Path and CS GI

wire that measures of pressures in the esophagus and LES. Evaluation of peristalsis

CT and endoscopic ultrasound. defining esophageal wall thickening, submucosal lesions, extent of malignancy

Lower esophageal sphincter (LES) pressure is elevated (incr resting tone), esophageal aperistalsis. incomplete relaxation of lower esophageal sphincter in response to swallowing --> functional obstruction of esophagus.

loss of intrinsic inhibitory innervation of lower esophageal sphincter and smooth muscle segment of the esophageal body. Myenteric ganglia usually absent. Most common.

• Chagas caused by Trypanosoma cruzi, which causes destruction of myenteric plexus
• Esophageal cancer
• Scleroderma may manifest with hypomotility esophageal wall becomes fibrotic. Minimal LES tone

Most commonly occur in 3rd to 5th decade. dysphagia, nocturnal regurg, may manifest in young adults, chest fullness. progressive dilation of esophagus above lower esophageal sphincter. Bird's beak deformity on esophagram.

esophageal squamous cell carcinoma

bitter taste in mouth, heartburn related to food, posture, anxiety.

Low LES pressure*, Increased gastric refluxate, Transient LES Relaxation (TLESR)

Hiatal hernia, Widened crural diaphragm and proximally displaced gastroesophageal junction, smoking, mint, chocolate, coffee, alcohol, carbonated drinks, tomato juice, citrus juices

avoid eating w/in 3 hrs of bedtime, sleep on left side, lose weight, Elevate head of your bed 4-6 inches by placing bricks under headboard

Hemorrhage, Peptic strictures, *Barrett’s esophagus, Precursor to esophageal adenocarcinoma

Hypopharyngeal. incomplete or uncoordinated UES relaxation.

halitosis (bad breath), regurgitation of undigested material, dysphagia

outpouching of mucosa, submucosa, muscular layers

traction from lymph nodes due to TB, cancer

• only mucosa and submucosa herniate. Outer longitudinal muscle fibers form teniae.
• Increased elastin in teniae. NO hypertrophy or hyperplasia. Change in collagen

thickening of the circular muscle layer, shortening of teniae, luminal narrowing

• Stage I -- Pericolic abscess or phlegmon
• Stage II -- Pelvic, intra-abdominal, or retroperitoneal abscess
• Stage III -- Generalized purulent peritonitis
• Stage IV -- Generalized fecal peritonitis

(transmural): spontaneous rupture of esophagus, usually associated w/ incr in intraluminal pressures and rupture of esophageal wall. Pt presents w// crepitus (crackling sound) in neck, alcoholics

nontransmural): Frequent cause of upper GI bleeding, assoc w/ retching (longitudinal tear at GE junction) and abrupt changes in pressures. Bleeding after vomiting, hematemesis.

hiatal hernia, chronic alcoholic w/ severe vomiting, coughing

Infection, inflammatory ulcer, mediastinitis

Usually related to reflux. CNS depressants, NSAIDs, radiation, tetracyclines, alcohol or tobacco exposure may be some of the contributing causes. More common in Iran and China.

eosinophils w/ or w/o neutrophils in epithelial layer. basal zone hyperplasia and elongation of lamina propria papillae. Intraepithelial neutrophilic infiltration indicates severe injury

Candida (tan yellow plaques in lower esophagus, mucosal hyperemia), CMV, herpes

• benign or malignant.
• Peptic induced (erosive esophagitis, esophageal ulcers) most common.
• Can also be due to caustic injury (after alkaline or strong acid ingestion in suicidal attempts)

Mucosa and submucosa. seen in distal esophagus, intermittent dysphagia to solids. “steakhouse syndrome”.

mucosa and submucosa involved. iron deficiency anemia involved. Often in Swedish women.

90% of esophageal cancers (except in US). smoking and alcohol excesses risk factors, also risk factors include nitrosamine containing food products, hx of achalasia. More frequent in China and Africa. Common in middle 1/3 esophagus

dysphagia, odynophagia, weight loss, fatigue, anorexia. Age >50

• polypoid exophytic masses that protrude into lumen
• necrotizing cancerous ulcerations that extend deeply and sometimes erode into resp tree, aorta, or elsewhere
• diffuse infiltrative neoplasms that cause thickening and rigidity of the wall and narrowing of the lumen.

more common in whites, M>F, assoc w/ Barrette's esophagus, distal 1/3 esophagus, large nodular masses or show deeply ulcerative or diffusely infiltrative features

replacement of normal distal stratified squamous mucosa by columnar epithelium containing goblet cells. Complication of long-standing gastroesophageal reflux. M>F, whites > blacks.

ulceration and stricture. adenocarcinoma

3cm. Polypoid lesions after 5 yrs would be detected at this level.

• Severe recurrent aphthous ulcers (canker sores).
• Tends to be familial in the Middle East. Strep may be involved

HSV1 cold sores. intranuclear acidophilic viral inclusions.Form giant cells known as multinucleated polykaryons. Tzanck test.

• (thrush, moniliasis) is most common, particularly among persons w/ diabetes mellitus, anemia, antibiotic or glucocorticoid therapy, immunodeficiency, or debilitating illnesses such as disseminated cancer.
• Pseudohyphae seen

• whitish, well-defined mucosal patch or plaque caused by epidermal thickening or hyperkeratosis. strong link to tobacco, alcohol, HPV.
• Can transform to squamous cell carcinoma esp if lesion is red.

vermilion border of lateral margins of lower lip, floor of mouth, & lateral borders of tongue. HPV 16 + 18, leukoplakia/erythroplakia, tobacco abuse, alcohol abuse

paramyxovirus (- strand ssRNA), parotid gland inflammation, orchitis, pancreatitis

usually by Staph aureus or strep viridans

ductal obstruction via stone

dominant cause is autoimmune (bilateral). Seen in Sjögren syndrome. Linked to other connective tissue dz: rheumatoid arthritis, SLE, scleroderma

usually in superficial parotid glands, well demarcated, encapsulated, most common benign, saliva contains epidermal growth factors, painless swelling, 6/7th decade

Heterogeneity: tumor cells form ducts, acini, tubules, strands, or sheets of cells

papillary cystadenoma lymphomatosum. parotid glands, less common benign, swelling at angle of jaw.

• mucoepidermoid carcinoma. malignant mixed. malignancy less in parotid gland, more in submandibular.

When primary or recurrent benign tumors are present for many (10-20) years and malignancy transformation occurs. Assoc w/ mucoepidermoid carcinoma

separation of diaphragmatic crura & widening of space btwn muscular crura & esophageal wall permits a dilated segment of stomach to protrude above diaphragm. Incr incidence w/ age

• 95% of hiatal hernias. Heartburn, regurg. those w/ severe reflux esophagitis are likely to have a sliding hiatal hernia. Other complications include mucosal ulceration, bleeding, and even perforation.
• Many go on to develop Barrett esophagus

Caused by portal hypertension (most often secondary to cirrhosis) May cause massive bleeding into lumen or hematemesis

epigastric pain relieved by food or antacids, periodic or nocturnal pain, pain before meals or when hungry

nausea or vomiting, bloating and distention, anorexia or weight loss, pain aggravated by food or after meals

common in longstanding type I diabetes. Nausea, vomiting, early satiety. Cause is autonomic neuropathy causing delayed emptying of gastric contents

early satiety nausea & vomiting, sweats, syncope, diarrhea and flushing. Rapid emptying causes distension and release of gut hormones (serotonin) which contributes to symptoms

1st part of duodenum or stomach lesser curvature. NOT precursor for malignancy. Recurs, most in middle aged to older pts. M>F. Punched-out mucosal defect, penetrates gastric or intestinal wall deeper than muscularis mucosa. Small lesions, margins not elevated

smoking, corticosteroids, NSAIDs

Epigastric pain 1-3 hours after eating, pain relief with food. more frequent in persons with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism (hypercalcemia).

Excess production of gastrin from a (pancreatic) tumor in individuals w/ Zollinger-Ellison syndrome --> HCl secretion -- > multiple peptic ulcerations in stomach, duodenum, and even jejunum.

Epigastric burning pain tends to be worse at night & occurs usually 1 to 3 hours after meals during day. Nausea, vomiting, bloating, belching, and significant weight loss. Bleeding is chief complication.

Obstruction from edema or fibrotic scarring

may be aggravated by food

Mucosal defect not deeper than the muscularis mucosa

lymphoma or adenocarcinoma

assoc w/ peptic ulcer. H pylori tends to attack antrum of stomach & induce prox duodenal ulcers. Epithelial injury is by vacuolating toxin called VacA, regulated by cytotoxin-associ gene A (CagA). Secretes urease & phospholipases that breaks down urea to form toxic compounds such as ammonium chlorid

Superficial to deep: Necrotic zone, inflammatory zone, granulation tissue, fibrosis.

• Gastric metaplasia of the duodenum occurs in response to protect epithelium by making mucus --> Colonization
• of metaplastic epithelium by H. pylori, which then makes the epithelium susceptible to ulceration

• Hemorrhagic, erosive, stress gastritis, Epigastric pain, nausea, vomiting, bleeding
• Mucosal edema and congestion. May see hemorrhage, neutrophils.
• Etiology: toxins, drugs, alcohol, spices, systemic dz, opportunistic infections.

Uncommon. Abs against acid-producing parietal cells, and intrinsic factor (IF) leading to mucosal atrophy (chronic atrophic gastritis) loss of acid production (hypochorhydria). Pernacious anemia. Associated w/ other autoimmune disorders. Lymphocytes, plasma cells, intestinal metaplasia (incr likelihood of gastric carcinoma)

More common. Due to H. pylori. Most severe in antrum. infiltrate of lymphocytes, plasma cells and neutrophils with eventual intestinal metaplasia. Linked with gastric adenocarcinoma and MALT lymphoma. End result of both types A and B is chronic atrophic gastritis

most common gastric polyp. Mucosal overgrowth secondary to chronic inflammation. Dilated and cystic gastric pits, lined by bland mucous cells

Precursers to gastric carcinomas. Found in older patients with chronic gastritis and intestinal metaplasia

higher incidence in Japan, most common malignancy in stomach, dysphagia, Linitus plastica- diffusely infiltrative (rigid thickened stomach wall- “leather bottle”) - advanced beyond submucosa, poor outcome. mostly involves pylorus, antrum, and lesser curvature of stomach

H pylori, smoking, genetics (HER2 NEU), chronic atrophic gastritis, nitrosamines.

fungating, polypoid. protrusion of tumor mass into lumen; flat or depressed, in which there is no obvious tumor mass within the mucosa

exophytic, superficial spreading (limited to mucosa and submucosa), and excavating (most common)

gastric mucous cells that have undergone intestinal metaplasia in setting of chronic gastritis (H pylori). M>F. incr risk w/ blood group A for chronic gastritis w/ intestinal metaplasia (H pylori)

earliest lymph node spread (of gastric carcinoma) that goes to supraclavicular lymph node

gastric carcinoma that spreads intraperitoneal to ovaries in females

• gastric-type mucous cells that generally do not form glands but rather permeate mucosa & wall as scattered individual "signet-ring" cells or small clusters in an "infiltrative" growth pattern
• cells are filled with mucin vacuoles that push the nucleus to one side

arise de novo from native gastric mucous cells, mutations in E-cadherin, not assoc w/ chronic gastritis or H pylori infection, and poorly differentiated. Early age w/ female predominance.

most assoc w/ H pylori (setting chronic gastritis), B cell origin, t(11,18) translocation is common, Celiac dz is associated w/ higher risk of intestinal T-cell lymphomas

tumor in pancreas, sometimes stomach and duodenum. Releases excessive gastrin. Diarrhea due to large volume of gastric acid and malabsorbtion secondary to inactivation of pancreatic enzymes by low pH.

Derived from enterochromaffin-like cells of fundus/body or gastrin-producing cells of antrum. potentially malignant. Elevated levels of 5-HT, hepatic dysfxn. Show markers for chromogranin A, synaptophysin, and neuron-specific enolase

excessive gastrin release similar to ZE syndrome, Cushing syndrome, hyperinsulin (hypoglycemia)

appendix. rectal and appendiceal carcinoids almost never metastasizes. solid, yellow-tan appearance on transection. Tumors are exceedingly firm cuz of desmoplasia

• derived from interstitial cells of Cajal (pacemaker cells) w/in muscle layers. Contain KIT antigen. smooth
• muscle tumors, either benign leiomyomas or malignant leiomyosarcomas

congenital. a nidus of gastric mucosa in the esophagus or small intestine ("ectopic rest")

heartburn, epigastric pain, nausea, vomiting, hematemesis (coffee grounds appearance of vomit), melana. Or no sx

Steiner silver stain

Vit B12. Achlorhydria pts will also show pernacious anemia.

lymphocytic infiltration, plasma cells. development of peptic ulcer and gastric carcinoma

• heavy use of NSAIDs, particularly aspirin. Excessive alcohol, Heavy smoking, chemotherapeutic drugs,
• Uremia, Systemic infections, Severe stress , Ischemia and shock, Suicide attempts with acids and alkali, mechanical trauma, Reflux of bilious material after distal gastrectomy

hematemesis, melena, epigastric pain, nausea, vomiting, and potentially fatal blood loss. Major causes of hematemesis, particularly in alcoholics.

Severe trauma, sepsis, shock, or grave illness of any type, Chronic exposure to NSAIDs & corticosteroids, Extensive burns (Curling ulcers) , CNS injuries or intracerebral hemorrhage (called Cushing ulcers) can all be causes

anywhere in stomach, multiple lesions, small and circular. Doesn’t affect adjacent mucosa

rare, May occur at ampulla causing obstructive jaundice or bleeding, Pts with familial adenomatous polyposis (FAP) at increased risk

rare, incr incidence in celiac dz, May also *present with obstructive jaundice or bleeding

multiple Hamartomatous Polyps in GI tract, non dysplastic. uncommon, usually in cecum.

autosomal dominant. FAP accounts for most (APC gene, tubular adenomas, risk of colonic cancer is virtually 100% by midlife). Peutz-Jeghers polyps and Cowden syndrome both involve hamartomatous polyps

• almost exclusively non-Hodgkin lymphoma, 7th decade, Ab pain, wt loss, and small bowel obstruction.
• Increased incidence in celiac sprue.

focal nodular hyperplasia. F>M. Not linked to oral contraceptives