Cyberfriends: The help you're looking for is probably here.
Welcome to Ed's Pathology Notes, placed here originally for the convenience of medical students at my school. You need to check the accuracy of any information, from any source, against other credible sources. I cannot diagnose or treat over the web, I cannot comment on the health care you have already received, and these notes cannot substitute for your own doctor's care. I am good at helping people find resources and answers. If you need me, send me an E-mail at scalpel_blade@yahoo.com Your confidentiality is completely respected.
DoctorGeorge.com is a larger, full-time service.
There is also a fee site at
www.afraidtoask.com.
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With one of four large boxes of "Pathguy" replies. |
I'm still doing my best to answer
everybody.
Sometimes I get backlogged,
sometimes my E-mail crashes, and sometimes my
literature search software crashes. If you've not heard
from me in a week, post me again. I send my most
challenging questions to the medical student pathology
interest group, minus the name, but with your E-mail
where you can receive a reply.
Numbers in {curly braces} are from the magnificent Slice of Life videodisk. No medical student should be without access to this wonderful resource. Someday you may be able to access these pictures directly from this page.
Also:
KCUMB Pathology Club
Freely have you received, freely give. -- Matthew 10:8. My
site receives an enormous amount of traffic, and I'm
handling about 200 requests for information weekly, all
as a public service.
Pathology's modern founder,
Rudolf
Virchow M.D., left a legacy
of realism and social conscience for the discipline. I am
a mainstream Christian, a man of science, and a proponent of
common sense and common kindness. I am an outspoken enemy
of all the make-believe and bunk that interfere with
peoples' health, reasonable freedom, and happiness. I
talk and write straight, and without apology.
Throughout these notes, I am speaking only
for myself, and not for any employer, organization,
or associate.
Special thanks to my friend and colleague,
Charles Wheeler M.D.,
pathologist and former Kansas City mayor. Thanks also
to the real Patch
Adams M.D., who wrote me encouragement when we were both
beginning our unusual medical careers.
If you're a private individual who's
enjoyed this site, and want to say, "Thank you, Ed!", then
what I'd like best is a contribution to the Episcopalian home for
abandoned, neglected, and abused kids in Nevada:
My home page
Especially if you're looking for
information on a disease with a name
that you know, here are a couple of
great places for you to go right now
and use Medline, which will
allow you to find every relevant
current scientific publication.
You owe it to yourself to learn to
use this invaluable internet resource.
Not only will you find some information
immediately, but you'll have references
to journal articles that you can obtain
by interlibrary loan, plus the names of
the world's foremost experts and their
institutions.
Alternative (complementary) medicine has made real progress since my
generally-unfavorable 1983 review linked below. If you are
interested in complementary medicine, then I would urge you
to visit my new
Alternative Medicine page.
If you are looking for something on complementary
medicine, please go first to
the American
Association of Naturopathic Physicians.
And for your enjoyment... here are some of my old pathology
exams
for medical school undergraduates.
I cannot examine every claim that my correspondents
share with me. Sometimes the independent thinkers
prove to be correct, and paradigms shift as a result.
You also know that extraordinary claims require
extraordinary evidence. When a discovery proves to
square with the observable world, scientists make
reputations by confirming it, and corporations
are soon making profits from it. When a
decades-old claim by a "persecuted genius"
finds no acceptance from mainstream science,
it probably failed some basic experimental tests designed
to eliminate self-deception. If you ask me about
something like this, I will simply invite you to
do some tests yourself, perhaps as a high-school
science project. Who knows? Perhaps
it'll be you who makes the next great discovery!
Our world is full of people who have found peace, fulfillment, and friendship
by suspending their own reasoning and
simply accepting a single authority that seems wise and good.
I've learned that they leave the movements when, and only when, they
discover they have been maliciously deceived.
In the meantime, nothing that I can say or do will
convince such people that I am a decent human being. I no longer
answer my crank mail.
This site is my hobby, and I do not accept donations, though I appreciate those who have offered to help.
This page was last updated February 9, 2008.
During the thirteen years my site has been online, it's proved to be
one of the most popular of all internet sites for undergraduate
physician and allied-health education. It is so well-known
that I'm not worried about borrowers.
I never refuse requests from colleagues for permission to
adapt or duplicate it for their own courses... and many do.
So, fellow-teachers,
help yourselves. Don't sell it for a profit, don't use it for a bad purpose,
and at some time in your course, mention me as author and KCUMB as my institution. Drop me a note about
your successes. And special
thanks to everyone who's helped and encouraged me, and especially the
people at KCUMB
for making it possible, and my teaching assistants over the years.
Whatever you're looking for on the web, I hope you find it,
here or elsewhere. Health and friendship!
We have two ends with a common link;
--Author unknown
QUIZBANK GI tract (all)
I am presently adding clickable links to
images in these notes. Let me know about good online
sources in addition to these:
MedEdPORTAL -- American Association of Medical Colleges. Primarily for medical school faculty.
Pathology Education Instructional Resource -- U. of Alabama; includes a digital library
Pathopic -- Swiss site; great resource for the truly hard-core
Syracuse -- pathology cases
Alabama's Interactive Pathology Lab
"Companion to Big Robbins" -- very little here yet
Alberta
Pathology Images --hard-core!
Alberta Tumor Photos -- and lots more. Highly recommended.
Bristol Biomedical
Image Archive
EMBBS Clinical
Photo Library
Chilean Image Bank -- General Pathology -- en Español
Chilean Image Bank -- Systemic Pathology -- en Español
Connecticut
Virtual Pathology Museum
Australian
Interactive Pathology Museum
Semmelweis U.,
Budapest -- enormous pathology photo collection
Iowa Skin
Pathology
Loyola
Dermatology
History of Medicine -- National Library of Medicine
KU
Pathology Home
Page -- friends of mine
The Medical Algorithms Project -- not so much pathology, but worth a visit
National Museum of Health & Medicine -- Armed Forces Institute of Pathology
Telmeds -- brilliant site by the medical students of Panama (Spanish language)
U of
Iowa Dermatology Images
U Wash
Cytogenetics Image Gallery
Urbana
Atlas of Pathology -- great site
Visible
Human Project at NLM
Karolinska Institutet -- pathology links
Johns Hopkins CPC's
U. of Virginia Case Studies
Oklahoma Teaching Cases
Indiana U. Teaching Cases
SUNY Histopathology
West Virginia Case of the Month
Upstate NY Cases -- works only on some browsers
Society for Ultrastructural Pathologi -- electron microscope cases
WebPath:
Internet Pathology
Laboratory -- great siteEd Lulo's Pathology Gallery
Bryan Lee's Pathology Museum
Dino Laporte: Pathology Museum
Tom Demark: Pathology Museum
Dan Hammoudi's Site
Claude Roofian's Site
![]()
Medmark Pathology -- massive listing of pathology sites
Pathology Handout -- Korean student-generated site; I am pleased to permit their use of my cartoons
Estimating the Time of Death -- computer program right on a webpage
Pathology Field Guide -- recognizing anatomic lesions, no pictures
St.
Jude's Ranch for Children
I've spent time there and they are good. Write "Thanks
Ed" on your check.
PO Box 60100
Boulder City, NV 89006--0100
More of my notes
My medical students
Clinical
Queries -- PubMed from the National Institutes of Health.
Take your questions here first.
HealthWorld
Yahoo! Medline lists other sites that may work well for you
We comply with the
HONcode standard for trustworthy health
information:
verify
here.
With one we sit, with one we think.
Success depends on which we use;
Heads we win, tails we lose!
Gastrointestinal Images
University of Washington
Pictures and comments
Gastrointestinal
Utah cases for path students
Juliana Szakacs MD
Gastrointestinal System I
Great pathology images
Indiana Med School
Gastrointestinal System II
Great pathology images
Indiana Med School
Gastrointestinal Pathology
Virginia Commonwealth U.
Great pictures
Tulane Pathology Course
Great for this unit
Exact links are always changing
Gastrointestinal Diseases
Mark W. Braun, M.D.
Photomicrographs
GI Tract Ia
Introductory Pathology Course
University of Texas, Houston
GI Tract Ib
Introductory Pathology Course
University of Texas, Houston
GI Tract II
Introductory Pathology Course
University of Texas, Houston
KCUMB students: Questions for this system
Esophagus and Stomach GI Tract 1-187
Small Bowel GI Tract 188-256
Large Bowel GI Tract 257-280, 322-332
Colon Cancer GI Tract 281-321
Hepatobiliary I Liver 1-86
Hepatobiliary II Liver 87-172
Pancreas Pancreas Do 'em all
Consider this mastery material.
Be sure you can use the following terms correctly, and tell how and where they apply to the gut.
achalasia
atresia
diverticulum
erosion
fistula
hematemesis
hematochezia
hernia
melena
polyp
pseudo-diverticulum
reflux
stenosis
tenesmus
ulcer
Be sure you can recognize each of the kinds of lesions presented on the videodisc!
INTRODUCTION
Disease of the gut troubles most people at some time during their lives, and claims the lives of many people.
This easy unit focuses on problems with the alimentary canal. Conceptually, the material presents no serious problems. Some of the "why"'s are only now being clarified, and several common problems have complex causes. The human gut withstands considerable abuse. For a review of how to injure the gastroduodenal mucosa, see J. Clin. Gastroent. 13(S1): S1, 1991.
A few terms for review now:
POLYP: Any bump on the gut that sticks up above the inner surface into the lumen.
HERNIA: Presence of a portion of an organ in a body space where it doesn't belong. INCARCERATED HERNIA: One that can't be REDUCED, i.e., put back in its proper place. STRANGULATED HERNIA: Where venous drainage is compromised and infarction is imminent / present.
EROSION: A portion of the epithelium
of a mucosal surface has been lost due to necrosis, but there has been no loss of the
underlying connective tissue. In the stomach, as the term is generally
used, there may be loss of some
connective tissue but sparing the muscularis mucosae.
ULCER: A portion of the epithelium AND some of the
connective tissue has been lost due to necrosis. In the stomach, an "ulcer"
is typically diagnosed only if the muscularis mucosae is lost.
DIVERTICULUM: An outpouching of all the layers of the wall of a hollow organ.
PSEUDO-DIVERTICULUM:
Outpouching of mucosa through a defect in the muscularis propria.
PARACRINE / ENDOCRINE CELLS ("Kulchitsky cells", "enterochromaffin", "neurosecretory", "argentaffin /
argyrophil", formerly "APUD" cells) are found individually all along the gut, and various ones
produce various peptide hormones of known and unknown significance. (You met these in the lung
when we studied oat cell carcinoma and bronchial carcinoid.)
Strangulated umbilical hernia
EMBBS
In the GI tract in particular, "atypia" and "dysplasia" are probably interchangeable terms.
The common cancers of the GI tract are carcinomas. Often the first physical finding is Virchow's sentinel lymph node, where the thoracic duct joins the left internal jugular vein.
For the basics of the GI viruses, click here.
ESOPHAGUS
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The "gullet" begins at the cricophagyngeus (the short "upper esophageal sphincter" starts here) and ends at the diaphragmatic hiatus or thereabouts ("lower esophageal sphincter"). Solid food may hang up at either site, or where the esophagus passes behind the left main-stem bronchus or between enlarged hilar nodes. Neither sphincter is fool-proof (or even anatomic). Considerable coordination is required for a proper swallow (the big word for "swallowing" is "deglutition"). Most of the time, the esophagus performs its simple but important task well.
You remember that the upper esophagus (i.e., the first inch or so) has mostly skeletal muscle (and is thus subject to diseases of nerve and skeletal muscle), the middle esophagus (i.e., maybe another inch) has both skeletal and smooth muscle, and the distal esophagus (i.e., most of the esophagus) has mostly smooth muscle. Unlike most of the rest of the gut, the esophagus has no serosa to help limit the spread of rips or cancers.
Problems with the esophagus manifest as difficulty and/or pain on swallowing, and/or problems with regurgitation.
BIRTH DEFECTS of the esophagus are relatively common.
AGENESIS of some or all of the esophagus is uncommon. ATRESIA of the esophagus, as elsewhere, is failure of a normally-hollow organ to develop its lumen. An atretic esophagus is represented, over part or all of its length, by a fibromuscular cord without a lumen. Less severely, portions of the esophagus may be congenitally STENOTIC (i.e., too narrow).
{20073} esophageal atresia, from behind. Lungs at the sides, stomach at the bottom
TRACHEO-ESOPHAGEAL FISTULAS of several varieties are common neonatal surgical problems. The proximal esophagus may enter the trachea or bronchus, producing coughing upon feeding (* original movie of M*A*S*H). The proximal esophagus may end blindly and the distal esophagus arise from a large airway, preventing feeding and causing the stomach to fill with air (the most common version). Or there may simply be a window between the two organs.
THROAT PROBLEMS: A little bit higher than the real esophagus, but worth mentioning here:
GLOBUS HYSTERICUS ("globus syndrome", "globus pharyngeus"), a "lump in the throat", is spasm of the back of the throat and perhaps the upper esophagus. It creates the feeling of a mass in the hypopharynx. Sometimes the cause is organic (i.e., a reflex from something wrong nearby, perhaps reflux from the esophagus spilling into the larynx; or a thyorid nodule that was missed -- J. Laryngol. Otol. 121: 242, 2007); often it's psychosomatic. Psychiatrists attribute it to "swallowed tears", and the cure is to cry. (Despite its banal nature, the sensation of a mass may frighten a patient. "Spontaneous cures of non-biopsy-proven throat cancer" sound like globus.)
ZENKER'S "PULSION" DIVERTICULUM: Adjacent to the cricophagyngeus muscle. A hiding-place for last week's spaghetti and last month's pills (so THAT'S why they didn't work....) The smell alone may create a serious social problem.
* An EPIPHRENIC DIVERTICULUM, also of mysterious origin, occurs just above the diaphragm. It can harbor large amounts of fluid that are disgorged back to the mouth shortly after the patient goes to bed.
ACHALASIA means "failure of a sphincter to relax when it should". Usually, this means the lower esophageal sphincter.
In the U.S., the problem is usually idiopathic failure of the lower sphincter to relax. The etiology is just now becoming clarified; the cause is usually inflammation of the myenteric plexus (Am. J. Surg. Path. 24: 1153, 2000; Histopathology 35: 445, 1999; Gastroenterology 111: 648, 1996), with eventual nerve damage, but nobody knows why this happens. In other cases, the ganglion cells are simply lost instead; no one knows why.
The esophagus remains filled with food. The patient (typically a young adult) will notice regurgitation and bad breath. The situation may become really nasty as more and more food accumulates in a mega-esophagus. Fortunately, most patients are cured by a single endoscopic dilatation of the sphincter; there's also "botox", or laparoscopic myotomy and partial fundoplication for the hard cases (Am. J. Surg. 181: 471, 2001.)
Untreated, achalasia is a life-threatening problem (carcinoma, aspiration pneumonia).
* Pseudo-achalasia usually results from cancer obliterating the myenteric plexus (Am. J. Surg. Path. 26: 784, 2002).
You remember that Chagas' disease (T. cruzi) is an important cause of mega-esophagus worldwide.
GLYCOGEN PLAQUES are acanthotic (i.e., thick spiny layer) epithelium with extra glycogen. The most common lesion of the esophagus, and of no consequence. You'll see it frequently if you do endoscopies.
* Occasionally, endoscopists see a very dark-pigmented esophagus without any other pathology. This is esophageal melanocytosis (Arch. Path. Lab. Med. 130: 552, 2006); its significance remains unknown.
WEBS are contracted, localized fibrous scars that form little shelves ("ledges") that may obstruct the lumen.
* No one knows quite what to make of a supposed association between upper esophageal webs, iron deficiency anemia, and a risk for squamous cell carcinoma in the proximal esophagus. Whether or not this really exists, it's called "Plummer-Vinson syndrome". Current thinking is that somehow iron deficiency causes the webs to form just beyond the cricoid (Am. J. Gastro. 97: 190, 2002).
SCHATZKI'S RING is a washer-shaped partially-obstructing fibrous ring at the squamo-columnar junction just above the gastroesophageal junction. It is a radiologist's delight and may be seen in any adult; long a mystery, cases that occur in the absence of reflux may be due to pill enlodgement (Am. J. Surg. 158: 563, 1989). A-RING is the same, at the gastro-esophageal junction.
A big chunk of solid food (i.e., poorly-chewed beef) may hang up on a web or ring. In bad cases, softer food may have trouble negotiating the obstruction.
{09433} Schatzki ring
{09434} Schatzki ring
{09435} web
HIATUS HERNIA is said to be present whenever a portion of the stomach pooches up through the diaphragmatic hiatus. Said to be present in up to 10% of adults (typically the overweight), they are most often sub-clinical.
SLIDING HIATUS HERNIA (the usual kind) is present when a short (congenital, fibrous scarring from years of reflux, diaphragm pulled low by obesity) pulls the proximal stomach into the chest. As the esophagus contracts during swallowing, radiologists watch the stomach slide further up through the diaphragm. As with "reflux esophagitis", the distal esophagus is likely to become inflamed and damaged as a result of exposure to pepsin and acid.
PARA-ESOPHAGEAL ("ROLLING") HIATUS HERNIA (the less common kind) is present when a portion of the stomach rolls up through the diaphragm alongside an esophagus of normal length. This is typically a non-problem, but the herniated portion of stomach may become strangulated.
Future pathologists: Don't expect to see either type of hernia (or, for that matter, a Schatzki's ring, or an intestinal hernia) after death, when the muscles of the body relax / go into rigor mortis.
TRACTION DIVERTICULUM, illustrated without comment in "Big Robbins", probably result from scar
contraction in the mediastinum (i.e., TB
). They are uncommon.
* APHTHOUS ULCERS, the familiar painful white "canker sores" that most people have experienced on the oral mucosa, may be a serious problem in the esophagus for people with HIV infection. No one knows why. Thalidomide for this problem: J. Inf. Dis. 180: 61, 1999.
GASTROESOPHAGEAL REFLUX (GERD, formerly, "peptic esophagitis") is THE common esophagal problem, the result of an incompetent lower esophageal sphincter.
The sphincter is inflamed, scars, and becomes further damaged. The epithelium keeps getting digested and regrowing, with much more opportunity to select for mutated cells. Pathophysiology Am. J. Med. Sci. 326, 274, 2003.
Update for clinicians: JAMA 287: 1972 & 1982, 2002. The correlation between clinical symptoms and endoscopy is remarkably poor. Only about half of the patients with severe "GERD" on endoscopy even have heartburn (Dig. Dis. Sci. 48: 2237, 2003.)
* Like most other diseases of children, pediatric GERD has been blamed on cow's milk. Since the disease also occurs in children who do not drink cow's milk, it cannot be the sole cause. And since the only test is an elimination diet and response to challenge (still true Arch. Dis. Child. 92: 902, 2007), and since strongly-held emotionally-based beliefs are involved, getting at the truth will be difficult. A pop claim that eosinophils in the upper GI mucosa correctly identified the subset of cases caused by milk allergy failed a scientific study miserably (J. Clin. Path. 59: 89, 2006),
The cause of common "reflux" remains obscure. Mechanical problems (including overweight and
sliding hiatus hernia) must contribute, and the problem is more severe if there's "excess stomach acid
/ pepsin / bile" or the gastric contents stays for some reason within the esophagus. Other things that
irritate the esophagus (swallowing spicy food, alcohol (Gut 34: 727, 1993, others), very hot
beverages, and/or tobacco juice) will not help either. Pregnancy, benzodiazepines, intubation, and
tobacco use are all implicated as well. Lying flat makes matters worse (tip: try propping the head of
the bed up on cinder blocks).
The diagnosis of GERD is made clinically on endoscopy
(Dig. Dis. Sci. 45: 217, 2000),
but pathology may be obtained for confirmation.
Pathologists diagnose reflux based on the following criteria (older review: Gast. Clin. N.A. 19: 631,
1990; update Am. J. Surg. Path. 20(S1): S-31, 1996):
Future pathologists: Be sure you've got that specimen properly oriented, and consider asking the
clinician to send it up on cardboard;
Why the thickness of the basal cell layer? In reflux, the surface cells get digested and the basal cells
are multiplying overtime to replace them.
Peptic esophagitis ulcers
WebPath Photo
If replacement of the normal squamous epithelium by a columnar epithelium has occurred, you may have a BARRETT'S ESOPHAGUS. All about Barrett's: Gastroenterology 122: 1569, 2002; NEJM 346: 836, 2002; Med. Clin. N.A. 86: 1423, 2002.
Today's definitions of Barrett's usually require goblet cells, and for the truly hardcore, the non-goblet cells are both absorptive and secretory. Older definitions of Barrett's allowed any columnar epithelium type.
Ignore hamartomas of gastric-type mucosa; cancer probably only occurs if there is metaplasia with goblet cells, so perhaps one day Barrett's will be redefined as limited to this.
There are at least 2 million "Barrett's" patients in the U.S. In Sweden, 1.6% of the population is affected, with alcohol and tobacco being risk factors (Gastroent. 129: 1825, 2005).
As you'd expect ("Nowell's law triumphant"), finding a Barrett's esophagus means there's been some hits on the genome, and the genetically damaged cells have had a chance to overgrow the area because of repeated healing from reflux. This is a fertile breeding ground for adenocarcinoma of the esophagus.
The molecular biology of transformation to cancer is now fairly clear: Lancet 360: 1587, 2002.
* Anti-reflux therapy may be helpful, but don't count on it to reverse the process. This includes the new, popular procedure of laparoscopic fundoplication (Ann. Thor. Surg. 77: 393, 2004).
In today's cost-conscious era, it seems reasonable to screen adults who complain of heartburn once for Barrett's, with follow-up if and only if there is dysplasia (numbers Ann. Int. Med. 138: 176, 2003).
More on mutations in Barrett's: Arch. Surg. 132: 728, 1997. Deciding on therapy (lasers, electrocoagulation, mechanically removing the mucosa, surgery) based on how bad the dysplasia is: Br. J. Surg. 84: 760, 1997, Am. J. Med. 111 S 8A: 147A, 2001; lasers see Gut 51: 776, 2002. Some pathologists recommend waiting to resect until there is "superficial adenocarcinoma", but the truth is that pathologists can't seem to distinguish this reliably from high-grade dysplasia (Gut 51: 671, 2002).
Future pathologists: You'll look at dysplasias from Barrett's biopsies frequently, and there are likely to be further refinements that will help you let the surgeons know when to operate (laser, scrape, etc). All Barrett's have some hyperchromasia of the nuclei in the lower portions of the glands. Low-grade dysplasia features loss of mucus production, stratified nuclei in the crypts, and elongated nuclei in parallel. High-grade dysplasia features stratification on the surface, branching glands, and/or cribriform stuff in the crypts. Be careful about calling "severe dysplasia" if there is inflammation; it might be better to treat the reflux and repeat the biopsy. One major criterion that says "operate" is loss of the basal orientation of the nuclei, i.e., this is more than just the kind of atypia that one finds in an adenomatous polyp. Grading updates: J. Clin. Path. 55: 910, 2002; J. Clin. Path. 59: 1029, 2006. Biomarkers Mayo Clin. Proc. 76: 438, 2001. Does screening really save enough lives to be worthwhile? It's still a tough call (Am. J. Gastro. 98: 1931, 2003; Gastroenterology 127: 310, 2004 from KU).
* HCA, an immunostain to help spot the aggressive dysplasias: Am. J. Clin. Path. 122: 747, 2004.
{15428} Barrett's esophagus (note tan columnar, rather than white squamous, mucosa)
{15429} Barrett's esophagus
{15427} acute reflux esophagitis (one heck of a case of heartburn;
stomach is on the left)
Reflux leads to fibrosis (scarring, shortening, perhaps narrowing) of the esophagus, difficulty on swallowing ("DYSPHAGIA"), pain in swallowing ("ODYNOPHAGIA"), retrosternal pain ("heartburn") and/or slow GI bleeding leading to iron-deficiency. In severe cases, massive GI bleeding (hematemesis, melena) can occur.
Other noteworthy causes of ESOPHAGITIS include candida
,
CMV
,
herpes
,
radiation, generalized
diseases of stratified squamous epithelium (* pemphigus, other) or keeping a stomach tube down for
more than a few minutes. All the above can give some nasty ulcers.
You also remember the esophageal changes ("rubber hose") in scleroderma (review for pathologists
Gut 55: 1697, 2006)
and graft-vs.-host disease.
Herpes esophagitis
Joel K. Greenson MD
U. of Michigan
CMV Esophagitis
Joel K. Greenson MD
U. of Michigan
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{11096} candida esophagitis (scrapes off, unlike glycogen acanthosis)
{11099} candida esophagitis
{49128} candida esophagitis
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{19449} herpes, histology
{25910} herpes, pap smear
* Future pathologists: Herpes
of the esophagus is often relatively devoid of good herpes-inclusion
cells. Look instead for clusters of macrophages (Hum. Path. 22: 541, 1991).
Drinking lye (Drano, etc., an extremely painful and unreliable method for would-be suicides) or some other caustic substance leads to corrosive esophagitis, strictures, etc., etc.
{11772} lye burn of stomach
{15554} lye burn of stomach
PERFORATED ESOPHAGUS can result from swallowing the wrong thing. Chicken bones are infamous (AJFMP 19: 166, 1998) -- these can pierce the heart or cause other dreadful problems.
LACERATED ESOPHAGUS usually results from heavy-duty vomiting during which the esophagus fails to relax (alcohol abuse, pregnancy, post-anesthesia; MALLORY-WEISS SYNDROME). Endoscopists and pathologists see little longitudinal tears, usually in the distal esophagus. They are a problem only if bleeding is massive, or if the esophagus actually ruptures (BOERHAAVE'S SYNDROME; at these sites of rupture, the muscularis mucosae is apparently absent: Am. J. Surg. 158: 420, 1989).
{15420} lacerated esophagus
ESOPHAGEAL VARICES are dilatations of the esophago-gastric venous plexus. These result from portal vein hypertension from any cause, as the blood from the stomach and intestines seeks the low-pressure pathway back to the heart.
You won't know varices are there until they bleed. And they bleed massively when their attenuated overlying mucosa is rubbed away, or they just pop from pressure. This is the fast way out of life for many problem drinkers.
{38629} varices, gross
{38632} varices, gross
{15419} esophageal varix, histology
{24406} varices, histology
{40724} varix with clot, histology
Portal hypertension patients will also commonly exhibit hemorrhoids and dilated veins around the umbilicus ("caput medusae", why?) Remember that portal hypertension will greatly accelerate GI bleeding from non-variceal causes (gastritis, peptic esophagitis, ulcer, Mallory-Weiss) as well.
Learn now: THE CAUSES OF PORTAL HYPERTENSION....
BENIGN TUMORS OF THE ESOPHAGUS: Banal, and relatively uncommon. For example, fibrovascular hamartomas: AJR 166: 781, 1996.
CARCINOMA OF THE ESOPHAGUS strikes around 8000 people each years and kills most of them.
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SQUAMOUS CELL CARCINOMA has historically been the most common esophageal cancer in the United States, but is becoming less common.
Most patients are males (more than 4:1), black men are at higher risk than others, and in the U.S., the large majority are both smokers (cigarets, cigars) and drinkers.
Old lye strictures are also frequent sites for esophageal cancer, as is the Chagas-disease ridden mega-esophagus (Digestion 47: 138, 1990).
The epidemic of highly-aggressive squamous cell carcinoma in Mainland China (Cancer 73: 2027, 1994;
Cancer 74: 573, 1994) has been attributed to
aspergillus
fungus contamination, nitrosamines,
vitamin deficiency, zinc deficiency, molybdenum deficiency, ethnic teas, and ethnic delicacies that
are pickled (i.e., rendered rich in certain fungi).
* The South Carolina lowlands have a great excess of squamous cell carcinoma of the esophagus, and these cancers have a distinctively high rate of p53 mutations, suggesting some chemical in the environment (J. Thor. Card. Surg. 108: 148, 1994). Still a mystery: South. Med. 95: 900, 2002. In West Kenya, it is a common disease of teens and young adults (Lancet 360: 462, 2002).
Any portion of the esophagus can be involved; the middle third is slightly more common than the others.
Like most squamous cell carcinomas, esophageal cancer arises in squamous dysplasia (update Gut 54: 187, 2005), is often multifocal (Cancer 73: 2687, 1994), grows as a fungating lesion (less often, just an ulcer), and produces symptoms (dysphagia, food "sticking") only late. Because of its location, the later stages of this disease are particularly cruel.
* Biomarkers: Surgery 127: 552, 2000.
* A claim from the 1990's that many esophageal carcinomas contained HPV remains unconfirmed.
* Honesty or the impact of managed care? The surgeons finally tell it like it is: radiation and chemotherapy for cancer of the esophagus have little or no impact beyond making life more miserable for these patients (Arch. Surg. 133: 722, 1998).
{15423} carcinoma of the esophagus, exophytic growth
{15421} carcinoma of the esophagus, growing as ulcer
{15422} carcinoma of the esophagus, annular growth
{15424} squamous carcinoma of the esophagus, histology
{15552} carcinoma of esophagus invaded aorta
{19345} yet another squamous cell carcinoma of the esophagus (x-ray)
{26876} and another
{42231} and still another
ADENOCARCINOMA is now almost as common as squamous cell carcinoma, and is probably increasing in frequency. It arises most often arising in a Barrett's esophagus. Again, the male predominance is marked (more than 6:1) and as you'd expect, symptomatic reflux is a strong risk factor (NEJM 340: 825, 1999). Tobacco and obesity are risk factors, alcohol consumption is not. It's basically the same lesion as cancer of the gastric cardia: Br. J. Surg. 529: 529, 1999. The longer the Barrett's region (Gut 33: 1155, 1992), the higher the risk, and smoking also increases risk: Cancer 72: 1155, 1993 (big study). Histopathology of Barrett's cancer: Hum. Path. 19: 942, 1988.
Other tumors of the esophagus are banal (little leiomyomas) or curiosities (sarcomas; melanomas,
Am. J. Clin. Path. 92: 802, 1989, others).
Barrett's esophagus with cancer
Joel K. Greenson MD
U. of Michigan
{49132} leiomyoma, gross
Histopathology and cell-of-origin of cancers of the esophagus: Cancer 75(S6): 1440, 1995.
* ESOPHAGEAL ANGINA: Spasm simulating myocardial infarct (including "crushing chest pain radiating to the left arm and jaw", etc., etc.) Once said to be common, we hear little about this now.
|
|
{11889} stomach with biscuit
Most stomach problems start with the mucosa. Review of the healthy mucosa:
Surface, pits ("crypts" / "foveolae") in all areas... Tall surface mucous cells (make "neutral mucus")
Deep in pits, all areas... Neck cells (reserve cells for both above and below; "the proliferative zone")
Cardiac glands... More neck-type cells
Gastric glands... Parietal cells (eosinophilic, packed with mitochondria; make acid and intrinsic factor);
Chief cells (pale, granular)
Pyloric glands... Neck-type cells; G-cells (gastrin producers)
In 1999, Lancet 354: 134, 1999
published a short report on
biotech-enhanced potatoes thickening the mucosa of the stomach
and elongating the crypts of rats to which they were fed.
A small-sample study with a conclusion that didn't make sense...
and the small differences could easily be explained by differences
in the angles produced by hand-cutting and hand-embedding, as happens on human biopsies
routinely. Did the author compare the heights of the villi to the
depths of the crypts for control purposes? Or for that matter,
the relative thickening of crypt layer and gland layer?
Of course not! Your instructor wrote to Lancet (who turned down my letter)
and to the author (Arpad Pusztai,
who had gone on TV and made inflammatory statements
about the public being used as guinea pigs;
he didn't respond either and is now a leading antibiotechnology activist
and celebrated "persecuted genius").
Lancet ended up admitting (May 29, 1999) that
it knew the paper was junk science when it was published but that if it
hadn't published it, it would have been smeared for "suppressing
information" by
anti-biotechnology militants. I am not making any of this up.
Regrettably
"environmental activism" thrives on this kind of stuff.
Greenpeace USA's website
(2005) is still citing the paper as proof of the dangers of
bioengineered food ("damaged immune systems and stunted growth of vital organs").
* The mucosa protects itself with a host of protease-inhibitors, phospholipids, glycoproteins, etc., etc.;
neutrophils and lots of other things damage it (Dig. Dis. Sci. 39: 138, 1994), etc., etc. You'll go
crazy trying to keep them all straight.
* CURIOSITIES
It's not rare to find a bit of ectopic pancreas.
You may also find lung, complete with bronchus -- the famous "pulmonary sequestrum." It's harmless.
DIEULAFOY'S MALFORMATION is an extra-large artery running along the
mucosa of the lesser curvature. It can cause severe bleeding, even into the chest
(Chest 110: 567, 1996; Ann. Thorac. Surg. 80: 1126, 2005).
INTESTINAL METAPLASIA (review Gut 52: 1, 2003):
A common finding. Most often it's caused by helicobacter; you might see it
in autoimmune atrophic gastritis with achlorhydria (perhaps due to the associated bacterial
colonization); bile reflux and previous radiation. An experienced endoscopist can spot areas of intestinal metaplasia
by their slightly more whitish color.
Intestinal metaplasia is clearly the precursor lesion for "intestinal type" stomach cancer.
* Some pathologists distinguish subtypes of worsening severity: TYPE I: Straight crypts, regular architecture, mature enterocytes, Paneth cells, and goblet cells, neutral
mucin
{15432} type I intestinal metaplasia (right)
TYPE II: Mild distortion of glands, few enterocytes or Paneth cells, many mucin-producers and goblet cells,
neutral mucin, * carboxymucin
TYPE III: Variable degrees of glandular distortion, cells less differentiated, mostly sulfo-mucin ("colonic differentiation").
Any kind of stomach cancer can harbor any kind of mucin. In case
somebody (not me) asks:
SULFOMUCIN... Very acid... Intestine; if in stomach, the epithelium is atrophic-metaplastic and is likely to turn
nasty (?)
CARBOXYMUCIN... Acid... Intestine (also called "acid sialomucin")
NEUTRAL MUCIN... Neutral... Stomach (also called "neutral sialomucin").
Future pathologists: Use alcian blue to stain the acid mucins!
I am almost sorry to have to add that newer work indicates that all three types may represent
either multistep-mutations-of-carcinogenesis or just tissue regeneration (Cancer 74: 556, 1994);
the distinction is of no importance (J. Clin. Path. 54: 679, 2001).
This is sad because for the past decade, we pathologists have been honing our
color-vision to distinguish normal gastric neck cells from "small-intestinal type"
intestinal metaplasia, etc., etc. * Stay tuned for prognosticating "intestinal metaplasia", judging whether it is reversible
upon eradicating helicobacter (consensus is now that this is the norm: Gut 54:
1536, 2005), based on gene studies (Gut 52: 1, 2003)
and/or immunostaining and/or repeat endoscopy (Dig. Dis. Sci. 45: 1754, 2000). "Das-1 positive is premalignant": Gut 52: 80, 2003).
BIRTH DEFECTS
DIAPHRAGMATIC HERNIAS result from failure of the diaphragm to form properly. Portions of stomach,
intestines, and other organs end up in the chest.
{15607} diaphragmatic hernia, left leaf never formed
Congenital PYLORIC STENOSIS is probably a hereditary defect of variable penetrance in which the
pylorus of the stomach is hypertrophic, and the gastric outlet may become fully obstructed, typically
at the end of the first month of life. The infant experiences projectile vomiting, and the surgeon feels
a mass ("feels like an olive") in the upper abdomen. Surgical splitting of the pylorus effects a cure.
It is more common in boys, and Turner's XO is also a risk.
* A claim that some of
these kids lack nitric oxide synthetase (NEJM 330: 969, 1994) has failed to find
additional support (Clin. Genet. 53: 421, 1998).
* More recently, the understudied "interstitial cells of Cajal",
little cells that have a lot to do with gut motility, have been found to be
somewhat lacking both in numbers and a key enzyme in the pylorus in these kids
(Arch. Path. Lab. Meed. 127: 1182, 2003). Stay tuned.
Often impressive. Causes include beer chug-a-lugging, bowel obstruction, misplaced endotracheal
tubes, gastroparesis (think of diabetic autonomic neuropathy),
and (in the dead) inept CPR attempts. (Amateurs first blow air into the stomach, then rupture
it by pressing in the wrong place. See Ann. Int. Med. 30: 343, 1997.)
{49141} gastric dilatation
BEZOARS
These are swallowed goodies that remain permanently in the stomach.
Hairballs (TRICHOBEZOARS) are seen in people who enjoy nibbling their long hair ("Rapunzel
syndrome"). Or ask a pet cat. Review Mayo Clin. Proc. 73: 653, 1998.
PHYTOBEZOARS may be chunks of ill-chewed vegetable matter, or (worst) persimmon remnants. The
latter contain a substance that, complexed with acid, turns into cement and may require surgery.
Things that interfere with gastric emptying (diabetes, other dysautonomias, post-vagotomy, anti-cholinergic medicines)
enhance one's ability to personally experience a bezoar.
{49150} bezoar
ACUTE GASTRITIS: Acute damage to the gastric mucosa from any cause.
If there is necrosis of any epithelial cells, it is "erosive gastritis" --
you remember that an erosion is inflammation plus necrosis of an epithelium without necrosis
of the underlying connective tissue (at least not yet).
Pathogenetic mechanisms include:
"Big Robbins" listed, or could have listed, these important causes:
You can figure out for yourself what the mechanisms might be in each case. Anatomically, you may
see anything from mild edema and a few polys to bloody sloughing of chunks of the upper mucosa,
and symptoms can range from "upset stomach" to vomiting blood by the pint.
AUTOIMMUNE ("FUNDIC", "CHRONIC ACTIVE", "DIFFUSE ATROPHIC", "TYPE A")
CHRONIC GASTRITIS is an autoimmune process
that attacks primarily the fundic glands.
You'll see loss of mucous secretion, striking shortening of the glands, and usually loss of the parietal cells.
Patients usually (60+%) have autoantibodies against parietal cell H+/K+ ATPase (and usually others against intrinsic
factor). This is the usual cause of the achlorhydria (i.e., greatly diminished or no stomach acid) and
Addisonian pernicious anemia. JAMA 278: 1946, 1997; update Gastroenterology 120: 377, 2001.
Around 10% of these patients go on to develop stomach cancer.
Many of these patients have other autoimmune endocrine diseases as well. The
three to remember are Addison's disease of the adrenals, Hashimoto's disease of the thyroid (Arch. Int. Med. 159: 1726, 1999), and
insulin-dependent diabetes.
* Future pathologists: Since there is no acid and no feedback,
the G-cells undergo hyperplasia in the antrum. They are a single layer of clear cells. This is a breeding-ground
for carcinoids supposedly.
Work on autoimmune gastritis is overshadowed nowadays by
helicobacter, but the finding of anti-parietal cell autoantibodies
seems solid. Perhaps those lacking the antibody were really helicobacter-induced
atrophy (see below). And helicobacter itself can supposedly trigger
the autoantibodies (you think?: Gastroent. 115: 340, 1998).
Update: Blood 107: 1673, 2006.
{15426} "atrophic gastritis", gross
HELICOBACTER GASTRITIS is a serious problem worldwide.
The vast majority of the old "unexplained chronic gastritis" ("type B gastritis")
cases are caused by helicobacter. You'll have no trouble recognizing
the familiar wiggly creatures on the surface of (often obviously damaged)
gastric mucosa. Giemsa, immune, or silver stains show them to advantage.
* Much confusion is being generated right now by talk of various
gross patterns on helicobacter gastritis. Usually the antrum gets it worst
("antral predominant", often with hyperacidity), or the whole stomach is involved
("pangastritis"). A minority of patients with helicobacter have the antrum
spared ("corpus predominant"), and these people supposedly have atrophy and a low stomach
acid that returns to normal after helicobacter is eradicated; obviously this
has a lot in common with autoimmune gastritis without helicobacter. Wait
to try to figure this out until the matter is more settled.
Helicobacter flourishes in the stomach because it cleaves urea to ammonia
under acid conditions (Science 287: 482, 2000).
Helicobacter's virulence factor, CagA protein, actually gets inoculated
into the stomach cells (Science 287: 1497, 2000). Nobody knows
yet exactly what it does to cells after it enters, though it deregulates
at least one growth control gene (J. Inf. Dis. 187: 334, 2003).
The other virulence
factor, VacA (vacuolizing cytotoxin A) is even more mysterious.
There's a chronic infiltrate with both lymphocytes and neutrophils.
Lymphoid follicles in the mucosa suggest "Helicobacter".
Pyloric metaplasia advances from the antral area into the fundus,
perhaps decreasing acid production, and the fundic glands may atrophy as well.
You may see intestinal metaplasia,
especially near any ulcers that may be present.
Acid production may be increased, decreased, or normal.
When the fundus is involved, the fundic glands become shallow
("patchy atrophic gastritis", to be distinguished from autoimmune
atrophic gastritis), and typically exhibit intestinal
metaplasia (i.e., enterocytes, goblet cells; it's especially pre-malignant -- type III -- when they are
filled with "acid mucus/sulfomucus" as in the real intestine) and/or antral metaplasia (neck cells, G-cells). In advanced autoimmune
gastritis only, the parietal cells are completely gone.
In any portion, the rugae are likely to flatten and vanish. The process begins at the surface and work
downward into the glands. Lesions of various stages are present simultaneously in different parts of
the stomach. Eventually, the surface will come to exhibit at least some intestinal metaplasia and
probably some degree of dysplasia.
Helicobacter gastritis involving most of the stomach is the precursor lesion
to the epidemic stomach cancers seen in much of the world.
Removing helicobacter cures this illness (J. Clin. Path. 4: 22, 1994).
Most people with significant
duodenitis (i.e., polys) have helicobacter gastritis (Am. J. Clin. Path. 90: 711, 1988, kids Am. J.
Clin. Path. 102: 188, 1994 & Dig. Dis. Sci. 39: 1488, 1994), etc., etc.
{11728} Helicobacter in gastritis (look close)
OTHER FORMS OF GASTRITIS:
MENETRIER'S DISEASE ("idiopathic hypertrophic gastritis";
"enlarged fold gastitis"): Idiopathic hyperplasia of the surface
mucous cells, with corresponding atrophy of the glands. Makes for some big folds, and a lot of protein loss in the excessive mucus. Intestinal
metaplasia and neoplasia may form (nice case: NEJM 1/14/88).
Menetrier's is caused (at least sometimes) by helicobacter, and resolves when you
clear the bacteria (Gut 35: 701, 1994). Growth factors producing
the huge folds: Gut 39: 787, 1996.
{19486} Menetrier's, gross
* HYPERTROPHIC HYPERSECRETORY GASTROPATHY: Idiopathic hyperplasia of the stomach glands themselves,
with excessive numbers of parietal and chief cells.
ZOLLINGER-ELLISON SYNDROME: Gastrinoma (often in the pancreas) causing hyperplasia of the gastric
glands. Makes for a very upset, ulcerated stomach.
* GRANULOMATOUS GASTRITIS: Sarcoid, Crohn's, idiopathic (for the latter see Dig. Dis. Sci. 39: 1649,
1994). All are non-caseating, of course.
STRESS ULCERS (the usual "acute erosions") are small (less than 1 cm) areas of loss of some (or all) the mucosa. Note
that nobody really knows where "acute gastritis" leaves off and "stress ulcers" begin; probably
they're part and parcel of the same reaction pattern.
Nomenclature: If the patient has burns, they are "Curling's ulcers" (* think of a hot curling iron). If
the patient has intracranial trauma, they are "Cushing's ulcers" (attributed to vagal stimulation of
gastric acid secretion, named for famous neurosurgeon Harvey Cushing).
Their pathogenesis constitutes a major mystery of medicine. Except in Cushing's ulcers,
hyperacidity does not seem to be the problem. Most of the factors that produce "acute gastritis" can
also help produce stress ulcers. Some workers now favor catecholamine effect (i.e., ischemia)
and/or some glucocorticoid effect.
Pre-pyloric erosions are due to stress (Scan. J. Gastr. 24: 522, 1989).
{15425} "stress ulcer", gross
* A sweet-and-simple test for the integrity of your gastric mucosa: swallow some sucrose and
test for sucrose in the blood! Lancet 343: 998, 1994.
{10471} benign stomach peptic ulcer
Ulcers resulting from the digestive action of acid-pepsin ("no acid, no ulcer") on the gastric mucosa.
A common problem, somewhat more common in men, usually subclinical, prone to remit and
relapse ("once an ulcer, always an ulcer"). "Ulcers" can occur anywhere along the GI tract.
Frequency:
80% duodenum
19% stomach
1% elsewhere
The early wisdom was that almost all patients with either gastric or
duodenal ulcer patients have helicobacter on board (Gut 35:
19, 1994), and eliminating the creature eliminates the disease. Of course that was an
exaggeration; a large minority of stomach ulcer patients are helicobacter-negative (Gastroent. 128: 1845, 2005).
Other risk factors for ulcer include...
None of these are overwhelmingly powerful.
You WILL get
an ulcer, and probably several, if you develop a gastrinoma.
Ask a gastroenterologist about the differences among ulcer patients.
Those with duodenal ulcers tend to secrete acid too abundantly when stimulated, and to empty their
stomachs too readily.
Gastric ulcer types tend to have low-normal levels of acid, and tend either to have chronic gastritis
or take lots of aspirin or other substances noxious to the stomach. People with longstanding gastric
ulcers almost all have "chronic gastritis" in the antrum, and intestinal metaplasia near the ulcer.
* Whether or not helicobacter is on board, gastric ulcers seem to be preceded by abnormalities of the
phospholipids in the gastric epithelium, with loss of their normal protective function. This may be a
common pathway by which helicobacter, atrophic gastritis, cirrhosis, certain animal models, and
others produce ulcer (Gastroent. 107: 362, 1994).
Most (almost all) patients with duodenal ulcers, and a majority of those with gastric ulcers, now are
known to have helicobacter on board, and the bug is thought to be an important part of the
pathogenesis.
In the duodenum, there appears to be a vicious cycle between helicobacter infection and
antral
metaplasia (J. Clin. Path. 43: 981, 1990, Am. J. Clin. Path. 102: 188, 1994) that permits the bugs
to thrive. This is not surprising, considering the abrupt appearance and disappearance of ulcers.
Antral metaplasia is a common finding in normal duodenum (Am. J. Clin. Path. 90: 711, 1988), and
perhaps this how duodenal ulcers begin.
The rare helicobacter-negative duodenal ulcer patient may have Crohn's, Zollinger-Ellison, taking
steroids or NSAID's (review Gut 35: 891, 1994; nobody knows how it works), or just be unlucky
(Gut 34: 762, 1993; Am. J. Med. 91: 15, 1991).
Peptic ulcers are usually single, and most are less then 3 cm across. They look sharply punched-out
(as you'd expect, rolled borders suggest malignancy). However, they may penetrate deeply. The
base is always keep clean by digestive juice. Gastric ulcers are usually on the lesser curvature, and
the favorite site is near or in the antrum. Duodenal ulcers are usually in the first portion, but may be
anywhere. As scar contracts, the mucosal folds radiate from the ulcer.
Peptic ulcers may cause pain (relieved when food or antacid neutralizes stomach acid, recurring
after a meal stimulates stomach acid), hemorrhage, perforate (call the surgeon!) and/or cause
fibrosis leading to obstruction (notably of the pylorus). We believe they do not undergo malignant
transformation ("cancers often ulcerate, but ulcers seldom/never cancerate").
Future surgeons: You may "CHOP" out the ulcer if it is Chronic, Hemorrhaging uncontrollably,
Obstructing the gastric outlet, or Perforated.
BENIGN TUMORS
HYPERPLASTIC POLYPS ("inflammatory polyps") are extremely common and thought to result from exuberant
regeneration of the mucosal epithelium. They usually look like multiple little rice grains, but may
be larger. Microscopically, they are composed of dilated glands lined with pit-type cells.
The big ones (over 1.5 cm) can turn cancerous (Dig. Dis. Sci. 41: 377, 1996).
{09292} hyperplastic polyps of stomach
* INFLAMMATORY FIBROID POLYP is a mass of vessels and stroma
looking like granulation tissue, plus a lot of eosinophils.
* JUVENILE POLYPS resemble those we'll meet later in the colon.
ADENOMATOUS POLYPS ("neoplastic polyps", "adenomas") tend to be pedunculated, with villi and/or
crypts, and the current definitions require
some dysplasia. They are premalignant, there is a link to syndromes
and a
familial tendency, and maybe half would turn into cancer if left alone (but who wants to do that
study?)
{09333} adenomatous polyp
{09299} leiomyoblastoma
* Subclassifying them: Ann. Surg. 242: 64, 2005. Those resulting
from atrophic gastritis almost never kill, other types are more aggressive.
GASTRIC ADENOCARCINOMA (common "stomach cancer"; Lancet 362: 305, 2003; Ann. Surg. 241: 27, 2005)
While its prevalence in the U.S. has decreased strikingly in recent decades, this continues to be an
important cancer killer in every country. Around 15,000 people per year die of stomach cancer in
the U.S. Rates in the rest of the world are also declining. Risk factors include:
Diet and environment are evidently much more important than ethnic
background. First-generation immigrants
have the risk of their home countries; second-generation immigrants the risk of their new countries
(Ann. Surg. 241: 27, 2005).
There are two major types of gastric adenocarcinoma, with different cells of origin.
(1) DIFFUSE INFILTRATIVE GASTRIC ADENOCARCINOMA
arises from the neck cell.
Helicobacter, autoimmune gastritis, and intestinal metaplasia are not
risk factors.
The frequency of this cancer is actually increasing dramatically
in the US (CDC: Arch. Path. Lab.
Med. 128: 765, 2004). No one knows why.
* Hereditary diffuse gastric adenocarcinoma, an anti-oncogene
deletion syndrome, is caused by mutated
E-cadherin (CDH1): Gut 53: 814, 2004; JAMA 297: 2360, 2007. Signet-ring cancers
begin at the body-antral junction, and are already invading the upper mucosa
long
before they are visible on endoscopy. Prophylactic gastrectomy
seems like a good idea.
(2) INTESTINAL TYPE GASTRIC ADENOCARCINOMA
typically arises in the setting of longstanding "atrophic gastritis" or other
"chronic gastritis", usually in the presence of helicobacter and/or autoimmune gastritis and/or
intestinal metaplasia and/or
bile reflux. How we discovered
the link to helicobacter: Am. J. Clin. Path. 100: 236, 1993); Cancer
73: 2691, 1994; Cancer 75: 2203, 1995; Dig. Dis. Sci. 41: 950, 1996.
Does eradicating helicobacter prevent progression of intestinal metaplasia to cancer?
Yes! (Gut 53: 1244, 2004. No! JAMA 291: 187, 2004.
* News: Around half of stomach cancers arising in the gastric cardia (but not elsewhere) probably
arise from Barrett's esophagus (Arch. Surg. 129: 609, 1994).
* Some cancers, espsecially after partial gastrectomy,
are rich in lymphocytes and these are almost always packed with
Epstein-Barr
virus The gross is the usual for a cancer (a cauliflower, an ulcer, or diffuse invasion). The histology is
what you'd expect. In either case, you may see invasive glands, papillae, signet-ring cells, mucus
lakes, desmoplasia, and most anything else, though when you see signet ring cell
invasion, it is usually the "diffuse" type rather than the "intestinal" type.
Terms: LINITIS PLASTICA: "leather bottle" stomach from a
diffusely-infiltrating, desmoplastic cancer. KRUKENBERG TUMOR: Drop-metastases causing
enlargement of the ovaries. SISTER MARY JOSEPH'S NODE: metastasis to the umbilicus (named for the
Mayo brothers' scrub nurse). RECTAL SHELF ("of Blumer"): Drop-metastases to the lowest place on the peritoneum
(remember the "pouch of Douglas"?)
* Grading stomach cancer is based on whether the cancer makes tubules and/or mucus (Goseki I-IV): Gut 35: 758, 1994;
some studies claim this gives no useful prognostic information beyond the stage;
Cancer 88: 2114 & 2426, 2000 did find it to be of some help.
Symptoms are also what you'd expect -- nausea, vomiting,
early satiety, GI bleeding. As you'd also expect, there are usually
no symptoms until it's too late. (If you have an extra cauliflower
in you stomach, you'd never know it.) There is so much stomach cancer in Japan that people get
endoscoped routinely in search of it, and there are many cures (unlike in the US). (For some reason
that no one understands, the Japanese have a tremendously high rate of
atrophic gastritis, conceivably from the local strains of helicobacter,
and this is where most of these
cancers arise: Gut 55: 1545, 2006). Biopsy all stomach ulcers you see -- even a cancer may shrink
on a regimen of H2-blockers and antacids.
{17511} Stomach cancer, exophytic
Most gastric adenocarcinomas are probably preceded by high-grade carcinoma-in-situ/dysplasia (see
Arch. Surg. 140: 644, 2005; dysplasia usually invades the mucosa soon,
and until it penetrates the muscularis propria, it's
called "early gastric cancer" (EGC). It can stay in the mucosa for a long time (Arch. Path. Lab. Med. 114: 1046,
1990). Some diffuse-infiltrating cancers may start de novo, without
dysplasia. {15443} early stomach cancer
Detected late (and it still usually is), stomach cancer has a generally poor prognosis.
{15441} non-metaplastic dysplasia
The mainstay of therapy for stomach cancer is still surgery.
* Serum tumor markers: CA 19-9, CA 72-4. Am. J. Surg. 169: 595, 1995.
STOMACH LYMPHOMAS (and other GI lymphomas) are less common than carcinomas but have a better
prognosis. Since they tend to be bulky, patients present with obstruction.
WESTERN ("American") LYMPHOMAS are usually familiar B-cell lymphomas. Helicobacter seems to be
the big risk factor: J. Clin. Path. 47: 437, 1994, J. Clin. Path. 47: 436, 1994; Lancet 345: 26, 723,
724 & 798, 1995 (no surprise, since helicobacter makes lymphoid follicles grow). However, many
gastric lymphomas are helicobacter-negative and different genetically
(Gut 52: 641, 2003).
* MEDITERRANEAN LYMPHOMAS occur especially around the Near-East, and usually feature
plasmacytoid differentiation. A subset is alpha-heavy chain disease.
* SPRUE-ASSOCIATED LYMPHOMA exhibits T-cell markers (reviews Gut 49: 804, 2001;
Am. J. Clin. Path. 127: 701, 2007; the more anaplastic primary small bowel lymphomas
tend to be preceded by celiac sprue while the less anaplastic ones don't);
* PSEUDOLYMPHOMA of the stomach is an old term that has no meaning
in light of today's molecular diagnostic techniques (Cancer 79:
1656, 1997). You can't always tell severe chronic inflammation from true lymphoma
just on histopathology, but today's biotech resolves even the toughest calls
by demonstrating clonality (Gut 55: 782, 2006).
Gastric Pathology
Sampurna Roy, MD
Lots of photos and good text
{09332} normal gastric rugae
{11740} normal stomach fundus histology
{50459} normal stomach fundus histology
{15534} type I intestinal metaplasia
{49138} diaphragmatic hernia, left leaf never formed
DILATED STOMACH
Gastroparesis
Spectacular x-ray
Brazilian Medical Students
Trichobezoar
Rapunzel syndrome
AFIP
Treating a gastric phytobezoar with meat tenderizer: Dig. Dis. Sci. 46:
1013, 2001.
{10160} trichobezoar
Pathologists define this to be neutrophils in the epithelium above the basement
membrane.
Eosinophilic / allergic gastroenteritis
Joel K. Greenson MD
U. of Michigan
Helicobacter pylori
Joel K. Greenson MD
U. of Michigan
food poisoning
Pernicious anemia
Immunoglobulin on parietal cells
WebPath Photo
{15434} "atrophic gastritis"
{15561} early atrophic gastritis, starting on surface
* The atrophy caused by helicobacter, from the molecular point of view:
Dig. Dis. Sci. 49: 1615, 2004.
Acute gastritis
Me after beer, pizza, and aspirin
WebPath Photo
Helicobacter pylori
Stained black
New England Journal of Medicine
{15440} Helicobacter
{19492} type B, antrum
{19491} type B, antrum
{26903} type A
{26906} type A
{26909} type A, some atypia
REACTIVE GASTROPATHY, without helicobacter but with loss of / changes in the antigens of mucin (different
changes from helicobacter cases),
is today the second-most-common diagnosis made by pathologists
on stomach biopsy today (Arch. Path. Lab. Med. 131: 86, 2007).
Often the cause is obscure; NSAIDS and bile reflux supposedly are often responsible.
{19487} Menetrier's, histology
{18711} "stress ulcers", gross
{19350} "gastric erosion", histology
{39426} hemorrhagic gastritis, nasogastric tube erosions
{07184} hemorrhagic gastritis, nasty case
Peptic Ulcer
Text and photomicrographs. Nice.
Human Pathology Digital Image Gallery
{15438} benign stomach peptic ulcer
{15439} benign stomach ulcer, with clot
{15560} histology of ulcer, arrow marks bleeding point
{19372} peptic ulcer
{26888} peptic ulcer, stomach
NSAID Gastritis
Joel K. Greenson MD
U. of Michigan
{38656} hyperplastic polyps of stomach
* Patients with familial adenomatous polyposis of the colon are
especially likely to get these (morphology and genes Am. J. Path. 161:
1735, 2002).
{09312} adenomatous polyp
{09331} adenomatous polyp
GASTROINESTINAL STROMAL TUMORS are the common spindle-cell neoplasms
of the stomach, usually bearing a trademark c-kit mutation and stainable antigen,
and responding to Gleevic (imatinib). They range from totally benign to highly
malignant (South. Med. J. 96: 512, 2003).
The cell of origin is probably most often the interstitial cell of Cajal,
in the nerve plexus (Lancet 369: 1731, 2007).
Most "leiomyomas", "leiomyoblastomas", and "leiomyosarcomas" are probably "GIST"'s.
GASTRIC CARCINOID is worth mentioning here because
of the big medicolegal flap about long-term gastric acid
suppression
perhaps causing gastric carcinoids. High levels of gastrin
causes enterochromaffin cell hyperplasia, and most people who get gastric
carcinoid have high gastrin levels (atrophic gastritis or Zollinger-Ellison).
And rats actually get such tumors
after lifetime omeprazole.
Stay tuned.
* Gastric carcinoinds that produce ghrelin: J. Clin. Endo. Metab. 86: 5052, 2001).
It
exhibits small glands made of polyhedral cells with round, tame-looking nuclei,
or cells infiltrating singly.
The most common subtype Is the signet-ring cancer.
It features large glands made of tall cells with rod-shaped nuclei (as in
the more common, more familiar primary carcinomas of the colon). This is the common type of
stomach cancer in the high-risk countries.
(Cancer 74: 805, 1994). Similar tumors are common
in the Far East regardless of previous surgical procedures.
Stomach cancers "with lymphoid stroma"
are less aggressive than common gastric cancers (Arch.
Surg. 129: 615, 1994), even if they are not the result of
previous surgery, and regardless of Epstein-Barr positivity (the virus is usually
present). Histopathology 36: 252, 2000; molecular biology
Gastroent. 121: 612, 2001; Am. J. Path. 161: 1207, 2002;
Am. J. Clin. Path. 121: 237, 2004.)
Gastric Adenocarcinoma
Text and photomicrographs. Nice.
Human Pathology Digital Image Gallery
Gastric Carcinoma
Text and photomicrographs. Nice.
Human Pathology Digital Image Gallery
{10472} Stomach cancer, ulcerated
{15509} Stomach cancer, linitis plastica, gross
{15562} Stomach cancer, linitis plastica, histology
{08818} Stomach adenocarcinoma, intestinal type
{17517} Stomach adenocarcinoma, intestinal type
{10473} Stomach adenocarcinoma, diffuse type
{39380} Stomach adenocarcinoma, diffuse type
{39392} Stomach adenocarcinoma, diffuse type
{15510} Signet ring stomach cancer
{19346} Stomach cancer, superficial
{35258} Stomach adenocarcinoma, Pap smear
{15444} non-metaplastic dysplasia