Git pathology m scyear2011 12

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  • For as notoriously complex as all this sounds, they look like boring leiomyomas, and in the days PRE-immunochemistry, they probably WERE called smooth muscle tumors.
  • Git pathology m scyear2011 12

    1. 1. GASTROINTESTINAL TRACTDr. Jalal A. JalalDept. of PathologyCollege of Medicine-HMU
    2. 2.  Oral cavity Salivary glands Esophagus Stomach Small bowel Large bowel Appendix2
    3. 3. I.DISEASES OF THE ORAL CAVITY A. Inflammatory disorders Herpes labialis (fever blisters, cold sores): is a common vesicular lesion caused by herpes simplex virus (HSV),most often type 1 (HSV-1). It tends to recur, with activation by febrile illness, trauma, sunshine, or menstruation. Aphthous stomatitis is characterized by painful, recurrent, erosive oral ulcerations. Oral candidiasis (thrush, moniliasis): is a local white, membranous lesion caused by Candida albicans. It occurs most commonly in debilitated infants and children,immunocompromised patients, and individuals with diabetes.3
    4. 4. B. TUMORS AND TUMOR-LIKECONDITIONS Benign tumors of the oral mucosa Papilloma is the most common benign epithelial tumor of theoral mucosa. It can occur anywhere in the mouth; the mostcommon sites are the tongue, lips, gingivae, or buccalmucosa. Fibroma is most often a non-neoplastic hyperplastic lesionresulting from chronic irritation. Hemangioma occurs most commonly on the tongue, lips, orbuccal mucosa. Epulis refers to a benign (usually non-neoplastic) growth ofthe gingivae. It is most often a reparative growth rather than atrue neoplasm.4
    5. 5. LEUKOPLAKIA AND ERYTHROPLAKIA Leukoplakia Leukoplakia refers to any whitish mucosal patch or plaquecaused by epithelial thickening. Microscopically, leukoplakias show a range of changes, varyingfrom hyperkeratosis with or without epithelial dysplasia tocarcinoma in situ. About 3 to 25% of leukoplakias can progress to invasive cancer.5
    6. 6. 6
    7. 7. 7
    8. 8.  Erythroplakia refers to red, velvety, often granular, circumscribedareas that may or may not be elevated, having poorlydefined, irregular boundaries. Histologically, erythroplakia almost invariably revealsmarked epithelial dysplasia (the malignanttransformation rate is >50%), So recognition of this lesion becomes even moreimportant than identification of oral leukoplakia.8
    9. 9. CANCERS OF THE ORAL CAVITY ANDTONGUE Most frequently squamous cell carcinoma.o The three predominant sites of origin of oral cavitycarcinomas are (in order of frequency) :(1) Lower lip.(2) Floor of the mouth.(3) Lateral borders of the tongue.9
    10. 10. RISK FACTORS FOR ORAL CANCERFactor CommentsLeukoplakia, erythroplakia Risk of transformation in leukoplakia 3% to25%More than 50% risk in erythroplakiaTobacco use Best-established influence.Human papillomavirus types 16 and18Identified by molecular probes in 30% to50% of cases; probably have a role in asubset of casesAlcohol abuse Weaker influence than tobacco use, but thetwo habits interact to greatly increase riskProtracted irritation Weakly associated10
    11. 11. 11
    12. 12. 12
    13. 13.  What is the relationship between location and prognosisfor cancers of the oral cavity? The prognosis is best for carcinomas of the lip andpoorest for carcinomas of the floor of the mouth and thebase of the tongue13
    14. 14. II. DISEASES OF THE SALIVARY GLANDS A. Sialadenitis. inflammation of the salivary glands may be caused by infection,immune-mediated mechanisms, or occlusion of the salivary ductsby stones (sialolithiasis). B. Acute parotitis: This condition occurs in mumps, but may also be caused by otherinfectious agents. Although childhood mumps is self-limited and rarely createsresidual problems, mumps in adults may be accompanied bypancreatitis or orchitis; the latter sometimes causes permanentsterility.14
    15. 15.  C.Chronic sialadenitis : arises from decreased production of saliva with subsequentinflammation. The dominant cause is autoimmune sialadenitis, whichis almost invariably bilateral. This is seen in Sjögren syndrome. This condition is most likely of autoimmune origin. Characteristics include keratoconjunctivitis sicca (dry eyes),xerostomia (dry mouth), and an associated connective tissue disease,most often rheumatoid arthritis. Sjögren syndrome is associated with an increased incidence ofmalignant lymphoma15
    16. 16.  D. Mucocele. This cyst-like pool of mucus, lined by granulation tissue, developsnear a minor salivary gland. It results from mucous leakage caused byrupture of obstructed or traumatized ducts. E. Ranula. This is a large mucocele, of salivary gland origin, characteristicallylocalized to the floor of the mouth.16
    17. 17. F. TUMORS OF THE SALIVARY GLAND The majority of salivary gland tumors occur in the parotid gland. The majority of tumors of the parotid gland are benign. In contrast, about half of the tumors of the sub maxillary gland aremalignant. Whatever the type, they present clinically as a mass causing a swellingat the angle of the jaw.17
    18. 18. PLEOMORPHIC ADENOMA (MIXEDTUMOR) is the most frequently occurring salivary gland tumor. It occurs withgreatest frequency in women between 20 and 40 years of age This is a benign tumor that frequently recurs; it rarely becomesmalignant. It has been called "mixed tumor" because of the presence of myxoidand cartilage-like elements, as well as epithelial cells.18
    19. 19. 19
    20. 20. Histologically, pleomorphic adenomas demonstrate irregularmasses or anastomosing strands of stellate or fusiform epithelialcells, some forming ducts or tubules, all of which are embeddedin a myxoid stroma that may display fibrous, cartilage-like, orhyalinized areas.The tumor is most often localized to the parotid gland (~90%).Usually, the tumor presents as a firm, nontender swelling.Often, the tumor is difficult to remove completely because of itsproximity to the facial nerve, and it is likely to recur afterresection.20
    21. 21. 21
    22. 22.  Other salivary gland tumors Papillary cystadenoma lymphomatosum (Warthin tumor):benign tumor composed of epithelial cells and dense lymphoidtissue. Mucoepidermoid carcinoma: most common malignant salivary gland tumor. Adenoid cystic carcinoma22
    23. 23. SALIVARY GLAND TUMORS: LOCATION,HISTOLOGY, AND CHARACTERISTICSType Typical Location HistologyPleomorphic adenoma(mixed tumor)Parotid gland Variable mixture of epithelial andmesenchyme-like elementsPapillary cystadenomalymphomatosum(Warthin tumor,adenolymphoma)Parotid gland Cystic spaces lined by double-layered eosinophilicepithelium, all embedded inlymphoid stroma23
    24. 24. Type Typical Location HistologyMucoepidermoidcarcinomaParotid gland Comprised of mucus-producingand epidermoid componentsand cells intermediatebetween the twoAdenoid cysticcarcinomaMinor salivary glands Variable; most characteristicappearance consists ofcribriform pattern with massesof small, dark-staining cellsarrayed around cystic spaces24
    25. 25. III. DISEASES OF THE ESOPHAGUS Tracheoesophageal fistula. Esophageal diverticula Achalasia Hiatal Hernia Esophageal varices Inflammatory and related disorders of the esophagus EsophagusTumors25
    26. 26. SYMPTOMS OF ESOPHAGEALDISORDERS Dysphagia (difficulty in swallowing),which is attributed either to deranged esophageal motorfunction or to narrowing or obstruction of the lumen.o Heartburn (retrosternal burning pain) usually reflectsregurgitation of gastric contents into the loweresophagus.o Less commonly, hematemesis (vomiting of blood) andmelena (blood in the stools) are evidence of severeinflammation, ulceration, or laceration of the esophagealmucosa.o Massive hematemesis may reflect life-threateningrupture of esophageal varices.26
    27. 27. NORMAL ANATOMY Extends from C6 to T11 or T12 Length 25 cm in adult (on average) Three points of luminal narrowing:1. Cricoid cartilage2. Where left mainstem bronchus crosses anterior to theesophagus (midway down)3. Diaphragm Upper and lower sphincters defined manometrically; nomophological landmarks Outer longitudinal muscle layer is striated for the first 6-8 cm No serosa - lesions can easily spread into mediastinum27
    28. 28. HISTOLOGY28
    29. 29. CONGENITAL ANOMALIES A. Tracheoesophageal fistula. This congenital disorder is suggested in a newborn bycopious salivation associated with choking, coughing,and cyanosis on attempts at food intake. It occurs inthree distinct variants: In the most common variant (90%), the lower portionof the esophagus communicates with the trachea near thetracheal bifurcation. The upper esophagus ends in a blindpouch (esophageal atresia). Maternal polyhydramnios(increased amniotic fluid) is a frequently associatedabnormality.29
    30. 30. TRACHEOESOPHAGEAL FISTULA The second most common variant is characterized by a fistulousconnection between the upper esophagus and the trachea; the loweresophageal segment is not connected to the upper esophagus. In a third variant, there is a fistulous connection between the tracheaand a completely patent esophagus.30123
    31. 31. B. ESOPHAGEAL DIVERTICULA are pouches lined by one or more layers of the esophageal wall. Most commonly, false (pulsion) diverticula result from herniation ofthe mucosa through defects in the muscular layer. Less commonly, true (traction) diverticula consist of mucosal,muscular, and serosal layers. Traction diverticula result from periesophageal inflammation andscarring. Esophageal diverticula occur in three characteristic locations:Immediately above the upper esophageal sphincter (Zenkerdiverticulum).Near the midpoint of the esophagus.Immediately above the lower esophageal sphincter (epiphrenicdiverticulum).31
    32. 32. C. ACHALASIA The term achalasia means "failure to relax," and here denotesincomplete relaxation of the lower esophageal sphincter in responseto swallowing. This produces functional obstruction of the esophagus, withconsequent dilation of the more proximal esophagus. The condition is caused by a loss of ganglion cells in the myentericplexus, which leads to the progressive dilation of the esophagus.32
    33. 33. ACHALASIA One important source (principally in South America) is Trypanosomacruzi infection in Chagas disease. In other cases, ganglion cells are lost for reasons that are not known. Clinical characteristics include difficulty in swallowing. Achalasia can lead to esophageal squamous cell carcinoma in about5% of subjects.33
    34. 34. HIATAL HERNIA Sac-like dilatation of stomach present above the diaphragm1. Sliding Hernia (90%) Congenitally short esophagus or acquired from esophagealscarring induced with traction on the stomach Predisposes to reflux.2. Rolling (Paraesophageal) Hernia (10%) Portion of cardia protrudes through the diaphragm into thethorax along side the esophagus Vulnerable to strangulation and infarction35
    35. 35. E. ESOPHAGEAL VARICES These dilated submucosal esophageal veins that occur secondary toportal hypertension can result in upper gastrointestinal hemorrhage. The other important causes of upper gastrointestinal hemorrhage are bleeding peptic ulcer Mallory-Weiss syndrome,36
    36. 36. F. INFLAMMATORY AND RELATEDDISORDERS OF THE ESOPHAGUS Gastroesophageal reflux disease (GERD) is reflux of gastric acid contents into the esophagus. Characteristic manifestations often include substernal pain (heartburn)relieved by antacids.o Most commonly, associated conditions include: hiatal hernia incompetent lower esophageal sphincter. excessive use of alcohol tobacco increased gastric volume, pregnancy, scleroderma. Assuming a recumbent position.37
    37. 37. REFLUX/GERD• Morphology:• Inflammatory Cells– Eosinophils– Neutrophils– Lymphocytes• Basal zone hyperplasia• Lamina Propria papillae elongated and congested38
    38. 38. REFLUX/GERD39
    39. 39. GASTROESOPHAGEAL REFLUX What are the major complications of reflux esophagitis?(a) ulcer;(b) bleeding;(c) development of stricture;(d) development of Barrett esophagus.40
    40. 40. BARRETT ESOPHAGUS Is columnar metaplasia of esophageal squamous epithelium; thecolumnar epithelium is often of the intestinal (specialized) type withprominent goblet cells. Occurring in as many as 5% to 15% of persons with persistentsymptomatic reflux disease. Barrett esophagus affects males more often than females (ratio of 4:1)and is much more common in whites than in other races This condition is a complication of long-standing gastroesophagealreflux and is a well-known precursor of esophagealadenocarcinoma.41
    41. 41. BARRETT ESOPHAGUS IS APPARENT AS A SALMON-PINK, VELVETYMUCOSA BETWEEN THE SMOOTH, PALE-PINK ESOPHAGEALSQUAMOUS MUCOSA AND THE MORE LUSH LIGHT BROWN GASTRICMUCOSA42
    42. 42. 43
    43. 43. OTHER CAUSES OF ESOPHAGITIS Candida esophagitis (moniliasis) Associated conditions often include: antibiotic use, diabetes mellitus, malignant disease, immunodeficiency caused by AIDS or immunosuppressive drugs. Herpetic esophagitis is caused by HSV-1 infection. Characteristics include painful, difficult swallowing. Less common forms of esophagitis : cytomegalovirus (CMV) infection, uremia, radiation therapy, 44
    44. 44. G. Esophagus Tumors1. Leiomyoma Most common benign tumor of esophagus arising from Smooth muscle cells2. Squamous cell carcinoma Incidence: common in China, Rare in US (Adenocarcinoma – MC in USA)M>F, age >50 yr. “Early carcinoma” = upto submucosa ( 90%- 5 year survival goodprognoses even though lymph nodes are involved) Spreads locally into mediastinal structures & to lymph nodes Clinically: Insidious dysphagia, weight loss, anemia. Overall 5-year-survival is 5%.45
    45. 45. Risk Factors for Squamous Cell Carcinoma of the EsophagusEsophageal DisordersLong-standing esophagitisAchalasiaPlummer-Vinson syndrome (esophageal webs, microcytic hypochromic anemia,atrophic glossitis)Life-styleAlcohol consumptionTobacco abuseDietaryDeficiency of vitamins (A, C, riboflavin, thiamine, pyridoxine)Deficiency of trace metals (zinc, molybdenum)Fungal contamination of foodstuffsHigh content of nitrites/nitrosaminesGenetic PredispositionTylosis (hyperkeratosis of palms and soles)46
    46. 46. MORPHOLOGY Squamous cell carcinomas are usually preceded by a longprodrome of mucosal epithelial dysplasia followed bycarcinoma in situ and, ultimately, by the emergence ofinvasive cancer. In months to years, these lesions become tumorous, taking oneof three forms:(1) polypoid exophytic masses that protrude into the lumen.(2) necrotizing cancerous ulcerations that extend deeply andsometimes erode into the respiratory tree, aorta, or elsewhere(3) diffuse infiltrative neoplasms that cause thickening andrigidity of the wall and narrowing of the lumen.o About 20% arise in the upper third of esophagus, 50% in themiddle third, and 30% in the lower third. 47
    47. 47. ESOPHAGUSSQUAMOUS CELL CARCINOMA48
    48. 48. Esophagus Tumors3. Esophageal adenocarcinoma Incidence: 25% of esophageal cancers world wide up to half of all esophageal cancers reported in US Primary risk factor - Barrett’s esophagus Most arise in distal 1/3rd of the esophagus. Histology: Mucin producing adenocarcinoma. present with dysphagia Overall 5-year survival - 15%49
    49. 49. 50
    50. 50. ESOPHAGUSMALIGNANT TUMORSFeature Squamous AdenoIncidence 75% 25%Geography Asia USAAge >50 >40Site Middle1/3 rd Lower 1/3rdRisk factors Smoking,alcohol, foodsReflux Esophagitis(Barretts)Prognosis 5yr.-5% 5yr.-15%51
    51. 51. IV. DISEASES OF THE STOMACH Congenital pyloric stenosis Gastritis: Acute, Chronic Peptic ulcer of the stomach Tumors of the stomach52
    52. 52.  The stomach is divided into four major anatomicregions: the cardia, fundus, body, and antrum. The cardia and antrum are lined mainly by mucin-secreting foveolar cells that form small glands. The antral glands are similar but also contain endocrinecells, such as G cells, that release gastrin to stimulateluminal acid secretion by parietal cells within the gastricfundus and body. The well-developed glands of the body and fundus alsocontain chief cells that produce and secrete digestiveenzymes such as pepsin.53
    53. 53. 54
    54. 54.  A. Congenital pyloric stenosis This stenosis is caused by hypertrophy of the circularmuscular layer of the pylorus, often leading to apalpable mass. The resulting obstruction of the gastric outlet causesepisodes of projectile vomiting beginning in the first 2weeks of life. This condition is much more common inboys. The condition is corrected by surgical incision of thehypertrophied muscle55
    55. 55. B. GASTRITIS Acute (erosive) gastritis CausesNonsteroidal anti-inflammatory drugs (NSAIDs)Cigarette smokingHeavy alcohol intakeBurn injury; Curling ulcer, an acute gastric ulcer inassociation with severe burnsBrain injury; Cushing ulcer, an acute gastric ulcerin association with brain injury56
    56. 56. ACUTE (EROSIVE) GASTRITIS CharacteristicsFocal damage to the gastric mucosa, withacute inflammation, necrosis, andhemorrhageManifested as acute gastric ulcers, which areoften multiple57
    57. 57. CHRONIC GASTRITIS is characterized by chronic mucosal inflammation and atrophy of themucosal glands.A. Autoimmune gastritis: is associated with: Presence of antibodies to parietal cells (and sometimes to intrinsic factor) Achlorhydria (lack of gastric acid secretion) pernicious anemia Autoimmune diseases, such as Autoimmune thyroiditis and Addison disease. It is also associated with aging, partial gastrectomy, gastric ulcer, and gastriccarcinoma.58
    58. 58. B. Helicobacter pylori–associated gastritisis the most common form of chronic gastritis.There is no association with pernicious anemia, antibodies toparietal cells, or reduced gastric acid secretion.Often, increased gastric acid secretion occurs.H. pylori is also strongly associated with gastric and duodenalpeptic ulcerIs a high suspect in the causality of carcinoma of the stomach andgastric lymphoma of the mucosa-associated lymphoid tissue(MALT) type.59
    59. 59. H. PYLORI GASTRITIS - SILVERSTAINBacteria overepithelial cells60
    60. 60. H. pylori–Associated AutoimmuneLocation Antrum BodyInflammatory infiltrate Neutrophils, subepithelialplasma cellsLymphocytes, macrophagesAcid production Increased to slightly decreased DecreasedGastrin Normal to decreased IncreasedOther lesions Hyperplastic/inflammatorypolypsNeuroendocrine hyperplasiaSerology Antibodies to H. pylori Antibodies to parietal cellsSequelae Peptic ulcer, adenocarcinoma Atrophy, pernicious anemia,adenocarcinoma, carcinoidtumorAssociations Low socioeconomic status,poverty, residence in ruralareasAutoimmune disease;thyroiditis, diabetes mellitus,Graves disease61
    61. 61. C. PEPTIC ULCER OF THE STOMACH Most often, the stomach ulcer occurs at or near the lessercurvature, in the antral and prepyloric regions. The ulcer is not a precursor lesion of carcinoma of thestomach. Unlike peptic ulcer that occurs elsewhere, peptic ulcer ofthe stomach is not dependent on increased gastric acidsecretion; however, acid and pepsin are believed to playa role, because gastric peptic ulcers rarely occur inassociation with absolute achlorhydria.62
    62. 62.  Postulated etiopathogenic mechanisms of gastric pepticulcer production include: H. pylori–mediated processes, in which bacterial ureases andproteases break down glycoproteins in gastric mucus, thusinterfering with epithelial protection Increased permeability of the gastric mucosa to hydrogen ion,resulting in back diffusion of hydrogen ion with injury to thegastric mucosa Bile-induced gastritis leading to gastric ulceration63
    63. 63. 64
    64. 64. BENIGN, CHRONIC, GASTRIC PEPTICULCERSharp edges, converging folds of mucosa in the upper half. The ulcer bed is covered by fibrinopurulent exudate.65
    65. 65. 66
    66. 66. ESOPHAGEAL LACERATIONS (MALLORY-WEISS SYNDROME)67oLongitudinal tears at the gastroesophageal junctionoClinical setting: chronic alcoholics after a bout of severevomitingoTear may be superficial or deep affecting all layersoClinical picture: Pain, bleeding, superimposed infectionoHiatal hernia is found in 75% of patientsMost often bleeding stops w/o intervention, but life-threateninghematemesis may occur.Supportive therapy and balloon tamponade. Healing is promptwith minimal or no residue
    67. 67. 68
    68. 68. D. BENIGN TUMORS- GASTRIC POLYPS69•INFLAMMATORY AND HYPERPLASTIC POLYPS:o Approximately 75% of all gastric polyps are inflammatory orhyperplastic polyps.oThey are most common between 50 and 60 years of age.o usually develop in association with chronic gastritis, whichinitiates the injury and reactive hyperplasia that leads to polypgrowth.oAmong individuals with H. pylori gastritis, polyps may regressafter bacterial eradication.oBecause the risk of dysplasia correlates with size, polyps largerthan 1.5 cm should be resected and examined histologically.
    69. 69. D. MALIGNANT TUMORS OF THESTOMACH Carcinoma of the stomach General considerationsCarcinoma of the stomach is most common after 50 years of age,with an increased incidence in men. It occurs more frequently inpersons with blood group A, suggesting a genetic predisposition.Incidence varies greatly from one geographic area to another,with incidence much higher in Japan, Finland, and Iceland.The incidence is decreasing in the United States.70
    70. 70. CARCINOMA OF THE STOMACH Etiologic factorsH. pylori is a high suspect.Nitrosamines from dietary amines and nitrites used as foodpreservatives may play a role. Incidence of the disease is greatlyincreased in populations who eat large amounts of smoked fishand meat and pickled vegetables.Increased incidence is also associated with excessive salt intakeand a diet low in fresh fruits and vegetables.AchlorhydriaChronic gastritis with or without pernicious anemia71
    71. 71. GROSS MORPHOLOGIC VARIANTS OFSTOMACH CARCINOMAA-Intestinal typeOften, this variant is manifest as polypoid (fungating)carcinoma, which forms a solid mass projecting into the lumenof the stomach. It has a high degree of association with H.pylori infection.The intestinal variant can become ulcerated and must bedifferentiated from peptic ulcer. Peptic ulcer usually exhibits asmooth base with nonelevated, punched-out margins. Incontrast, carcinoma tends to form an ulcer with an irregularnecrotic base and firm, raised margins.72
    72. 72. Malignant gastric ulcer.This ulceratingadenocarcinoma of thestomach .Rolled elevated edges in thecancer are suggestive signs,but differentiation bybiopsy is essential.73
    73. 73. B-Infiltrating or diffuse carcinoma (linitisplastica, leather-bottle stomach) is not associated with H. pylori infection.characterized by a thickened, rigid stomach wall,caused by diffuse infiltration of tumor cells withaccompanying extensive fibrosis.74
    74. 74. Infiltrating carcinoma (linitisplastica).The stomach with stiff rigidwalls caused by infiltratingtumor cells and extensivefibrosis has been referred to asa "leather-bottle stomach."75
    75. 75. 76
    76. 76. CLINICAL FEATURES. Intestinal-type gastric cancer : The mean age of presentation is 55 years, and the male-to-female ratio is 2 : 1. Diffuse gastric cancer is relatively uniform acrosscountries, there are no identified precursor lesions, andthe disease occurs at similar frequencies in males andfemales. Notably, the remarkable decrease in gastric cancerincidence applies only to the intestinal type, which ismost closely associated with atrophic gastritis andintestinal metaplasia. As a result, the incidences ofintestinal and diffuse types of gastric cancers are nowsimilar.77
    77. 77.  The depth of invasion and the extent of nodal and distantmetastasis at the time of diagnosis remain the most powerfulprognostic indicators for gastric cancer. In advanced cases gastric carcinoma may first be detected asmetastases to the supraclavicular lymph node, also calledVirchows node. Another somewhat unusual mode of intraperitoneal spread infemales is to both the ovaries, giving rise to the so-calledKrukenberg tumor.78
    78. 78. GASTROINTESTINAL STROMAL TUMORS GI stromal tumor (GIST) is the most common mesenchymal tumor of theabdomen, and more than half of these tumors occur in the stomach. Epidemiology: Overall, GISTs are slightly more common in males. The peak age of GIST diagnosis in the stomach is approximately 60 years, withfewer than 10% occurring in individuals under 40 years of age. Pathogenesis. Approximately 75% to 80% of all GISTs have mutations of the gene encodingthe tyrosine kinase c-KIT, which is the receptor for stem cell factor. GISTs appear to arise from the interstitial cells of Cajal, which are located in themuscularis propria and serve as pacemaker cells for gut peristalsis.79
    79. 79. MORPHOLOGY (GIST) They usually form a solitary, well-circumscribed, fleshy masscovered by ulcerated or intact mucosa. GISTs composed of thin elongated cells are classified as spindlecell type, whereas tumors dominated by epithelial-appearing cellsare termed epithelioid type; mixtures of the two patterns alsooccur. The most useful diagnostic marker is c-KIT, which isimmunohistochemically detectable in 95% of gastric GISTs. The prognosis correlates with tumor size, mitotic index, andlocation, with gastric GISTs being somewhat less aggressive thanthose arising in the small intestine. Recurrence or metastasis is rare for gastric GISTs under 5 cm butcommon for mitotically active tumors larger than 10 cm.80
    80. 80. GASTROINTESTINAL STROMAL TUMOR (GIST). A, GIST FROM THESTOMACH WALL. B, HISTOLOGY OF THE TUMOR SHOWING SPINDLECELLS WITH ELONGATED NUCLEI WITH FINE CHROMATIN, ANDEOSINOPHILIC FIBRILLAR CYTOPLASM.81
    81. 81. C, KIT STAIN SHOWING STRONG AND UNIFORM REACTIVITY OF THETUMOR CELLS.82
    82. 82. GASTRIC LYMPHOMA accounts for 4% of malignant gastric tumors. They are of the MALT type. Gastric MALT lymphomas arise in the setting of mucosallymphoid activation, as a result of Helicobacter-associatedchronic gastritis. With H. pylori infection, there is an intense activation of Tand B cells in the mucosa. This leads to polyclonal B-cellhyperplasia and eventually to the emergence of amonoclonal B-cell neoplasm. About 50% of gastric lymphomas can regress with antibiotictreatment for H. pylori. The prognosis is better than it is for denocarcinoma.83
    83. 83. V. DISEASES OF THE SMALL INTESTINE Meckel diverticulum Peptic ulcer Bowel obstruction Malabsorption syndromes Crohn’s disease Tumors of the small intestine84
    84. 84. ANATOMY AND HISTOLOGY The adult small intestine is approximately 6 m in length. The most distinctive feature of the small intestine is its mucosallining, which is designed to provide maximal surface area for thepurpose of food absorption. It is studded with innumerable villi. These extend into the lumen as finger-like projections covered byepithelial lining cells. In normal individuals, the villus-to-crypt height ratio is about 4 : 1. Within the duodenum are abundant submucosal mucous glands,termed Brunners glands. These glands secrete bicarbonate ions,glycoproteins, and pepsinogen II.85
    85. 85. ANATOMY AND HISTOLOGY The surface epithelium of the small intestinal villicontains three principal cell types. Columnar absorptive cells are recognized by the densearray of microvilli on their luminal surface (the “brushborder”). Interspersed regularly between absorptive cells aremucin-secreting goblet cells, Endocrine cells.86
    86. 86. 87
    87. 87. A. MECKEL DIVERTICULUM is the most common congenital anomaly of the small intestine. occurs as a result of failed involution of the vitelline duct, whichconnects the lumen of the developing gut to the yolk sac. is located in the ilium. It may contain ectopic gastric, or pancreatictissue.“Rule of 2” is used to remember characteristics of Meckel diverticulae: Occur in approximately 2% of the population, Generally present within 2 feet (85 cm) of the ileocecal valve, Approximately 2 inches (5 cm) long, are twice as common in males as in females, and are most often symptomatic by age 2. The condition is usually asymptomatic but complications, includingpeptic ulceration in ectopic gastric mucosa with bleeding orperforation, may occur.88
    88. 88. 89
    89. 89.  B. Peptic ulcer Occurrence is most frequent in the first portion of the duodenum, thestomach, or the lower end of the esophagus, all of which are exposedto acid and pepsin. Except for peptic ulcer of the stomach, peptic ulcer is alwaysassociated with hypersecretion of gastric acid and pepsin. Ulceration is closely related to gastric H. pylori infection, whichaffects essentially all patients with duodenal ulcer and the majority ofpatients with gastric ulcer. H. pylori increases gastric acid secretion and apparently impairs bothgastric and duodenal mucosal defenses.90
    90. 90.  Frequency of occurrence is increased in persons of blood group O,suggesting that genetic factors may play a role. Peptic ulcer is not a precursor of malignancy. Complications often include hemorrhage with melena (black stools containing blood). Obstruction perforation.91
    91. 91. PEPTIC ULCER IS SOMETIMESASSOCIATED WITH:1. Intake of aspirin or other NSAIDs. The ulcerogenic effect of thesedrugs may be mediated by inhibition of prostaglandin synthesis.2. Smoking. The incidence of peptic ulcer is two-fold greater in smokers.3. Zollinger-Ellison syndrome, increased tendency toward peptic ulcerformation, which is caused by gastric acid hypersecretion due togastrin-secreting islet cell tumor of the pancreas. Recurrent pepticulcer or peptic ulcer in aberrant sites, such as the jejunum issuggestive of the Zollinger-Ellison syndrome.4. Primary hyperparathyroidism5. Multiple endocrine neoplasia (MEN) type I (Wermer syndrome):an autosomal dominant syndrome characterized by pituitary,parathyroid, and pancreatic islet cell adenomas or hyperplasia.Associated with hypergastrinemia and peptic ulcer92
    92. 92. C.BOWEL OBSTRUCTION Although any part of the gut may be involved, because of itsnarrow lumen, the small bowel is most commonly affected. Four entities -account for at least 80% of the cases: hernias, intestinal adhesions, intussusception, Volvulus Tumors and infarction account for only about 10% to 15% ofsmall bowel obstructions.o The clinical manifestations of intestinal obstruction includeabdominal pain and distention, vomiting, and constipation.o Surgical intervention is usually required in cases of mechanicalobstruction or severe infarction.93
    93. 93. 1. Hernias, a weakness or defect in the wall of the peritoneal cavity,may permit protrusion of a pouch like, serosa-lined sac ofperitoneum, called a hernial sac. The usual sites of weakness are anteriorly at the inguinal andfemoral canals, at the umbilicus, and in surgical scars. Hernias are of concern because segments of viscera frequentlyintrude and become trapped in them. The most frequent intruders are small bowel loops, but portions ofomentum or large bowel also may become trapped.94
    94. 94. 2. Surgical procedures, and infection often cause localized orgeneralized peritoneal inflammation (peritonitis). With healing,adhesions may develop between bowel segments or the abdominalwall and the operative site. These fibrous bridges can create closedloops through which the intestines may slide and become trapped(internal herniation). The sequence of events is much the same aswith external hernias.3. Intussusception (invagination of a proximal segment of bowel intoa more distal segment), causing bowel obstruction.Intussusception occurs more often without preexisting bowelpathology and is seen most often in infants and young children.4. Volvulus (twisting of a portion of the gastrointestinal tract aboutitself), often causing bowel obstruction95
    95. 95. 96
    96. 96. D. MALABSORPTION SYNDROMES Malabsorption is characterized by defective absorption of fats, fat-soluble and other vitamins, proteins, carbohydrates, electrolytes andminerals, and water. The most common presentation is chronic diarrhea; the hallmark ofmalabsorption syndromes is steatorrhea (excessive fat content of thefeces).97
    97. 97. THE MAJOR MALABSORPTIONSYNDROMESDefective Intraluminal DigestionDigestion of fats and proteinsPancreatic insufficiency, due to pancreatitis or cystic fibrosisZollinger-Ellison syndrome, with inactivation of pancreatic enzymesby excess gastric acid secretionSolubilization of fat, due to defective bile secretionIleal dysfunction or resection, with decreased bile salt uptakeCessation of bile flow from obstruction, hepatic dysfunctionNutrient preabsorption or modification by bacterial overgrowthDistal ileal resection of bypassTotal or subtotal gastrectomy 98
    98. 98. Primary Mucosal Cell AbnormalitiesDefective terminal digestionDisaccharidase deficiency (lactose intolerance)Bacterial overgrowth, with brush-border damageDefective transepithelial transportAbetalipoproteinemiaReduced Small Intestinal Surface AreaGluten-sensitive enteropathy (celiac disease)Short-gut syndrome, after surgical resectionsCrohn disease99
    99. 99. InfectionsAcute infectious enteritisParasitic infestationTropical sprueWhipple diseaseLymphatic ObstructionLymphomaTuberculosis and tuberculous lymphadenitis100
    100. 100. CELIAC DISEASE Celiac disease is caused by sensitivity to gluten incereal products Clinical manifestations include weight loss, weakness, anddiarrhea with pale, bulky, frothy, foul-smelling stools. It isalso characterized by growth retardation and general failureto thrive. Disease most often becomes symptomatic in infancy whencereals are first added to the diet. Diagnosis involves documentation of malabsorption, smallintestinal biopsy demonstrating blunting of small intestinalvilli, and clinical improvement and restoration of normalintestinal morphology on a gluten-free diet.101
    101. 101. Incidence increases in association with humanleukocyte antigens (HLAs) HLA-B8 and HLA-DW3. This finding and the presence of antibodies directedagainst gliadin (a glycoprotein component of gluten)and transglutaminase suggest that both genetic andimmune-mediated mechanisms may be involved.These antibody tests may also be used for screeningprior to definitive diagnosis by biopsy.Approximately 10%–15% of cases lead to smallintestinal malignancy, most often enteropathy-typeT-cell lymphoma.102
    102. 102. THE HISTOPATHOLOGY IS CHARACTERIZED BYINTRAEPITHELIAL LYMPHOCYTOSIS, CRYPT HYPERPLASIA,VILLOUS ATROPHY, AND INCREASED NUMBERS OF PLASMACELLS, MAST CELLS, AND EOSINOPHILS, WITHIN THE UPPERPART OF THE LAMINA PROPRIA.103Celiac disease Duodenum, normal
    103. 103. Disorder Morphologic Features CommentsTropical sprue Histologic findings vary from nochanges to abnormalities similarto those of celiac diseaseTropical disease ofprobable infectious origin;often responds to antibioticsWhipple disease Distinctive PAS-positivemacrophages in intestinalmucosa Tropheryma whippeliibacilli visualized by electronmicroscopyMay affect any organ, mostcommonly the smallintestine; arthralgias andcardiac and neurologicsymptoms are common104
    104. 104. Disorder Morphologic Features CommentsDisaccharidasedeficiencyNo characteristic histologicchangesDeficiency ofdisaccharidases sited in brushborder of mucosal cells ofsmall intestine; lactasedeficiency, which leads tomilk intolerance, is mostfrequentAbetalipoproteinemia No characteristic features in theintestine; circulatingacanthocytes (red cells withspiny projections) suggest thediagnosisβ-lipoprotein deficiency iscaused by hereditarydeficiency of apoprotein β105
    105. 105. D. CROHN’S DISEASE General considerations This chronic inflammatory condition of unknown etiologymay affect any part of the gastrointestinal tract but mostcommonly involves the distal ileocecum, small intestine, orcolon. Crohn disease tends to affect young people in the second andthird decades of life, although no age group is exempt. Itoccurs most frequently in people of Jewish descent. The disease can lead to carcinoma involving the smallintestine or colon. However, neoplastic transformation ismuch less frequent in Crohn disease than in ulcerative colitis.106
    106. 106. CROHN’S DISEASE Morphology Chronic inflammation involving all layers of the intestinal wall (transmuralinvolvement). Thickening of involved segments, with narrowing of lumen Linear ulceration of the mucosa. Submucosal edema with elevation of the surviving mucosa, producing acobblestone appearance Skip lesions (segments of normal intestine between affected regions). Discrete noncaseating granulomas (in about 50% of the cases). Submucosal fibrosis.107
    107. 107. CROHN’S DISEASE Clinical manifestations Abdominal pain and diarrhea. Malabsorption. Fever. Intestinal obstruction resulting from fibrous stricture. Fistulas between loops of intestine and between the intestine, bladder,vagina, and skin.108
    108. 108. Crohn disease. Linear ulcerations and edema result in thecobblestone appearance shown here.109
    109. 109. E. TUMORS OF THE SMALL INTESTINE General considerationsTumors of the small intestine make up a small percentage ofgastrointestinal neoplasms.The most common malignant tumors are adenocarcinoma,lymphoma, and carcinoid.110
    110. 110. Adenocarcinoma These tumors grow in a napkin-ring encircling pattern or aspolypoid fungating masses, in a manner similar to colonic cancers. Most small bowel carcinomas arise in the duodenum (including theampulla of Vater). Cramping pain, nausea, vomiting, and weight loss are the commonpresenting signs and symptoms, but such manifestations generallyappear late in the course of these cancers. By the time of diagnosis, most have already penetrated the bowelwall, invaded the mesentery or other segments of the gut, spread toregional nodes, and sometimes metastasized to the liver.111
    111. 111. GASTROINTESTINAL LYMPHOMA Any segment of the gastrointestinal tract may be involvedsecondarily by systemic dissemination of non-Hodgkinlymphomas. However, up to 40% of lymphomas arise in sites other than lymphnodes, and the gut is the most common extra-nodal location. 1% to 4% of all gastrointestinal malignancies are lymphomas. By definition, primary gastrointestinal lymphomas reveal no evidence of liver,spleen, or bone marrow involvement at the time of diagnosis; regional lymphnode involvement may be present. Intestinal tract lymphomas can be of B- or T-cell origin. The most common form in Western countries is MALT lymphoma.This is a sporadic lymphoma that originates in B cells of themucosa-associated lymphoid tissue (MALT) of the gastrointestinaltract.112
    112. 112. GASTROINTESTINAL LYMPHOMA This type of gastrointestinal lymphoma usually affects adults, lacksa sex predilection, and may arise anywhere in the gut: stomach (55% to 60% of cases), small intestine (25% to 30%), proximal colon (10% to 15%), and distal colon (≤10%). Celiac disease is associated with a higher than normal risk ofintestinal T-cell lymphomas.113
    113. 113. CARCINOID TUMOR Cells generating peptide and nonpeptide hormones, are normallydispersed along the length of the gastrointestinal tract mucosa andhave a major role in coordinated gut function. Endocrine cells are abundant in other organs, but most of thetumors that develop from these cells arise in the gut. Tumors arising from these endocrine cells are called carcinoidtumors; they may develop in the pancreas, lungs, and liver. The term carcinoid is an old reference to "carcinoma-like," whichhas persisted through the decades. The peak incidence of theseneoplasms is in the sixth decade, but they may appear at any age. They compose less than 2% of colorectal malignancies but almosthalf of small intestinal malignant tumors.114
    114. 114. CARCINOID TUMOR Although all carcinoids are potentially malignant tumors, thetendency for aggressive behavior correlates with the site of origin,the depth of local penetration, and the size of the tumor. For example, appendiceal and rectal carcinoids infrequentlymetastasize, even though they may show extensive local spread. By contrast, 90% of ileal, gastric, and colonic carcinoids havespread to lymph nodes and distant sites at the time of diagnosis. As with normal gut endocrine cells, the cells of carcinoid tumorscan synthesize and secrete a variety of hormones. Although multiple hormones may be synthesized by a singletumor, when a tumor secretes a predominant product to cause aclinical syndrome, it may be called by that name (e.g., gastrinoma,somatostatinoma, and insulinoma).115
    115. 115. Carcinoid syndrome:Caused by the elaboration of vasoactive peptidesand amines, especially serotoninManifest clinically by:Cutaneous flushingWatery diarrhea and abdominal crampsBronchospasmValvular lesions of the right side of the heart116
    116. 116. 117
    117. 117. VI. DISEASES OF THE COLON A. Hirschsprung disease Diverticula Vascular diseases of the colon Inflammatory disorders of the colon Tumors118
    118. 118. VI. DISEASES OF THE COLON A. Hirschsprung disease (congenital megacolon) is dilation of the colon due to the absence of ganglion cells of thesubmucosal and myenteric neural plexuses; dilation is proximal tothe aganglionic segment. Acquired megacolon may result from Chagas disease, in which the trypanosomes directly invade thebowel wall to destroy the neural plexuses. Organic obstruction of the bowel by a neoplasm or inflammatorystricture. Toxic megacolon complicating ulcerative colitis or Crohn disease.119
    119. 119. B. DIVERTICULA are pulsion (or false) diverticula (pockets of mucosa andsubmucosa herniated through the muscular layer) that mostfrequently involve the sigmoid colon. They are almost always multiple. Diverticula are most common inolder persons. Diverticulosis is defined by the presence of multiple diverticulawithout inflammation.Occurrence is most common in populations that consume low-fiber diets.The condition is most often asymptomatic or associated withvague discomfort.120
    120. 120.  Diverticulitis refers to inflammation of diverticula.Older persons are affected.Complications may include perforation, peritonitis,abscess formation, or bowel stenosis. Bright redrectal bleeding is frequent.Presenting features may include lower abdominal painand tenderness, fever, leukocytosis, and other signs ofacute inflammation.121
    121. 121. 122
    122. 122. C. VASCULAR DISEASES OF THECOLON1. Ischemic bowel diseaseThe cause is atherosclerotic occlusion of at least twoof the major mesenteric vessels.Most often affected are the splenic flexure and therectosigmoid junction, which lie in the relativelypoorly vascularized regions (so-called watershedareas) between areas supplied by the superiormesenteric artery and the inferior mesenteric andinternal iliac arteries.The result is mucosal, mural, or transmural infarctioninvolving the wall of the intestine.123
    123. 123. 124
    124. 124. 2. Angiodysplasia is tortuous dilation of small vessels inthe intestinal mucosa or submucosa.Lesions are multiple, most often involving the cecumor ascending colon.This condition is an extremely common cause ofotherwise unexplained lower bowel bleeding.3. Hemorrhoids are dilated internal and external venousplexuses in the anal canal. They are predisposed by alow-fiber diet.125
    125. 125. D. INFLAMMATORY DISORDERS OF THECOLON Ulcerative colitisGeneral considerationsUlcerative colitis is of unknown etiology.It is often grouped along with Crohn disease asinflammatory bowel disease.Crohn disease and ulcerative colitis share a similargeographic and racial distribution; some patientshave a family history of either ulcerative colitis orCrohn disease.126
    126. 126. extraintestinal manifestations:PolyarthritisUveitis and episcleritisSclerosing cholangitis, a chronic fibrosinginflammatory process of the biliary systemleading to chronic cholestasis and sometimes toportal hypertensionSacroiliitisSkin manifestations, including erythemanodosum and pyoderma gangrenosum127
    127. 127. Morphology:Mucosal inflammation and ulceration limited to thelarge intestine; the rectum is always affected but theentire colon may be involved. Inflammatory changes almost entirely confined to themucosa and submucosa; the most characteristic featureis the crypt abscess, in which there are infiltrates ofneutrophils in the crypts of Lieberkühn.128
    128. 128.  Red, granular appearance of the mucosa; ulceration may beminimal or quite extensive, with only islands of surviving mucosaremaining. Pseudopolyps, mucosal remnants of previous severe ulceration Chronic diarrhea associated with the passage of blood andmucus; the most frequent clinical manifestation is bleeding. Complications Toxic megacolon, a medical emergency in which there is a markeddilation of the colon Perforation of the colon Carcinoma of the colon129
    129. 129. 130Ulcerative colitis. In contrast to Crohn disease, which can involve any part of thegastrointestinal tract, ulcerative colitis is limited to the colon.
    130. 130. ULCERATIVE COLITIS -CRYPTABSCESS131
    131. 131. FEATURES THAT DIFFER BETWEEN CROHNDISEASE AND ULCERATIVE COLITISFeature Crohn Disease Ulcerative ColitisMACROSCOPICBowel region Ileum ± colon Colon onlyDistribution Skip lesions DiffuseStricture Yes RareWall appearance Thick ThinMICROSCOPICInflammation Transmural Limited to mucosaPseudopolyps Moderate MarkedUlcers Deep, knife-like Superficial, broad-basedLymphoid reaction Marked Moderate 132
    132. 132. FEATURES THAT DIFFER BETWEENCROHN DISEASE AND ULCERATIVECOLITISFeature Crohn Disease Ulcerative ColitisFibrosis Marked Mild to noneSerositis Marked Mild to noneGranulomas Yes ( 50%)∼ NoFistulae/sinuses Yes NoCLINICALPerianal fistula Yes (in colonic disease) NoFat/vitaminmalabsorptionYes NoMalignant potential With colonic involvement YesRecurrence after surgery Common NoToxic megacolon No Yes133
    133. 133. PSEUDOMEMBRANOUS COLITISThis condition is morphologically distinguished by superficialgrayish mucosal exudates consisting of necrotic, looselyadherent mucosal debris (pseudomembrane).The cause most often is overgrowth of exotoxin-producingClostridium difficile. Fibrinous necrosis of the superficialmucosa is caused by the exotoxin, not by bacterial invasion.Clinical characteristics include fever, toxicity, and diarrhea,most often occurring in patients on broad-spectrum antibiotictherapy.134
    134. 134.  Amebic colitisThe cause is infection of the colon with Entamoebahistolytica.Flask-shaped ulcers are characteristic. CholeraThe cause is infection with Vibrio cholerae, anoninvasive toxin-producing bacterium.Characteristics include toxin-mediated loss of fluidand electrolytes with mucosa of the small bowel andcolon remaining normal in appearance.135
    135. 135. E. TUMORS Benign polypsTerminology. A polyp is a descriptive term for any elevation of theintestinal surface.Pedunculated polyps are attached by a narrow stem.Sessile polyps have a broad-based attachment.136
    136. 136. Non-neoplastic polyps1. Hyperplastic polyps can occur anywhere in the colon orsmall intestine. They have no clinical significance but maybe mistaken for an adenomatous polyp.2. Inflammatory polyps include benign lymphoid polyps andinflammatory pseudopolyps consisting of granulationtissue and remnants of mucosa, caused by chronicinflammatory bowel disease.3. Hamartomatous polyps Juvenile polyps occur in the small intestine and colon. Theymost often occur in children but are also seen in adults.137
    137. 137.  Peutz-Jeghers polyps occur as part of the Peutz-Jeghers syndrome, whichincludes hamartomatous polyps of the colon and smallintestine and melanotic accumulations in the mouth and onthe lips, hands, and genitalia.Peutz-Jeghers polyps have no malignant potentialthemselves, but the syndrome is associated with increasedpropensity for adenocarcinoma of the colon and malignancyat other sites, such as the stomach, breast, or ovaries.138
    138. 138. NEOPLASTIC POLYPS Adenomatous polyps are true neoplasms rather than benignproliferations of tissue. They are usually asymptomatic but canresult in rectal bleeding.1. Tubular adenomasThese are the most common type (75%) of adenomatouspolyp.These polyps are usually small and pedunculated.They can contain malignant foci; the likelihood ofmalignancy is greater in larger polyps.139
    139. 139. 140
    140. 140. 141
    141. 141. 2. Tubulovillous adenomasThese adenomas account for about 15% of adenomatouspolyps.Tubulovillous adenomas resemble tubular adenomas buthave a surface covered by finger-like villi. They are similarhistologically to tubular adenomas.They are intermediate in malignant potential betweentubular adenomas and villous adenomas.142
    142. 142. 3. Villous adenomasThese polyps are much less common than tubular adenomasand account for approximately 10% of adenomatous polyps.Villous adenomas are usually larger than tubular adenomas,usually sessile, and are characterized by large numbers offinger-like villi.They have the highest potential for malignancy of all ofthe adenomatous polyps; they become malignant in morethan 30% of cases.143
    143. 143. 144
    144. 144. 145
    145. 145. WHAT VARIABLES DETERMINE THELIKELIHOOD OF MALIGNANT CHANGE IN APOLYP? Three interrelated features are determinants of the risk ofcancerous transformation: polyp size, histologic architecture, andseverity of dysplasia.1) Cancer is rare in tubular adenomas less than 1 cm in diameter.2) The likelihood of cancer is high (about 50%) in sessile villousadenomas that are greater than 4 cm in diameter.3) Severe dysplasia is likely to progress to cancer. Such dysplasiasare found in villous areas.Of all these, size is the most important factor.146
    146. 146. MULTIPLE POLYPOSIS SYNDROMES are associated with a greatly increased risk of malignanttransformation.1. Familial polyposis is an autosomal dominant conditioncharacterized by the presence of numerous adenomatouspolyps. The risk of malignant transformation approaches100%.2. Gardner syndrome is an autosomal dominant conditioncharacterized by the presence of numerous adenomatouspolyps along with osteomas and soft tissue tumors.3. Turcot syndrome is characterized by adenomatous polypsalong with tumors of the central nervous system.147
    147. 147. MULTIPLE POLYPOSIS. THE POLYPS ARE BENIGN, BUTEACH OF THE INNUMERABLE POLYPS HAS ABOUT A1% POTENTIAL FOR MALIGNANT CHANGE.148
    148. 148. Type CommentsNon-neoplastic polypsHyperplastic polyp No clinical significanceInflammatory polyps:Lymphoid polyp Most common site is the rectal mucosa; may be a reaction tolocal irritationInflammatorypseudopolypAssociated with ulcerative colitis and other inflammatorydiseases of the colon; consists of granulation tissue and residualand regenerating mucosaHamartomatous polyps:Juvenile polyp Occurs most frequently in childrenPeutz-Jeghers polyp Associated with Peutz-Jeghers syndrome149
    149. 149. Neoplastic polypsTubular adenoma Benign but may undergo malignant change; oftenmultiple; hereditary multiple polyposis syndromesassociated with greatly increased risk of malignancyTubulovillous adenoma Morphologically resembles tubular adenoma withadditional features similar to those of villousadenoma; greater malignant potential than tubularadenomaVillous adenoma Large sessile tumor with velvety surface comprisedof finger-like villi; high potential for malignantchange150
    150. 150. ADENOCARCINOMA OF THE COLON ANDRECTUMGeneral considerationsAdenocarcinoma of the colon and rectum is one of the mostcommon neoplasms in the Western world.The peak age incidence is in the sixth to seventh decades.This form of cancer is associated with increased serumconcentration of carcinoembryonic antigen (CEA).Because elevated CEA is not specific for colon cancer, thislaboratory determination is most useful for following thecourse of the disease rather than for making the initialdiagnosis.151
    151. 151. The cancer develops through a set of anatomicchanges progressing from normal mucosa toadenomatous polyp to carcinoma to metastatictumor, with a parallel set of molecularchanges in oncogenes and tumor suppressorgenes that have been presented as amodel of tumor progression.152
    152. 152. 153
    153. 153. Predisposing factors1. Adenomatous polyps2. Inherited multiple polyposis syndromes3. Long-standing ulcerative colitis4. Genetic factors; up to a four-fold increase in incidence isnoted among relatives of patients with colon cancer.5. A low-fiber diet that is high in animal fat; the disease isless common in much of the Third World, where populationsconsume a high-fiber diet that is low in animal fat.154
    154. 154. CharacteristicsAdenocarcinoma varies in gross presentationaccording to the region of the colon involved.Carcinoma of the rectosigmoid colon tends topresent in an annular manner, producing earlyobstruction.Carcinoma of the right colon usually does notobstruct early and often presents (sometimes quitelate) with iron deficiency anemia secondary tochronic blood loss.155
    155. 155. ADENOCARCINOMA OF THE COLON.156
    156. 156. INVASIVE ADENOCARCINOMA OF COLONSHOWING MALIGNANT GLANDS INFILTRATINGTHE MUSCLE WALL.157
    157. 157. Tumor Stage Histologic Features of the NeoplasmTis Carcinoma in situ (high-grade dysplasia) or intramucosalcarcinoma (lamina propria invasion)T1 Tumor invades submucosaT2 Extending into the muscularis propria but notpenetrating through itT3 Penetrating through the muscularis propria intosubserosaT4 Tumor directly invades other organs or structuresNx Regional lymph nodes cannot be assessedN0 No regional lymph node metastasisN1 Metastasis in 1 to 3 lymph nodesN2 Metastasis in 4 or more lymph nodesMx Distant metastasis cannot be assessedM0 No distant metastasisM1 Distant metastasis158
    158. 158. VII. DISEASES OF THE APPENDIX A. Acute appendicitis Occurrence is most frequent in the second and thirddecades of life. The disease is thought to be caused by obstruction of theappendiceal lumen, most often by a fecolith, resulting inbacterial proliferation and invasion of the mucosa. Gross changes include a congested appendix with aswollen distal half covered by purulent exudate; thelumen also contains a purulent exudate and often afecalith.159
    159. 159.  Histologic characteristics include an acute inflammatoryinfiltrate extending from the mucosa through the fullthickness of the appendiceal wall. Presenting features include anorexia, nausea, andabdominal pain, most commonly localized to the rightlower quadrant, and systemic signs of acuteinflammation, such as fever. If untreated by surgical resection, appendicitis mostoften leads to perforation or abscess, or both.160
    160. 160. B. TUMORS OF THE APPENDIX. The most common tumor of the appendix is the carcinoid. It is usually discovered incidentally at the time of surgery orexamination of a resected appendix. This neoplasm most frequently involves the distal tip of theappendix, where it produces a solid bulbous swelling up to 2 to 3cm in diameter. Although intramural and transmural extension may be evident,nodal metastases are very infrequent, and distant spread isexceptionally rare.161
    161. 161.  Mucocele, a dilated appendix filled with mucin, may simplyrepresent an obstructed appendix containing inspissated mucin orbe a consequence of mucinous cystadenoma or mucinouscystadenocarcinoma. In the latter instance, invasion through the appendiceal wall canlead to intraperitoneal seeding and spread. In women the resulting peritoneal implants may be mistaken formucinous ovarian tumors. In the most advanced cases the abdomen fills with tenacious,semisolid mucin, a condition called pseudomyxoma peritoneii.162
    162. 162.  A 47-year-old man has a history of drinking 1 to 2 liters ofalcohol per day for the past 20 years. He has had numerousepisodes of nausea and vomiting in the past 5 years. Heexperiences a bout of prolonged vomiting, followed bymassive hematemesis. Which of the following is the mostlikely diagnosis?1. Barrett’s esophagus2. Esophageal stricture3. Esophageal lacerations (Mallory Weiss syndrome)4. Esophageal squamous cell carcinoma5. Achalasia163
    163. 163.  All these statements about Barrett’s esophagus aretrue, except:1. It is associated with 30- to 40-fold greater risk todevelop adenocarcinoma2. It appears as salmon-pink mucosa on endoscopy3. It is associated with high risk for esophagealbleeding4. It represents replacement of the stratified squamousepithelium by columnar epithelium with gobletcells5. It could be a complication of long-standing refluxesophagitis164
    164. 164.  All these statement about Helicobacter pylori are correctexcept:1. H. pylori organisms are Gram negative bacilli2. It is associated with intestinal-type gastricadenocarcinoma3. It is associated with gastric lymphoma4. It is associated with diffuse-type gastric adenocarcinoma5. It is associated with peptic ulcer165
    165. 165.  A 20-year-old man has noted cramping abdominalpain for the past week associated with fever andlow-volume diarrhea. On physical examination,there is right lower quadrant tenderness. Bowelsounds are present. His stool is positive for occultblood. A colonoscopy reveals mucosal edema andulceration in the ascending colon, but the transverseand descending portions of the colon are notaffected. Which of the following microscopicfindings is most likely to be present in biopsies fromhis colon1. Entamoeba histolytica organisms2. Adenocarcinoma3. Non-caseating granulomas4. Diverticulosis166
    166. 166.  A 35-year-old woman has a 10 year history ofintermittent, bloody diarrhea. She has no other majormedical problems. On physical examination there areno lesions palpable on digital rectal examination, but astool sample is positive for occult blood. Colonoscopyreveals a friable, erythematous mucosa with focalulceration that extends from the rectum to the mid-transverse colon. Biopsies are taken and all revealmucosal acute and chronic inflammation with cryptdistortion, occasional crypt abscesses, and superficialmucosal ulceration. This patient is at risk fordevelopment of which of the following conditions?1. Diverticulitis2. Acute pancreatitis3. Colonic adenocarcinoma4. Peri-rectal fistula5. Appendicitis167
    167. 167.  A 25-year-old man complains of a low volume butchronic, foul smelling diarrhea for the past year. Hehas no nausea or vomiting. On physical examinationthere is no abdominal pain or masses and bowelsounds are present. His stool is negative for occultblood. Laboratory studies include a quantitative stoolfat of 10 g/day. Upper GI endoscopy is performedwith biopsies of the duodenum. The biopsies revealthe absence of villi, and increased surfaceintraepithelial lymphocytes. Which of the followingtherapies is most likely to be useful for this man?1. Antibiotics2. Anti-Entamoeba therapy3. Corticosteroids4. Gluten-free diet5. Surgical resection 168
    168. 168. REFERENCES ROBBINS AND COTRAN PATHOLOGIC BASISOF DISEASE, 8/E, 2010. Robbins basic pathology 8ed 2007 OUTLINES IN PATHOLOGYBy John H. Sinard, MD, PhD, May 2006169

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