Shahid Aziz

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Shahid Aziz Powered By Docstoc
					                                                                          GI Hr # 12
                                                             February 25, 2004 8 am
                                                                             Dr. Aziz
                                                             R. Eason for A. Asrabati
I.    Diagnosis
      A. Need to use clinical correlation with histological findings----there seems
         to be confusion about dx of this entity. A pt will present to the ER with
         upper quadrant abdominal discomfort and have a work-up including
         abdominal x-rays (plain films), blood chemistries, a CBC, an ultrasound,
         and is given Tagamet or Zantac to take home for a dx of gastritis when
         nothing is found and is told to follow-up with his/her doctor. What is
         gastritis? Is it defined by symptoms, what and where located on
         endoscopy (inflammatory changes)? Or is it defined on a pathological
         basis? Do above to dx.
      B. Gastroscopic bx include gastric erosion/ulceration, thickened gastric folds,
         polypoid masses or to dx H .pylori infections—if biopsy a polyp, try also
         to biopsy mucosa around it to be able to see what kind of bed it is growing
         in? Ask, is there any evidence of atrophic gastritis or intestinal
         metaplasia? May put pt at a higher risk for gastric adenocarcinoma. And
         depending on which location of the stomach is involved anatomically and
         pathologically, you may have certain risk for those entities.
      C. For chronic/nonspecific gastritis, need 5 bx
      D. Cause include NSAIDs, mainly the non-selective ones (Nuprin, Advil,
         Aleve), less with Celebrex and Vioxx (COX 2 inhibitors), H. pylori (T-
II.   Chronic, Nonspecific Gastritis
      A. Clinically silent (no c/o abdominal pain), risk for PUD or neoplasm (is
      B. Three groups
         1.      Diffuse antral predominant gastritis
                 a.       distal antral/prepyloric and due to H. pylori infections
                 b.        rates in Caucasians,  asymptomatic, no  CA risk
                 c.       Endo: normal/red streaks emanating from the pylorus
                          radiating to the body of the stomach (like they have been
                          painted on with a paintbrush). Streaky gastritis is
                          sometimes associated with superficial erosions found in
                          them if biopsied.
                 d.       Histo: diffuse, chronic inflammation=neutrophillic
                          infiltration through the lamina propria and epithelium.
                          Also, may see surface injury, foveolar epithelium with loss
                          of apical mucin and reactive nuclear change or erosion.
                          Lymphoid follicles with germinal centers indicating H.
                          pylori H. pylori are found superficial mucous layer along
                          mucosal surface and gastric pits (use a special stain for it)

                               Don’t do endoscopy specifically for it—there is a non-
                               invasive test for it—the hydrogen breath test.
                2.     Multifocal Atrophic Gastritis
                       a.      Involves the antrum, body with mucosal atrophy and
                               intestinal metaplasia. Causes: H. pylori in 85% pts.
                       b.       Genetic/environmental/diet plays role.
                       c.       incidence in AA, Scandinavians, Asians, Hispanic,
                               Central/S. Amer., Japanese, Chinese In some Japanese
                               groups, there is a marked risk for gastric adenocarcinoma
                               at the body, and the risk is so high, they recommend
                               endoscopic screening of those pts on a regular basis. In
                               some hospitals there, they do not use conscious sedation
                               like we do here for upper endoscopy. Here we use a local
                               anesthetic spray to anesthetize the throat, fentanyl, and
                               Versed, two drugs that take away discomfort, decrease
                               anxiety, and cause amnesia. In Japan, only use local
                       d.      With intestinal metaplasia=  risk dysplasia and CA—
                               biopsy polyp and mucosa around it to see what kind of bed
                               the polyp is growing out of. Looking for atrophic changes,
                               esp. atrophy with intestinal metaplasia, which increases
                               chance of these.
                       e.      Endo: pale mucosa, shiny surface, prominent submucosal
                       f.      Histo: inflammatory changes in gastric epithelial cells,
                               replaced by metaplastic (cell type usually not found in that
                               location-here are intestinal glandular cells-not belong in
                               the stomach) epithelial cells
                3.     Diffuse Corporal Atrophic Gastritis
                       a.      Autoimmune destruction of fundic glands, <5% chronic
                       b.      Accts for pernicious anemia (N. Euro/Scandinavian)
                       c.      Clinical: include hypo/achlorhydria, hypergastrinemia
                               (because of the effect of low gastric acid on stimulation of
                               gastrin), antral wall hyperplasia (due to trophic effects of
                               gastrin on the gastric wall). See circulating parietal
                               cell/intrinsic factors Antibodies—see a question that
                               pertains to circulating parietal cell Ab/intrinsic factor Ab,
                               think of this entity, diffuse corporal atrophic gastritis, is
                               autoimmune destruction of the fundic glands.
                       d.      Endo: effaced gastric folds and thin fundic mucosa
                       e.      Histo: incomplete (colonic) type intestinal metaplasia (
                               carcinoma), usually focal
        Remember that changes occurring here start as an autoimmune destructionlead
to hypergastrinemiatrophic changes in the wallsee endoscopically and
histologically. See intestinal metaplasia, and know that the pt is at increased risk of

getting adenocarcinoma of the body of the stomach. Also remember that for these pts
with this entity have no screening guidelines here in the Unites States. So if have a pt
with upper abdominal discomfort, and work-up is negative. Has endoscopy done, and
has endoscopic findings of effaced gastric folds and a thin fundic mucosa, and bx with
incomplete colonic type intestinal metaplasia. How do you monitor—every yr, 2yrs,
every 5 yrs and rescope and rebiopsy to check for adenocarcinoma. This is not done
because we do not know what occurs between intestinal metaplasia, dysplasia, and
cancer (do not have the steps outlined yet. The majority of people with intestinal
metaplasia do not develop dysplasia or carcinoma. Thus, there are no guidelines for
endoscopy recommended by the American College of Gastroenterlogists or the American
College of Physicians at this time. Then what do we do? Do pt education and reduction
of risk factors: Look at if use chewing tobacco, if they smoke, if they have family risks,
personal risks: previous history of adenomatous or hyperplastic polyps, , H pylori
infections that are symptomatic or caused ulcers, MALT type lymphomas. Are risks that
we want to remove. Pt education is very important.
         Gastric body adenocarcinoma in the U.S. is declining since the early 1980’s.
There is a high risk in Japan, and that is why screening endoscopies are done there. In
the U.S., esophageal adenocarcinoma and gastro esophageal junction adenocarcinoma,
however, are increasing by the same power. This decrease in gastric body
adenocarcinoma is possibly due to the aggressive treatment of H. pylori infections with
antibiotics. There are some studies coming out that suggest H.pylori infection is
protective for esophageal and gastro esophageal junction adenocarcinoma and with
wiping H. pylori out on a wide basis, possibly made these pts prone to developing these

        ? If a pt has other autoimmune co morbidities, do you follow them more closely?
No, other types of autoimmune d/o do not have an epidemiological, causative, or
etiological link here with this entity.

        For pt management, if suspect this (a pt presents to ER with upper abdominal
discomfort) and work-up is negative, pt has non-ulcer dyspepsia. Need to decide if do a
UGI series or endoscopy. UGI x-ray is ok, but there are limits with it. Needs to be a
double contrast exam to get greater mucosal detail (then with a single contrast UGI
series) Upper endoscopy is better: has greater magnification, can create digital pictures
to can actually see what is going on. Is ok to do UGI series. If don’t see anything will go
to endoscopy anyway.
        III.   Infectious
               A.      Viral—see in immunocompromised pts, eg with HIV or HIV/Hep
                       B and C
                       1.      CMV-also in esoph, SB, colon, Anus-not usu a diffuse dz,
                               is a discrete ulcer, are small and scooped out
                               a.      See in  imm person
                               b.      Clinical: epigastric pain, fever (low grade, usu
                                       lower than herpetic dz), atypical lymphocytosis
                               c.      Radio: rigid and narrow antrum—usu advanced
                                       case of CMV with diffuse involvement

                              d.        Endo: congested/edematous mucosa of antrum with
                                        ulceration, thick and bumpy, looks like
                                        malignancy—small, well-circumscribed
                        d.      Histo: enlarged ―owl eye‖ cells, may have multiple
                                granular, basophillic, cytoplasmic inclusions
        Case of HIV pt coinfected with Hep B and C on pegalated ? interferon for
presented with upper quadrant ab pain and low-grade fever. The blood work did not
show any other changes. The pt did have some nausea, early satiety, and nocturnal
epigastric pain. He also had systemic signs and symptoms: night sweats, wt loss, fevers,
chills. Did an upper endoscopy and found small, discrete ulcer with dirty exudative base
with irregular borders that looked like CMV located in prepyloric area, with bx showed
NSAID gastropathy. Pt had been taking Nuprin for body aches and fever and increasing
his dose steadily. CMV negative. Can mimic CMV ulcerations
                        2.      Herpes: rare, early infection and dormancy, with activation
                                secondary to radiation, chemo, lymphoma, CA
                                a.      Clinical:  imm person, gets n/v/f/c/fatigue/cough/
                                         wt.—worse odynophagia than with CMV; can be
                                        mimicked by NSAID abuse
                                b.       Barium: cobblestone, ragged shallow ulcers,
                                c.      Endo: multi small, raised ulcerated plaques/linear
                                        superficial ulcers, crisscross pattern (like chicken
                                        wire or snake skin appearance—like gastropathy
                                        from portal HTN), cobble stone in appearance,
                                        uniform ulcers
                                d.      Histo: numerous single/clumps with ground class
                                        nuclei and eosinophilic intranuclear (This is a
                                        correction from internuclearintranuclear)
                                        inclusion bodies, surrounded by halos
        Case of a 48 y.o. AA male from the federal correctional institute with hx of known
liver dz. Presented with encephalopathic changes, mentation changes. During the next
24-48 hrs, his encephalopathy worsened comarespiratory failure on ventilator.
Liver enzymes at presentation were moderately elevated AST/ALT at 200, Alk phos at 600
and Bilirubin total and direct at 6 and 4.5. Within 24-48 hours, they changed
significantly ALT to the 1000s, AST to 900, alk phos at 1200 and bilirubin continued to
rise. Pt was HIV and Hep C positive. But now with rapid deterioration of liver function.
Ask what is going on in the liver. Made pt coagulopathic, both extrinsic and intrinsic
pathways were affected; PT and PTT were both prolonged. Did an acetaminophen level
during this time, but it was below therapeutic levels. Case of undiagnosed etiology of
hepatic failure, had all criteria. Started on treatment for acetaminophen toxicity--
mucomyst. Did viral titers on him. Empirically started on acyclovir to treat for herpetic
hepatitis because is quickly reversible and side effects of med are acceptable here. Liver
bx by intrajugular route showed hepatic failure was from acetaminophen. Hx from
guards watching him in ICU that pt was taking Tylenol (loading up on it) after being
beaten up by former roommate because he was not showering regularly. Toxic

metabolites of Tylenol were still in body and Tylenol processed already. Also, damage to
P450 system still occurring. Upper endoscopy was negative for herpes, too.
               B.     Bacterial
                      1. Suppurative (phlegmonous) gastritis: rare, mortality ~60%,
                          submucosa/muscular propria of stomach, rare=acute
                              a. Peritoneo-jugular venous shunt
                              b. Clinical: upper abd pain, peritonitis, purulent ascites,
                              c. Gross: stomach=thick and edematous with perforations
                                   with granular green-black exudates
                              d. Histo: polymorphonuclear infiltrates, Gram +/-,
                                   vascular thrombosis
                      2. Mycobacterium TB: rare, associated with pulmonary TB
                              a. Clinical: abdominal pain, n/v, GIB fever,  wt
                              b. Radio: enlarged stomach with narrowed, deformed
                                   antrum with prepyloric ulcerations-mimic NSAID ulcers
                              c. Endo: ulcers, mass, gastric outlet-obstruction
                              d. Gross: multi small mucosal erosion, ulcer,
                                   hypertrophic mass, sclerosing inflammation, acute
                                   miliary dissemination, pyloric obstruction
                              e. Histo: necrotizing granulomas, acid fast bacilli
                      3. Mycobacterium avium (atypical): rare, imm people
                              a. Clinical: f/nt, sweat, anorexia,  wt, diarrhea, abd
                                   pain, chylous ascites, severe GI hemorrhage, chronic
                                   gastric ulcer
                              b. CT: mesenteric lymphadenopathy
                              c. Endo: chronic ulceration, coarse/granular duodenal
                                   mucosa, fine white nodules—with scalloping of
                                   duodenal folds that look like celiac dz –inflammatory
                                   bowel dz of upper tract, esp 1st part of small intestine (
                                   present with ab pain, wt loss, and diarrhea) folds are
                                   smaller, less prominent and almost flat. Also see
                                   Giardia, a parasite causing this, too.
                              d. Histo: foamy histiocytes with acid fast bacilli
                      4. Actinomyces: endo: circumscribed and ulcerative gastric
                              a. Histo: gram + filamentous anaerobes
                      5. Syphilis:
                              a. Endo: numerous shallow, irregular ulcers with white
                                   exudates and surround erythema. Edematous gastric
                              b. Barium: strictures (hourglass stomach)
                              c. Histo: severe gastritis, dense plasma cell in lamina
                                   propria, varying number neutrophil/lymphocytes, gland
                                   destruction, vasculitis, granulomas

       C.     Fungi
              1. Candidiasis: not uncommon, imm pt
                      a. usu involves the esophagus, c/o dysphagia—difficulty
                          swallowing, and if very remarkable, odynophagia—
                          pain with swallowing
                      b. Endo: large ulceration with diffuse superficial
                          erosion—see membrane formation in posterior pharynx,
                          and down into esophagus with long linear radiating
                          membranes that are friable and will bleed; use brush to
                          check and do KOH prep, also biopsy
                      c. Histo: layer of necrotic fibrinoid
                      d. Radio: tiny aphthoid erosions, later deep linear ulcers
              2. Histoplasmosis: rare, very young elder, imm pt
                      a. Endo: hypertrophic/red gastric fold, mass mimics
                                                             gastric CA
                      b. Histo: increased macrophage with histoplasma
              3. Phycomyosis: rare and lethal, systemic signs and symptoms
                      a. malnutrition, imm pt, abx, acidosis
                      b. A) invasive, deep invasion stomach wall and bld vessel
                      c. B) noninvasive, superficial mucosa without
                          inflammation response
                      d. Histo: nonseptae 10-20 um hyphae branched at right
                          angles. Infiltration to blood vessel walls
      D.      Parasites
              1.      Cryptosporidiosis-rare, assoc. with AIDS
              2.      Stronyloidiasis-rare, dg by bx
              3.      Anisakiasis-raw marine fish, mild peripheral eosinophilia
      (think of drug interaction or allergy here or eruption or I
              intradermal/intramucosal parasitic infections), dx by biopsy
                      a.      Radio: notched-shadow defects
                      b.      Gross: multi-erosive foci with hemorrhage, 5-10
              mm lesions in stomach wall
                      c.      Histo: eosinophilic granulomatous inflamm process
IV.   Granulomatous Gastritis
      A.      Crohn’s – rare in stomach
              1. Clinical: n/v/epigastric pain/anorexia/ wt
                      a.      Radio: antral fold thickening, antral narrowing,
              deep or shallow ulcers
                      b.      Endo: reddened mucosa, irregular ulcers, erosions,
                              nodular ulcerated lesions, atypical cobblestone with
                              fissure like ulceration
                      c.      Histo: noncaseating granulomas, ulcers, transmural
                      chronic inflammatory and submural fibrosis

                       2.    Sarcoidosis: rare
                             a.      Clinical: 3-5th decade, epigastric pain, n/v, wt,
                                     occasional hemorrhage, may lead to obstruction
                                     achlorhydria, pernicious anemia
                             b.      Endo: narrow distal stomach with multiple
                      prepyloric ulcers, atrophy, thick/cobblestone looking folds
                             c.      Histo: noncaseating granulomas, mimic NSAIDs
       V.       Xanthrogranulomatous Gastritis: associated with xanthogranulomatous
                Histo: foamy histiocytes, inflammatory cells, multinucleated giant cells,
        VI.      Distinctive Forms of Gastritis
                 A.       Collagenous gastritis: rare, 7 reported
                          1.      Barium: mosaic-like pattern in body of stomach
                          2.      Endo: multiple, diffuse, scattered discrete submucosal
                 hemorrhages, erosive, nodularity over the greater curvature
                          3.      Histo: patch, chronic, superficial gastritis, focal atrophy,
                          focal deposition of collagen in subepithelial region of the lamina
                          propria. 4.      Increased plasma cells/intraepithelial lymphocytes
                 B.       Lymphocytic Gastritis: Atypical host response, seen often with
                          gastric lymphomas. Dense lymphocytic infiltration of surface and
                          pit gastric epithelium
                          1.      Clinical: with gluten free diet, decrease lymphocytic
                 gastritis in two years
                          2.      Endo: thick mucosal folds, nodularity, apthous erosions
                          3.      Histo: expansion of lamina propria by plasma cell
                                  infiltrate, lymphocyte and rare neutrophils. Antral and/or
                                  body mucosal surface and superficial pit epithelium with
                                  many T-lymphocytes with flattening of epithelium and loss
                                  of apical mucin secretion
Case of 38 y.o. female with upper quadrant ab pain with a negative work-up. Had
endoscopy done showing a > 5 cm ulcer (giant ulcer) Cytology and biopsied from edges
(not center because at center have exudates (dead cells, WBCs and debris and can bleed;
also at edge, is where is actively dividing) Put on PPI and returned in 4 weeks with no
change in ulcer appearance. Symptomatically better—less early satiety and no systemic
signs and sx. Did spiral CT, rebiopsy and cytology. Showed nothing. Increased dose of
PPI. Came back in 6 weeks with symptoms much better, but ulcer still same. Required
surgical excision. Lymphocytic gastritis/ Lymphomas can present in a number of ways
including a benign ulcer that does not heal properly. MALT type lymphomas have a high
association with H pylori. If put on H pylori regimen, the lesion will regress and get
better. Need to do repeat endoscopies, get oncology consult, do complete lymphoma
serology work-up to make sure there is nothing else occurring.
                 C.       Eosinophilic: Etio=unk.
                          1.      Classified according to layer of the GI tract involved
                                  a.       Mucosal: clinic: abd pain, n/v, diarrhea, wt loss,
                          anemia, protein loss enteropathy, intestinal perf, Fe def anemia

                               b.       Muscular: obstructive symptoms
                               c.       Subserosal: eosinophilic ascites
                       2.      Radio: thickened mucosal folds, nodularity, ulcerations
                       3.      Endo: normal appearing mucosa/hyperemic edematous
               mucosa with superficial erosions or prominent gastric folds
                       4.      Histo: eosinophilic infiltrates, eosinophilic pit abscess,
               necrosis with neutrophils, epithelial regeneration
        VII. Reactive Gastropathies (Acute Erosive Gastritis)
               A.      Spectrum of hemorrhages, erosions, ulcers, usually 1-2 mm in
               B.      Histo: erosion with necrosis to level of the muscularis mucosa.
                       Acute ulcers go beyond muscularis mucosa. Reactive epithelial
                       changes secondary to regeneration and foveolar hyperplasia with
                       atypical nuclei. Often missed dg of dysplasia or carcinoma
               C.      Causes…
                       1.      MEDS
                               a.       ASA/NSAIDs
                               b.       FE, oral potassium
                               c.       Chronic fluoride intake (endoscopic petechiae,
                       erosions, erythema
                               d.       Chemotherapy (reactive gastric epithelial atypia and
                       gastric ulcerations)
                       2.      EtOH: After drink, get subepithelial hemorrhages seen
                               with endoscopy (usually without inflammation on
                               microscope) higher risk with H. pylori chronic antral
                               gastritis. Increased effects with NSAIDs
                       3. Cocaine: Exudative erosion throughout gastric fundus, body,
                           antrum and duodenal bulb. Occasionally GI
                           hemorrhage/pyloric perforation—
had a pt with using this intranasally and binge drinking to take pain away with
anesthetic. Cocaine wore off after an hour and then alcohol started wearing off., had
pain again. Had a complete work-up including cardiac because use of these substances
is associated with a dilated cardiomyopathy (there are changes in myocardiocytes). The
pt’s echocardiogram showed a ejection fraction of 45% at the age 38-39. With severe
epigastric ab pain, suspected ischemic gastritis. On endoscopy, saw streaky red
changes—could be ischemia or other things. Did a deep biopsy, and saw ischemic
changes associated with binge drinking and concomitant cocaine use. Pt hospitalized for
a long time because also had chronic alcoholic pancreatitis. Developed full-blown
malabsorption from pancreatic dz and became a diabetic.
                       4.      Stress: Physical/thermal trauma, shock, sepsis, head injury
                       5.      Radiation: Increased radiosensitive cells are differentiated
               cells as the parietal and chief cells. Usually solitary lesions.
                       6.      Bile Reflux: s/p partial gastrectomy with anastamosis to
                               duodenum (Billroth I) or jejunum (II), truncal vagotomy
                               and pyloroplasty for peptic ulcers, cholecystectomies,

                               a.      Occasionally seen in people without sg hx
                               b.      Endo: swelling, redness, erosions, bile stain
                               d. Histo: foveolar hyperplasia, dilated cystic glands,
                                   atypical glands
                               e. Must do a ph study on pt. Careful about dx here. Show
                                   what is occurring and that nothing has helped and that
                                   dz is severe. Pt also should have microcytic,
                                   hypochromic anemia before is sent to a surgeon.
                      7.       Ischemia: atherosclerotic disease, or in athletes, long
                               distance runners may have recurrent ischemic gastropathy
                               and chronic GI bleed with anemia
                      8.       Bezoars
                      9.       Prolapsed Gastropathy: fall into esophagus secondary to
               retching/vomiting. Mechanical injury can lead to GI hemorrhage
                      10.      Hiatal Hernias: linear gastric erosions
                      11       Congestive Gastropathy: Portal HTN gastropathy
       VIII. Hyperplastic
               Associated with:
               Manetrier’s dz (hyperplastic, hypersecretory gastropathy)
               Zollinger-Ellison’s Syndrome
               Others: neoplasm, granulomatous dz, gastric varices, infections,
       eosinophilic gastritis, H. pylori
Feldman, et al. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease:
Pathophysiology/Diagnosis/Management (2 Volume Set) WB Saunders Co; 7th edition
(June 15, 2002) pp 810-827
Shaye, P ―Gastritis and PUD‖, last
updated 7/17/02


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