wire that measures of pressures in the esophagus and LES. Evaluation of peristalsis
imaging tests for esophagus
CT and endoscopic ultrasound. defining esophageal wall thickening, submucosal lesions, extent of malignancy
Achalasia (general definition)
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.
primary achalasia pathphysio
loss of intrinsic inhibitory innervation of lower esophageal sphincter and smooth muscle segment of the esophageal body. Myenteric ganglia usually absent. Most common.
secondary achalasia pathogenesis
Chagas caused by Trypanosoma cruzi, which causes destruction of myenteric plexus
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.
Possible complication of achalasia
esophageal squamous cell carcinoma
bitter taste in mouth, heartburn related to food, posture, anxiety.
Low LES pressure*, Increased gastric refluxate, Transient LES Relaxation (TLESR)
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”.
Plummer-Vinson syndrome (cervical webs)
mucosa and submucosa involved. iron deficiency anemia involved. Often in Swedish women.
squamous cell carcinoma of esophagus
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
sx of esophageal carcinoma
dysphagia, odynophagia, weight loss, fatigue, anorexia. Age >50
stages of squamous cell carcinoma of esophagus
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.
Adenocarcinoma in esophagus
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.
complications of barrett esophagus
ulceration and stricture. adenocarcinoma
all endoscopic views are ____ above GE junction
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.
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.
oral cancer dominant sites and causes/risk factors
vermilion border of lateral margins of lower lip, floor of mouth, & lateral borders of tongue. HPV 16 + 18, leukoplakia/erythroplakia, tobacco abuse, alcohol abuse
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
Pleomorphic adenoma major histo feature
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.
most malignant tumor of salivary glands
mucoepidermoid carcinoma. malignant mixed. malignancy less in parotid gland, more in submandibular.
malignant mixed salivary gland tumor
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
delayed gastric emptying - gastroparesis
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
Major risk factors for peptic ulcer
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).
Peptic ulcers can also be caused by
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.
Peptic ulcer sx
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
In older pts w/ sudden onset of ulcer (H pylori associated), needs to check for
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
In chronic, open peptic ulcer, 4 zones can be distinguished
Superficial to deep: Necrotic zone, inflammatory zone, granulation tissue, fibrosis.
complication of gastritis
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
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)
Chronic antral gastritis (type B)
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
hyperplastic gastric polyps
most common gastric polyp. Mucosal overgrowth secondary to chronic inflammation. Dilated and cystic gastric pits, lined by bland mucous cells
adenomatous gastric polyps
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
gastric [adeno]carcinoma risk factors
H pylori, smoking, genetics (HER2 NEU), chronic atrophic gastritis, nitrosamines.
exophytic growth of gastric adenocarcinoma
fungating, polypoid. protrusion of tumor mass into lumen; flat or depressed, in which there is no obvious tumor mass within the mucosa
types of gastric adenocarcinoma
exophytic, superficial spreading (limited to mucosa and submucosa), and excavating (most common)
intestinal type adenocarcinoma
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
histo features of diffuse varient gastric adenocarcinoma
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
diffuse variant type gastric carcinoma
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
Zollinger Ellison (gastrinoma)
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)
most common site for gut carcinoid tumors
appendix. rectal and appendiceal carcinoids almost never metastasizes. solid, yellow-tan appearance on transection. Tumors are exceedingly firm cuz of desmoplasia
GI stromal tumors
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")
chronic gastritis sx.
heartburn, epigastric pain, nausea, vomiting, hematemesis (coffee grounds appearance of vomit), melana. Or no sx
H pylori staining
Steiner silver stain
Stomach acid releases...
Vit B12. Achlorhydria pts will also show pernacious anemia.
signs of VitB12 anemia/aplastic anemia
chronic gastritis features
lymphocytic infiltration, plasma cells. development of peptic ulcer and gastric carcinoma
causes of acute gastritis
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
acute gastritis can present as
hematemesis, melena, epigastric pain, nausea, vomiting, and potentially fatal blood loss. Major causes of hematemesis, particularly in alcoholics.
acute gastric ulceration signs/sx
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
acute gastric ulcerations are found...
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.
Familial polyposis syndromes
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