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Endo > GI path > Flashcards

GI path Flashcards

1
Q

Histo of normal esophagus

A
  • stratified nonkeratinizing squamous epithelium
  • proximal 1/3=striated muscle
    distal 2/3=smooth muscle
  • GE junction (where rugal folds begin)
  • Z-line (squamocolumnar junction): mucosal junction of squamous and columnar epithelium, may not correspond to GE junction when columnar metaplasia has occured
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2
Q

esophageal atresia and tracheoesophageal fistula

A

Def: Embryologic failure of tubal esophagus to connect mouth to stomach, ending in a blind pouch; fistula may connect segment to trachea

Clinical:

  • 50% have associated congenital anomalies–VATER syndrome (Vertebral defects, Anal atresia, TrachEoesophageal fistula, and Renal dysplasia)
  • Respiratory symptoms (aspiration pneumonia)

abnormal hedgehog signaling

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3
Q
A

normal gastroesophageal junction

stratified sqaumous of esophagus

simple columnar of gastric cardia

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4
Q

esophageal ring

A

Concentric, thin diaphragm of tissue in the distal esophagus, most commonly at GE junction (Schatzki’s ring

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5
Q

esophageal webs

A
  • Eccentric, thin membranes of tissue in the esophagus, most commonly proximal region
  • Plummer-Vinson syndrome: webs + iron deficiency anemia + glossitis; women; responds to iron supplementation
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6
Q

Esophageal diverticula

A

Outpouchings of the esophageal wall

  • True = all layers, including muscle
  • False = mucosa & submucosa only
  • Zenker’s diverticulum = false, cervical esophagus, elderly (motor dysfx)
  • Epiphrenic diverticulum = true, any age, just above diaphragm

Reflect underlying motor dysfunction

image=Zenker’s diverticulum

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7
Q

achalasia

def?

clinical?

microscopic?

A

Definition
Inability of the LES (lower esophageal sphincter) to relax after swallowing, resulting in periodic esophageal obstruction

Clinical
Dysphagia, odynophagia, regurgitation
inc. risk for squamous cell carcinoma

Microscopic Reduction or absence of myenteric ganglion cells

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8
Q

Symptoms: heartburn, acid regurg, dysphagia, globus sensation, chronic sore throat

Dx?

risk factors?

contributing factors?

A

Dx: GERD (Reflux of gastric acid into the esophagus with mucosal damage)

Risk Factors: Age, EtOH, tobacco (LES relaxation), chocolate

Contributing factors: hiatal hernia, weak LES, impaired esophageal peristalsis, delayed gastric emptying, inc gastric acid production

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9
Q
A

GERD

Hyperemia, vertical linear streaks represent superficial mucosal erosions/ulcers

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10
Q
A

GERD on bottom

squamous proliferation, papillae elongation, basal cell hyperplasia, inc. inflammation in lamina propria, decreased surface maturation

Note: biopsy findings are not specific! cannot make diagnosis w/ biopsy alone must have clinical info as well

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11
Q

Barrett’s esophagus

Def

A

Definition
Endoscopically recognizable columnar metaplasia of the esophageal mucosa that is confirmed pathologically to have intestinal metaplasia, the latter defined by goblet cells

Both the endoscopic and pathologic components should be present to establish BE.

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12
Q
A

Barrett’s esophagus: columnar metaplasia (intestinal metaplasia)+goblet cells

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13
Q
A

dysplasia in barrett’s

sequence of adenocarcinoma is metaplasia–>dysplasia–>carcinoma

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14
Q

Sx: dysphagia, food impaction

Hx: allergies, failed antireflux therapy

Tests: normal pH monitoring

Dx?

A

primary eosinophilic esophagitis (>15 eos/hpf from pts who lack a positive response to proton-pump inhibitors, have normal pH monitoring, or both)

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15
Q
A

herpes esophagitis

lateral margin of ulcer

cowdry A intranuclear inclusions (Multinucleation, chromatin Margination, nuclear Molding)

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16
Q
A

CMV esophagitis

  • Base of ulcer
  • Lg intranuclear inclusion with granular cytoplasmic inclusions
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17
Q
A

Candida esophagitis

  • Immunosuppressed, Diabetics, recent Abx
  • Pseudohyphae
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18
Q
A

esophageal varices: Dilatation of submucosal esophageal veins

most often due to portal hypertension secondary to cirrhosis

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19
Q
A
  • *Mallory-Weiss laceration**
  • at GE junction (usually on gastric side)
  • Forceful vomiting/retching forces prox stomach through diaphragm
  • Laceration may bleed profusely
  • Acute esophageal rupture –> Boerhaave’s syndrome
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20
Q
A

Fundus, body
Parietal (oxyntic) glands
Pink = parietal cell
Blue/purple = chief cell

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21
Q
A

Cardia and Antrum
Cardiac/antral glands
Mucus cells

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22
Q

Congenital hypertrophic pyloric stenosis

A
  • Concentric enlargement of the pyloric sphincter and narrowing of the pyloric canal that obstructs the gastric outlet
  • palpable epigastric mass (“olive”)

-M:F 4:1
Mostly Caucasian; rare in blacks & Asians

-Possible genetic as well as environmental (drugs, infection in utero) pathogenesis

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23
Q

gastritis:

acute vs chronic vs reactive

A

Acute gastritis
Erosive/hemorrhagic

Chronic gastritis
Autoimmune
H. pylori associated
Lymphocytic (see text)
Granulomatous (see text)
Eosinophilic (see text)
Collagenous (see text)

Reactive gastropathy
Chemical (see text)

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24
Q

Sx: abrupt onset abdominal pain and bleeding

Hx: alchohol use, NSAIDS

Dx?

Most common etiology?

Path findings?

Therapy?

A

Dx: Acute erosive/hemorrhagic gastritis (stress gastritis) (Abrupt onset of ab pain & bleeding a/w ETOH, NSAIDs, or low hemodynamic state following trauma)

Due to Breakdown of mucosal barrier (Direct irritant action, Drug mechanism of action, Hypoperfusion)

Most common etiologies: NSAIDS, post-op state

Gross: Petechiae, erosions, ulcers

Microscopic: Limited to mucosa: superficial lamina propria hemorrhage, mucosal sloughing/necrosis, neutrophils

Therapy: Acid-supression (histamine blockers, proton-pump inhibitors)

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25
Q

30yo female presents with fatigue and dyspepsia.

Labs: megaloblastic anemia, B12 deficiency, increased gastrin

Hx: SLE

Biopsy of body of stomach

Dx?

Path?

A

Dx: autoimmune gastritis (Immune-mediated form of chronic gastritis, results in loss of parietal cells, hypo- or achlorhydria, vit B12 deficiency)

Clinical: Autosomal dominant, <5% of chronic gastritis, Women, Pernicious anemia (megaloblastic anemia d/t ↓vit B12), Other autoimmune diseases

Labs: inc. gastrin, decreased vit B12

Path: Lymphoplasmacytic inflammation in deep, glandular lamina propria; limited to body/fundus

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26
Q
A

Fundic gland damage by patchy lymphocytic infiltrates
Loss of glands over time–> atrophy (atrophic gastritis)

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27
Q
A

autoimmune gastritis

*intestinal metaplasia is precursor to dysplasia and gastric carcinoma
*ECL cell hyperplasia is precursor to neuroendocrine tumors

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28
Q

Helicobacter pylori gastritis

def?

clinical?

A

Definition: Chronic antral-predominant gastritis caused by H. pylori

Clinical: A/w peptic ulcer disease (stomach & duodenum), gastric lymphoma & carcinoma

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29
Q
A

H. pylori gastritis

Lymphoplasmacytic inflammation admixed with neutrophils in superficial mucosa

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30
Q
A

Pititis, cryptitis, crypt abscesses (neutrophils = “activity”) due to H. pylori gastritis

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31
Q
A
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32
Q
A

H. pylori gastritis

Line epithelium in mucus layer
(do NOT invade, but secrete toxins)

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33
Q
A

Menetrier’s disease

Definition: Body & fundus-restricted hyperplasia of foveolar (mucous cell) epithelium with hypoproteinemia

Clinical: dec plasma proteins (albumin) from gastric mucosa, dec acid production

Pathogenesis: TFG-alpha overexpression

Gross: Markedly thickened rugal folds in fundus & body (resembling brain)

Microscopic: Foveolar (mucous cell) hyperplasia –>corkscrewing

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34
Q

histo features of normal small bowel mucosa

A

-villous height-to-crypt depth ratio of 3:1 to 5:1

-

-lamina propria contains mild physiologic mix of plasma cells, lymphocytes, and occasional eosinophils

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35
Q
A

Brunner’s glands are in the duodenum. They are in the submucosa

produce mucin rich alkaline (bicarbonate) secretion that protects duodenum from stomach acid and lubricates

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36
Q
A

normal terminal ileum w/ peyer’s patches

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37
Q

endoscopic findings celiac disease

A

scalloping and loss of folds

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38
Q

histologic features of celiac disease

A
  • increased intraepithelial lymphocytes with loss of so-called decrescendo pattern
  • blunted villi and crypt elongation
  • inc. plasma cells and lymphocytes in lamina propria (back is more “blue” and expanded from chronic inflammation)
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39
Q

Marsh classification

A

Used for classifying Celiac disease.

Most symptomatic celiac pts are Marsh3a-c.

classifies degree of villous blunting and crypt elongation

40
Q

serologic tests for Celiac Disease

A

1) Anti-tTG IgA: highly sensitive and specific. Best test!
2) Serium IgA levels simultaneously tested to exclude IgA deficiency which would give false negative

True gold standard diagnosis of CD is clinical/pathological response to gluten-free diet.

Other less good tests:

  • anti-endomysial IgA
  • Anti-gliadin (used to monitor response to gluten free diet)
41
Q

Genetics of Celiac Disease

A

almost all people w/ CD have MCH class II HLA-DQ2 or HLA-DQ8

absence makes diagnosis unlikely

but 20% of normal population have this, so not used for screening

42
Q

Other conditions besides Celiac that might have increased IEL and/or villous blunting

A
  • immune (common variable immunodeficiency, HIV entropathy, autoimmune disease)
  • Infection (H. pylori, cryptosporidium, bacterial overgrowth, )
  • NSAID injury

*NOTE: CVID mimics but has fewer plasma cells!

43
Q

Diseases assoc. with celiac disease

A
  • dermatitis herpetiform* (responds to GF diet)
  • lymphocytic collagenous colitis
  • lymphocytic gastritis
  • refractory sprue
  • collagenous sprue
  • enteropathy-assoc. T cell lymphoma*
  • small intestinal adenocarcinoma
44
Q
A
  • “test tubes in a rack” bases of crypts abut the muscularis mucosa
  • mild degree of chronic inflammation in lamina propria is normal (lymphocytes, plasma cells, eosinophils, mast cells)
45
Q
A

characteristic triangular folds of the colon

46
Q

microscopic colitis

A

lymphocytic and collagenous colitis

pts have chronic watery (non-bloody) diarrhea and normal endoscopy

middle aged-elderly

assoc. with certain drugs (long-term NSAIDS) and celiac disease

47
Q

lymphocytic vs collagenous colitis

A

Lymphocytic colitis:

  • *F:M ratio of 3:1
  • *increased IEL
  • no inc. subepithelial collagen
  • inc. lymphocytes, plasma cells and eosinophils in LP
  • no architectural changes

Collagenous colitis:

  • *F:M of 8:1
  • *increased IEL
  • *thickened subepithelial collagen
  • inc. lymphocytes, plasma cells and eosinophils in LP
  • no architectural changes
48
Q

Inflammatory bowel diseases (3)

A

1) Ulcerative colitis
2) Crohn’s disease
3) Intermittent colitis

49
Q

Gross pathology of IBD

A

active disease: erythematous, friable, edematous, ahaustral w/ or w/o ulcerations, pseudopolyps, cobblestoning

*biopsy alone can’t distinguish b/t Crohn or UC

50
Q

Pathologic findings in UC

A

-distribution: continuous colonic involvement of mucosa beginning in rectum

Gross findings:

  • inflammatory polyps
  • lead pipe colon (loss of haustral folds)
  • toxic megacolon

Microscopic changes: limited to mucosa

51
Q

Pathologic findings in Crohn’s disease

A
  • distribution: rectum usually spared, skip lesions, patchy disease both grossly and microscopically, disease can affect any part of columnar GI tract (classically terminal ileum)
  • Gross findings:
  • Long linear (bear claw-like) ulcers
  • cobblestone mucosa
  • creeping fat (mesenteric fat wrapping around serosal surface)
  • strictures (muscularis hypertrophy and hyperplasia)

Microscopic changes:

  • inflammatory change involving entire wall of bowel (Vs UC only in mucosa)
  • “transmural inflammation”: chronic inflammation and lymphoid aggregates
  • knife-like fissures
  • granulomata
  • combing fat
52
Q

Mucosal changes in IBD

chronicity

activity

A

chronicity:

  • architectural distortion
  • metaplasia
  • paneth cell metaplasia of left colon
  • pyloric metaplasia (terminal ileum in Crohn disease)

-muscularis hypertrophy and hyperplasia

**Activity: **how much acute inflammation

  • cryptitis: neutrophils in epithelium
  • crypt abscess: collection of neutrophils in lumen of a crypt
53
Q

chronicity in Crohn disease

A
  • architectural distortion (villous blunting)
  • pyloric metaplasia
  • muscularis hypertrophy and hyperplasia (both muscularis mucosa and muscularis propria)
54
Q

Acute self-limited colitis

A
  • typically transient (2-4wks) colitis w/ diarrhea (sometimes bloody)
  • most commonly assoc. w/ bacterial enterocolitis, can be viral or parasitic
  • usually not biopsied but when done: biopsy has acute inflammation but no features of chronicity (distinguish from IBD, no architectural distortion, no paneth cell metaplasia, no MM hypertrophy)
55
Q

C. difficile colitis

A
  • related to previous antibiotic exposure
  • “pseudomembranous colitis”:
  • not diagnostic: DDx includes C. diff and ischemia
  • PCR for C. diff toxins
  • pseudomembranes composed of fibrin, mucin and neutrophils. glands typically lose epithelial cells (C. diff toxin affects cell adhesion)
56
Q

Strictures in bowel

DDx?

A
  • chronic ischemia (d/t fibrosis)
  • crohn disease (d/t muscularis mucosae and propria hypertrophy and hyperplasia)
  • tumor
  • recurrent bouts diverticulitis
57
Q
A

celiac disease

tip of villi w/ inc. IEL. architecture preserved so Marsh 1 lesion

IEL are dark blue dots, enterocytes are lighter and more elongated

58
Q
A

celiac disease

small intestine is severely blunted so it looks completely flat

59
Q
A

common variable immune deficiency mimics celiac diseae (but no plasma cells)

60
Q
A

cryptosporidium mimics celiac disease

61
Q
A

lymphocytic colitis. lamina propria filled with chronic inflammatory cells. No crypt distortion. No thickened subepithelial collagen band

62
Q
A

lymphocytic colitis with surface damage (mucin depletion and reactive changes)

63
Q
A

collagenous colitis. pink collagen bands under surface. No architectural distortion.

64
Q
A

collagenous colitis. capilarries are entrapped in thickened subepithelial collagen band. lots of chronic inflammation in lamina propria and mildly inc. IEL and eosinophils.

65
Q
A

IBD w/ features of chronicity.

cyrpts have lifted off muscularis mucosa and are bifurcated–>architectural distortion

Muscularis mucosae is thickened (MM hypertophy and hyerplasia)

66
Q
A

terminal ileum w/ pyloric metaplasia

Pyloric metaplasia is feature of chronicity. glands look like pyloric glands of gastric antrum/cardia. pale/neutral in color w/ well-definied borders b/t cells

pyloric metaplasia classically occurs in terminal ileum in Crohn disease

Paneth cell metaplasia may rarely be seen in “backwash ileitis” of severe ulcerative colitis

67
Q
A

activity (acute inflammaiton) w/ cryptitis and crypt abscess seen in acute self-limited colitis.

neutrophils have faint pink cytoplasmic halo

68
Q
A

crohn disease: transmural inflammation with lymphoid aggregates

69
Q
A

granuloma in crohn disease

70
Q
A

combing fat crohns disease (mesenteric fat extends to serosal surface)

71
Q
A

acute self-limited colitis.

No features of chronicity (no architectural distortion, no paneth cell metaplasia, no MM hypertorohy) to distinguish from IBD. Presence of chronic infammatory cells is not a feature of chronicity

correlate w/ stool culture to exclude infection

72
Q
A

C. diff colitis

clue: epithelial cells fall of into lumen (due to C. diff toxin)

Gross path: pseudomembranes (fibrin, mucin, neutrophils)

73
Q
A

ischemia involving mucosa: hyalinization of lamina propria (pink), withered cypts, hemorrhage

best way to asses hemorrhage is presence of hemosiderin laden macrophages!

74
Q
A

pseudomembranes (fibrin, inflammatory cells) in ischemia

75
Q
A

chronic ischmiea w/ inc. fibrosis (trichrome stain)

76
Q

congenital anamolies of pancreas

A

o Accessory (ectopic pancreas): pancreatic tissue outside it’s normal location (often in stomach, small intestine, meckel’s diverticulum)

o Annular pancreas: abnormal ring of pancreas that encircles the duodenum; assoc w/ down’s syndrome

o Pancreas divisum: failure of dorsal and ventral buds/ducts to fuse leading to retention of 2 separate duct systems; duct of santorinin provides main drainagel may cause acute pancreatitis

77
Q

acute pancreatitis

common etiology

histo

A

Common etiologies: alcoholism, gallstones, mumps

Hist:

  • Edema by microvascular leakage
  • Fat necrosis by lipolytic enzymes (saponification)
  • Acute inflammation (neutrophils)
  • Proteolytic destruction of pancreatic parenchyma
  • Destruction of blood vessels and subsequent interstitial hemorrhage
78
Q

acute hemorrhagic pancreatitis

A

o Abrupt onset following heavy meal/alcohol

o Extensive tissue destruction w/ circulatory collapse and shock

o Elevated serum amylase and lipase

o 50% mortality

o may develop pseudocyst

79
Q

chronic pancreatitis

A

o Recurrent, progressive pancreatic tissue destruction

o Alcohol abuse is major cause

o Chronic inflammation, fibrosis, calcification

o Pancreatic insufficiency w/ malabsorption and/or diabetes

o 3-4% mortality/year

80
Q

autoimmune pancreatitis

A

o 40s-60s

o assoc. w/ autoimmune conditions (PSC, Sjogren)

o some w/ multifocal inflammatory fibrosclerosis (Reidel thyroiditis, orbital pseudotumor, mediastinal and retroperitoneal fibrosis)

o mimics pancreatic carcinoma both clinically (obstructive jaundice) and radiologically (mass-like lesion)—“sausage-like” appearance on imaging

o elevated serum IgG4

o respond well to steroids

o Histo:
• Dense “duct-centric” inflammation of predominantly lymphoplasmacytic cells and expansion of periductal fibrous tissue
• Periphlebitis and obliterative venulitis common
• Interstitial fibroblastic proliferaion w/ storiform architecture
• IgG4+ plasma cells

81
Q

hereditary pancreatitis

A

o AD, mutations in PRSS1 and SPINK1 result in autoactivation of trysinogen

o Same features of chronic pancreatitis except earlier age onset, less pancreatic calicification, and DM

o 40% develop pancreatic ductal adenocarcinoma

82
Q

pancreatic ductal adenocarcinoma

A

o Most lethal solid tumor; Highest incidence after age 60

o Risks: smoking, chemical exposure, high meat/fat diet, diabetes, chronic pancreatitis

o KRAS activating mutations; Tumor suppressor mutations in p16, TP53, SMAD4

o Precursor to cancer: pancreatic intraepithelial neoplasia

o Sx:
• Anorexia, wt loss
• Abdominal/back pain
• Jaundice
• Migratory thrombophlebitis (troussea’s sign)—hypercoagulability and tendency to venous thrombosis

o Derived from ductal cells; spreads by lymphatics and along nerves

o 5 year survival=5% (only 20% are surgical candidates)

o Gross: firm, gray poorly demarcated mass. Invasion of peripancreatic tissue and local structures common

o Microscopic: >75% are well-moderately differentiated, prominent desmoplastic rxn, perineural invasion

83
Q

pancreatoblastoma

A

o Children!
o Micro: acini and sqaumoid corpuscle
o 1/3 lymphn node/hepatic mets

84
Q

pancreatic neuroendocrine neoplasms

A

o Derived from islet cells; non-functional or functional; M & F equally; ages 30-60; MEN1 syndrome

o Insulinoma (Beta-cell tumors): most common islet cell tumor
• Excess secretion of insulin→hypoglycemia, sweating, nervousness, hunger, confusion, lethargy
• Most are benign, solitary, small
• Uniform nests of cells, richly vascular, amyloid deposition

o Gastrinoma: G cell tumor secretes excess gastrin
• Zollinger-Ellison Syndrome (intractable gastric hypersecretion, peptic ulceration, and elevated blood gastrin levels)

85
Q

serous cystadenoma

A

o Female predominance; pts with VHL at inc. risk
o Always benign, surgery is curative
o Composed of glycogen-rich cuboidal cells surrounding small (1 to 3 mm) cysts containing clear, thin, straw-colored fluid

86
Q

mucinous cystic neoplasm

A

o Women
o Body or tail pancreas
o Painless, slow growing mass
o 1/3 assoc. w/ invasive carcinoma
o The cysts are lined by columnar mucinous epithelium, and a dense ovarian-type stroma
o Not involving the major pancreatic duct

87
Q

intraductal papillary mucinous neoplasm

A

o Precursor to PDA
o Men
o Multifocal
o Can involve man pancreatic duct
o Lack ovarian type stroma

88
Q

solid pseudopapillary neoplasm

A

o Low grade malignant neoplasm, 15% get mets
o Women in 20s
o Sx: intra-abdominal mass, palpable on exam
o Activating Mutation in beta-catenin
o cystic areas filled w/ hemorrhagic debris,
o Histo: cells as solid sheets, pseudopapillary,

89
Q

cholelithiasis

A

o Gallstones in gallbladder or extrahepatic biliary tree
o Asymptomatic but may present w/ pain (biliary colic) if in cystic or common bile duct and fatty food intolerance

90
Q

cholesterol stones

A

o Yellow-tan; cholesterol calcium salts, mucin; radiolucent

o Risks: women of reproductive age, inc. age, obesity, ethnicity, diet, metabolic abnormalities, drugs

o Contributing factors (4)
• Hypersaturaiton of bile w/ cholesterol
• Gallbladder hypomotility
• Crystal nucleation accelerated
• Hypersecretion of mucus in gallbladder traps crystals leading to aggregation

91
Q

black pigment gallstones

A

o calcium bilirubinate, calcium salts, mucin; radioopaque

• Inc. conc. of unconjugated bilirubin in bile—chronic hemolysis, cirrhosis

92
Q

brown pigment stones

A

calcium bilirubinate, cholesterol, calcium salts, fatty acids; radiolucent

  • Bacterial cholangitis (E. coli), biliary heminthic infection, mechanical obstruction of bile flow (PSC)
  • More often found in bile ducts than gallbladder itself
93
Q

acute cholecystitis

A

o Diffuse inflammation of gallbladder 2/2 obstruction

o 95% assoc. w/ gallstones

o Acalculus cholecystitis: sepsis, severe trauma, polyarteritis nodosa, salmonella infection

o Gross:
• Gallbladder enlarged and tense; bright red or blotchy, violaceous to green-black discoloration, imparted by subserosal hemorrhages
• serosal covering is frequently layered by fibrin and, in severe cases, by suppurative exudate
• lumen may contain stones, is filled with a cloudy or turbid bile that may contain large amounts of fibrin, pus, and hemorrhage
• wall is thickened, edematous, and hyperemic.
• Perforation (bile peritonitis)

o Microscopic:
• Acute inflammation and edema
• Hemorrhage of the gallbladder wall
• Mucosal ulceration or widespread necrosis (gangrenous cholecystitis)

94
Q

chronic cholecystitis

A

o Persistent inflammation of gallbladder

o >90% associated with gallstones

o Gallbladder has thickened and fibrotic wall

o Rokitansky-Aschoff sinuses

o Gross:
• Wall is thick and firm 2/2 extensive fibrosis
• Gallstones in lumen
• Mucosa ulcerated and atrophic or intact

o Microscopic:
• Wall is fibrotic w/ prominent R-A sinuses
• Chronic inflammatory infiltrate
• Long standing inflammation→calcification (porcelain gallbladder; inc. risk cancer)

95
Q

Cholesterolosis

A

accumulation of cholesterol-laden macrophages in submucosa of gallbladder

o Gross: prominent scattered yellow flecks, strawberry gallbladder

96
Q

gallbladder adenocarcinoma

A

• Carcinoma: adenocarcinoma of gallbladder assoc. w/ cholelithiasis and chronic cholecystitis

o F>M

o >50yo

o RUQ abdominal pain, anorexia

o Metastatic disease

o Gross: diffuse wall thickening or polypoid growth

o Histo: adnocarcinoma w/ varying degrees of differentiation

Endo (7 decks)

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