The Upper GI and Pancreas

Question 1

Esophagus

Answer 1

25 cm long muscular tube.
Transports food to the rest of the digestive tract.
Begins with the cricopharyngeus muscle (upper esophageal sphincter) and ends just below the diaphragm at the lower esophageal sphincter (LES).
Designe to transiently relax when food passes through.
The LES IS NOT a muscular ring, but prevents reflux of stomach contents through…
1. tonic contraction of several cm of muscle.
2. A sharp angulation
3. A change in the mucosal lining.
4. The crus of the diaphragm.
The upper one third of the esophagus contains striated muscle, the lower two thirds contain smooth muscle only.

Question 2

Gastroesophageal Reflux Disease (GERD)

Answer 2

Heartburn; can lead to ulcers, bleeding, difficulty swallowing, cancer.
When acid from the stomach, combined with the stomach enzyme pepsin, and bile, refluxes into the esophagus it will cause pain and inflammation.
Hiatal hernia: cannot feel this happening; a condition where the upper aspect of the stomach is pulled up into the chest; this weakens the LES (valve designed to prevent reflux into the esophagus).
Stomach over distension is one reason why the LES can relax at the wrong time and allow reflux.
Symptoms: Heartburn (pyrosis), feeling of liquid coming back up esophagus or throat (gross reflux, acid brash), increased salivation, atypical presentations include laryngitis, asthma, aspiration pneumonia, loss of dental enamel.
Chronic inflammation of the esophagus.
Progression of a weak LES: TLESRs (NORMAL transient LES relaxations), then reflux and inflammation, then a weak LES.
Typical GERD symptoms: Erosive Reflux Disease
Atypical manifestations: Asthma, cough, laryngitis, chest pain, globus (the feeling like there is something in your GI tract).
Complications: Strictures (scarring which inhibits motor function), ulceration, Barrett’s esophagus, cancer.
Therapy: acid suppression (proton pump inhibitors-omeprazole, H2 blockers-ranitidine), lifestyle changes, weight loss, surgery.

Question 3

Long Term Complications of GERD

Answer 3

Chronic inflammation of the esophagus leads to…
1. Strictures: Scarring of the esophagus, which inhibits motor function and eventually causes narrowing. Leads to dysphagia (difficulty swallowing) for solid foods and then liquids.
2. Barrett’s Esophagus (intestinal metaplasia): chronic damage to the lining of the esophagus can lead to the mucosa changing from squamous cell to columnar epithelium (like the stomach and duodenum).
This metaplastic epithelium carries the risk of transforming into dysplasia and then to cancer.
Does not cause symptoms.
3. Adenocarcinoma: Almost all adenocarcinoma occurs in the setting of Barrett changes; frequency is on the rise; long term survival is low because the tumor grows large before presenting with symptoms.
The Road to esophageal adenocarcinoma: chronic reflux, intestinal metaplasia (Barrett’s), low grade dysplasia, high grades dysplasia, esophageal adenocarcinoma.

Question 4

Non Erosive Reflux Disease (NERD)

Answer 4

There is no visible damage to the esophagus, but there are symptoms.
Treat first! Ask later.

Question 5

Squamous cell Cancer of the Esophagus

Answer 5

Most common cancer worldwide, incidence in US is low (mainly adenocarcinoma in the US).
Adenocarcinoma is the fastest increase in incidence of all solid cancers in the Western World.
Risk factors: smoking, alcohol, nitrosamines in the diet, lye strictures, carcinogens, pickled foods, endemic microbes, regional practices, nutritional deficiencies, soil salinity.
Symptoms: dysphagia is the most common presenting symptom, weight loss, anemia/bleeding/hematemesis (vomiting of blood), chest/back pain, recurrent pneumonias, odynophagia (painful swallowing), choking, age > 45 years.
5 year survival is 10%.
Treatment: surgery and radiotherapy used for palliative treatment; chemotherapy treats metastases.

Question 6

Problems of motor function

Answer 6

Swallowing consists of an oropharyngeal phase and an esophageal phase.
Motor problems may cause dysphagia or odynophagia.
Causes include peripheral neuropathy (diabetes, alcohol), neurologic disease (stroke, ALS), or systemic disease (systemic sclerosis, amyloidosis, hypothyroidism).

Question 7

Non cardiac chest pain and esophageal spasm

Answer 7

Disorganized, spontaneous contraction of the esophagus.
Can cause pain that mimics an acute MI or angina.
Often due to reflux disease.

Question 8

Achalasia

Answer 8

The LES loses its ability to relax as a bolus of food travels down esophagus.
Eventually, peristalsis about he LES is lost (aperistalsis) and the esophagus bags out (bird beak esophagus) and is filled with food and liquid.
Gravity and hydrostatic pressure allow the esophageal contents to slowly drain into the stomach.
Cause is not known; however, there is a clear loss of nerve body cells in the myenteric plexus of the esophagus.
Bad breath.
Latin America, infection with Trypanosome cruzii is common and causes Chagas disease; loss of the ganglion cells in the myenteric plexus is one complication of this parasitic infection.
Treatment: drugs (nitrates, calcium channel blockers, botox that lasts 6 months to a year), pneumatic dilation (balloon), myotome (cut piece of LES muscle away, definitive therapy).

Question 9

The stomach and duodenum

Answer 9

J shaped stomach can hold 1.5 liters at one time.
Serves as a place for mechanical mixing and controls the rate of presentation of nutrients to the small bowel; rapid entry would cause diarrhea and loos of nutrition.
Stomach contains parietal cells that produce HCL and chief cells that make pepsinogen.

Question 10

Peptic Ulcer Disease

Answer 10

A break of the mucosa of the stomach or duodenum.
Low mortality.
Ulcers are common.
Causes: Smoking, use of aspirin and other NSAIDS.
Gastric ulcers seem to arise out of mucosa with non-erosive (chronic) gastritis, stress.
Blood group ): higher risk of developing duodenal ulcers.
HCl is a necessary component for developing duodenal ulcers and associated with most gastric ulcers. Treatment was H2 blockers and proton pump inhibitors or surgery.
Complications of PUD: bleeding is the most common, perforation into peritoneal cavity or into the pancreas.
Infection with helicobacter pylori is strongly associated with gastric and duodenal ulcers as well as chronic active gastritis, gastric adenocarcinoma, and gastric MALToma (mucosa associated lymphoid tissue)-lymphoma.
Has anchors and injects its DNA into the stomach lining cells.
Gram negative rod, flagellated, microaerophilic, urease producing cloud of acid neutralizing ammonia, lives under the mucus layer produced by the stomach lining.
Diagnosis of H. pylori: urea breath test, stool antigen, histopathology (biopsy by EGD), urea testing (biopsy by EGD), serology.
Treatment of H. pylori: oral antibiotics (amoxicillin or clatrithromycin and metronidazole OR tetracycline plus metronidazole plus bismuth) for 10-14 days-antibiotic resistance, proton pump inhibitors twice daily that promote ulcer healing and almost completely eliminates the chance for recurrent duodenal ulcer.
Treatment of ulcers: acid suppression for 8 weeks BID, get rid of offending agents (H. pylori, NSAIDS, smoking), ulcer surgery; billroth 1 and 2, vagotomy

Question 11

Dyspepsia

Answer 11

“Bad digestion”
Upper abdominal pain not associated with colon function; changes with eating, NOT POOPING.
Peptic Ulcer Disease symptoms: pain, bleeding (hematemesis, melena (black), hematochezia (red)), the last two are blood in stool), perforation, pancreatitis, gastric outlet obstruction.
Goes into mucosa=erosion
Submucosa=ulcer
Deeper=perforating ulcer
Protection of stomach depends on prostaglandins, NSAIDS block prostaglandins.

Question 12

Gastriis

Answer 12

1. Erosive (acute)
   Erosions, hemorrhages, ulcers may be present; NSAIDs currently most common cause; stress from trauma, critical illness, incapacitation also causative.
   Presents with vague abdominal pain, severe hemorrhage, chronic insidious bleeding leading to iron deficiency anemia.
   Treatment: remove inciting agent, acid suppression medications like histamine 2 receptor antagonists or proton pump inhibitors.
2. Non erosive (chronic)
   Under the microscope, ranges from mild chronic inflammation to severe atrophy.
   Autoimmune gastris is diffuse inflammation in the body and fungus of the stomach.
   It is associated with pernicious (B12) anemia and severe achlorhydria (no HCL in gastric secretions).
   Can lead to intestinal metaplasia, a precursor for gastric cancer.

Question 13

Adenocarcinoma

Answer 13

Less common in US, 4th most common malignancy in the world.
Still a problem in Japan and other parts of the world, 6 times greater incidence than in US; was most common cancer in men here.
Screen in Japan
Risk factors: H. pylori infection, diets high in meat and smoked foods, nitroamines, increased age, chronic atrophic gastritis, low SES, smoking.
Does not typically have symptoms early on, eventually will have weight loss, nausea, and abdominal pain.

Question 14

Malignant Lymphoma and MALToma

Answer 14

This tumor mimics gastric adenocarcinoma; the stomach is the most common extra-nodal non-Hodgkin lymphoma.
MALToma; a lymphoma of the stomach that is associated with H. pylori infection. For early tumors, eradicating HP can cure the MALToma.

Question 15

The Pancreas

Answer 15

Solid organ
Runs horizontally across the mid abdomen and is surrounded by the C shared sweep of the duodenum.
Deep in the retroperitoneum.
The pancreatic duct runs from the tail (near spleen) through the body and into the head of the pancreas where it drains into the second portion of the duodenum.
The common bile duct runs through the head of the pancreas to join the pancreatic duct.
Exocrine pancreas contains acing cells which produce digestive enzymes and bicarbonate.
Endocrine pancreas refers to islet cells which produce hormones including insulin and glucagon.

Question 16

Acute pancreatitis

Answer 16

Occurs when the acing cells of the exocrine pancreas become inflamed.
Spectrum ranges from mild, almost imperceptible symptoms to sever hemorrhage in pancreas and large scale necrosis of acinar cells.
Causes: obstructive (Gallstones mostly, can be tumors, worms, choledochcocoele, pancreas divisum), toxins/drugs-alcohol (mostly this and gallstones), DDI, sulfa, flagyl, azathioprine, aminosalicylates, pentamidine, trauma, viruses
What is happening?
Digestive enzymes formed in pancreas are sore in inactive form called zymogen granules.
Injury to pancreas causes these to become activated within cells of pancreas.
Trypsin is an early enzyme activated and in turn activates others.
Autodigestion, inflammation, and cell necrosis ensues.
Microscopically, you see necrosis of acinar and fat cells, as well as severe inflammation.
See increased WBC, serum lipase and serum amylase, but the amount of elevation does not equal severity.
Horrific pain, tenderness, pain above belly button, below chest and goes to the back, tachycardia, nausea and vomiting, fever.
Might develop a pseudocyst; fluid filled collection of enzyme and liquid with no lining cells.

Question 17

Alcohol and the pancreas

Answer 17

May stimulate increased secretions from the pancreas while causing the sphincter of Oddi (valve at head of duct) to spasm at the same time.

Question 18

Gallstones and the pancreas

Answer 18

As stones pass through the common bile duct, they cause a temporary obstruction of the pancreatic duct.
Upon exploration, the stone is gone.
Removing stone filled gallbladder greatly reduces recurrence of pancreatitis in these cases.

Question 19

Complications of acute pancreatitis

Answer 19

Inflammation causes fluid to collect in and around (phlegmon).
Pseudocyst; can put physical pressure on stomach or duodenum and cause obstructive symptoms.
May become infected.
Pancreatic necrosis worrisome because spot for potential infection, pancreatic abscess.
Systemic complications include hypocalcemia, pleural effusion, ARDS.
Care: nutrition, IV fluids, pain meds
No proven benefits: antibiotics, reduce pancreatic secretions.

Question 20

Chronic pancreatitis

Answer 20

Chronic inflammation in the pancreas that eventually leads scar tissue and fibrosis, loss of functional pancreatic cells, and deformities of the ducts.
The process can smolder on unnoticed by the patient.
Causes: alcohol (leading cause), cystic fibrosis, inheritance, idiopathic, hypertriglyceridemia.
Long term problems: pancreatic insufficiency;
exocrine insufficiency causes fat malabsorption induced diarrhea (steatorrhea) and secondary weight loss, vitamin deficiencies.
Endocrine insufficiency causes diabetes when

Question 21

Adenocarcinoma of the pancreas

Answer 21

Quiet killer
On the rise worldwide
In US, fourth leading cancer in men and fifth in women.
Later in life
Imaging tests insensitive, so incurable at time of discovery.
Smoking= higher incidence, also alcohol, chronic pancreatitis, high fat diet, certain chemicals.
Mostly found in head of pancreas.
Presents as painless jaundice for advanced stages.
More commonly presents as vague constant mid-epigastric pain with possible radiation to the back (ductal obstruction/perineural invasion)
Tumor also associated with depression, recurrent episodes of thrombophlebitis.
Often causes obstructive jaundice, severe abdominal pain from neural involvement, weight loss is seen and metastases to liver, lung and peritoneum.
CT guided needle biopsy for diagnosis.
Treatment: surgery- curative (whipple, pylorus sparing whipple), biliary bypass, chemo, radiation, celiac plexus nerve block.
Palliation: pain relief (narcotic, celiac ganglion block), biliary obstruction (surgical bypass vs endoscopic or percutaneous stenting), duodenal obstruction (bypass or stent), chemo/radiation.