia?

Back 6

• Widening of the muscular hiatal tunnel and circumferential laxity of the phrenoesophageal membrane, allowing a portion of the gastric cardia to herniate upward
  
• The squamocolumnar junction (SCJ) pokes right up into the esophagus

Front 7

What is the pathophysiology of a paraesophageal hiatal hernia?

Back 7

• The SCJ maintains its native position
• The gastric fundus herniates into next to esophagus

Front 8

Complications of paraesophageal hiatal hernia

Back 8

• obstruction
• diaphragmatic impingement on the stomach
• gastric volvulus
  

Front 9

Describe the key differences in the muscular layers in the upper and the lower part ofthe esophagus, which section of the esophagus exhibits skeletal muscle disorders and which sections exhibit smooth muscle disorders.

Back 9

Upper 1/4 to 1/3

• composed of skeletal muscle layer
• affected by skeletal muscle disorders (polymyositis; CVA and damage to the swallowing center or motor nuclei controlling striated muscles of hypopharynx and upper esophageal region.)

Lower portion

• Smooth muscle layer
• affected by smooth muscle disorders (achalasia, scleroderma)
  

Front 10

Neural network of esophagus

Back 10

Auerbach plexus (myenteric) lies between the longitudinal and circular muscle layers.

Meissner plexus (submucosal), is situated between the muscularis mucosa and the circular muscle layer

Muscularis mucosa -> Meissner -> circular -> Auerbach -> longitudinal

Front 11

Pathophysiology of achalasia, and cause

Back 11

• Damaged ganglion cells in myenteric (auerbach) plexus
  
• Lack nonadrenergic, noncholinergic,inhibitory ganglion cells, causing a hypertensive non-relaxed esophagealsphincter.

• Comes from idiopathic or Chagas

Front 12

Clinical features of Achalasia

Back 12

• Dysphagia for solids and liquids

• Putrid breath

• High LES pressure on esophageal manometry

• BIRD BEAK sign on barium swallow

• Increased risk for SCC

Front 13

Describe lymph flow of esophagus

Back 13

Upper 1/3

• Cervical, internal jugular, supraclavicular

Middle 1/3

• paratracheal and hilar, aortic, cardiac, and paraesophageal

Lower 1/3

• retroperitoneal, celiac, left gastric
  

Front 14

Pathway of metastatic spread of esophageal carcinoma

Back 14

• Lesions of the cervical esophagus may extend to the carotid arteries, pleura, recurrent laryngeal nerves, and trachea.

• Lesions of the middle third may invade the main stem bronchi, thoracic duct, aortic arch, subclavian artery, intercostal vessels, azygos vein, and right pleura.

• Tracheoesophageal or bronchoesophageal fistulas are most common in lesions of the middle third and develop in 15% of patients with esophageal cancer.

• Tumors of the lower third may extend into the pericardium, left pleura, and descending aorta.
  

Front 15

Describe the functional histology (related to a clinical disorder) of the stomach, including the muscular, submucosal, and mucosal layers.

Back 15

From surface of stomach to deep layer

• Mucus
• Mucosa
• Muscularis mucosae
• Submucosa

Lymphatics start in the deepest lamina propria just above the muscularis mucosae

Front 16

Morphology of acid secreting mucosa and function of chief and parietal cells

Back 16

Chief cells

• Mostly present in the lower half of gastric glands.
• Pepsinogen synthesis.

Parietal cells

• Synthesize hydrochloric acid and lipase.

Front 17

Parietal cells (oxyntic cells) and the physiology of this cell as it relates to acid secretion?

Back 17

• Gastrin (from antral gland G-cells), along with histamine and ACh from vagus stimulate luminal acid secretion by parietal cells in fundus and body
• When gastrin is released from G cells in response to a meal, it binds to CCK-2 receptors on both the parietal and ECL cells. The binding of gastrin to the parietal cell results in release of intracellular calcium and translocation and activation of the H+, K+-ATPase(the proton pump). The binding to the ECL cells causes release of histamine to go activate the parietal cells the same way.
  
• The parietal cells secrete acid, and the resulting drop in pH causes the antral D cells to release somatostatin, which inhibits gastrin release (negative feedback control).
  

Front 18

Define the clinical significance of the ligament of Treitz as it relates to GI bleeding.

Back 18

Ligament of Treitz holds up the small bowel at the junction of the duodenum and jejunum

Used to mark the difference between the upper and lower gastrointestinal tracts, which may determine the source of bleeding in the gastrointestinal tract.

Above = think stomach

Below = Lower GI bleed

Front 19

Describe the morphology and spread of gastric carcinoma into the normal components of the stomach wall, surrounding structures and regional lymph nodes.

Back 19

• All gastric carcinomas eventually penetrate the wall to involve the serosa and spread to regional and more distant lymph nodes.

• The abundant lymphatic channels within the submucosal and subserosal layers of the gastric wall allow for easy microscopic spread.

• Lymphatic drainage is through numerous pathways and can involve multiple nodal groups (e.g.,gastric, gastroepiploic, celiac, portal hepatic, splenic, suprapancreatic, pancreaticoduodenal, paraesophageal, and paraaortic lymph nodes).
  

Front 20

Vomiting blood or “coffee ground” material is indicative of?

Back 20

Gastritis and ulcer disease

Front 21

When the material vomited is pure gastric juice, what is suggested?

Back 21

Peptic ulcer disease

Zollinger–Ellison syndrome

Front 22

Lack of acid in vomit suggests?

Back 22

Gastric cancer

Front 23

Feculent material in vomit is a sign of?

Back 23

Distal small-bowel obstruction

Blind-loop syndrome

Front 24

Emesis of undigested food suggests?

Back 24

Zenker's diverticulum

Achalasia

Front 25

Vomitus containing food residue ingested hours or days previously suggests?

Back 25

Severe gastroparesis

Front 26

Pathophysiology of Meckel Diverticulum

Back 26

• The vitelline duct connects lumen of the developing gut to the yolk sac to provide nutrients to the growing fetus.
• Failed involution of this vitelline duct
• Leads to outpouching of all three layers of bowel wall (true diverticulum)
• Occurs in the ileum

Front 27

Intestinal wall layers from surface to deep

Back 27

1) Intestinal glands

2) Muscularis mucosa

3) Submucosa (enteric plexus and Peyer's patch)

4) Circular muscle layer

5) Myenteric plexus (Auerbach's)

6) Longitudinal muscle layer

7) Subserous

8) Serous

Front 28

Describe the key morphology as it relates to the mucosal folds and villi for absorption in the small bowel, relate to the clinical outcome with flattening of the mucosal folds

Back 28

• There is blunting and flattening of villi with celiac disease, and in severe cases a loss of villi with flattening of the mucosa.
• Celiac sprue leads to malabsorption.

Front 29

Digestion and absorption in 3 phases

Back 29

In general,the digestion and absorption of food materials can be divided into 3 major phases:–

1) Intraluminal: The luminal phase is the phase in which dietary fats, proteins, and carbohydrates are hydrolyzed and solubilized by secreted digestive enzymes and bile.

2) Terminal Digestion (Mucosal): The mucosal phase relies on the integrity of the brush-border membrane of intestinal epithelial cells to transport digested products from the lumen into the cells

3) Transepithelial (Postabsorptive): reassembled lipids and other key nutrients are transported via lymphatics and portal circulation from epithelial cells to other parts of the body.

Front 30

Describe the sphincter action of the ileocecal valve

Back 30

• Prevents backflow from the large intestine, once any material leaves the small intestine.

Front 31

Ulcerative colitis and ileocecal valve

Back 31

Ulcerative colitis occasionally involves the terminal ileum, as a result of an incompetent ileocecal valve.

Reflux of noxious inflammatory mediators from the colon results in superficial mucosal inflammation of the terminal ileum, called backwash ileitis.

Front 32

Locate the submucosal lymphoid tissue (Peyer’s patch) of the small intestines and describe the possible role the immunologic function plays in infectious, inflammatory, and neoplastic disorders (includes lymphoma)

Back 32

• The epithelium includes M cells which transport antigen across the epithelium to immune cells.
  
• The lymphoid tissue of Peyer's patches is similar to that of tonsils and appendix. These structures, together with other more diffuse lymphoid tissue,constitute the Gut-Associated tLymphoid Tissues, or GALT.
  
• Only found in the ileum

• Common site for extranodal marginal zone B-cell lymphomas (MALTomas)

Front 33

Describe the taeniae coli, longitudinal muscle bundles, haustra and mural defects (weakness) as it relates to potential for weakness and/or defects in the colon wall, specifically as it relates to diverticula

Back 33

• Where nerves and arterial vasa recta penetrate inner circular muscle coat of sigmoid, holes in muscle wall are created.

• In other intestine, these gaps are reinforced by the longitudinal layer of muscularis propia

• BUT, in the colon, we have the three banded taeniae coli. This means we can have outpouching diverticula

• The haustral folds represent folds of mucosa within the colon. They are formed by circumferential contraction of the inner muscular layer of the colon.
  

Front 34

Locate the most vulnerable sites in the colon for ischemia and explain why

Back 34

• Watershed area at the splenic flexure, rectosigmoid junction, and transverse colon
• These are the watershed areas that have the fewest vascular collaterals

Front 35

Describe the enteric plexuses, Meissner and Auerbach enteric plexuses of the colon

Back 35

Myenteric plexus = Auerbach

• Between inner circular and outer longitudinal muscle layers
• Regulates motility

Submucousal plexus = Meissner

• In the submucosa
• Regulates BF, secretions, absorption

Front 36

Pathophysiology of Hirschsprung Disease

Back 36

• Defective relaxation and peristalsis of rectum and distal sigmoid
• Congenital failure of ganglion cells (neural crest-derived) to descend into myenteric and submucosal plexus
• Failure to pass meconium
• Empty rectal vault on DRE
• Massive dilatation of bowel proximal to obstruction (megacolon)
• Commonly caused by Chagas (?)

Front 37

Explain the pathogenesis of hemorrhoids.

Back 37

• Enlarged veins located in the lower part of the rectum and the anus. The veins become swollen due to increased pressure within them, usually from constipation or profuse diarrhea, and during pregnancy because of the pressure of the enlarged uterus.

• Internal hemorrhoids are located in the inside lining of the rectum and cannot be felt. They are usually painless and make their presence known because blood is seen with a bowel movement. Internal hemorrhoids can prolapse or protrude through the anus.

• External hemorrhoids are located underneath the skin that surrounds the anus
  

Front 38

What does hematochezia indicate?

Back 38

The majority of cases are below the ligament of Treitz (junction of the jejunum with the duodenum)

Front 39

What does melena (black, tarry, foul smelling) stool indicate?

Back 39

The majority of cases are proximal to the ligament of Treitz (junction of the jejunum with the duodenum).

Stool remains in contact with bacteria that degrade hemoglobin during the transit time