Path and CS GI

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Path and CS GI
2010-10-28 16:59:04
Path CS GI

Path and CS GI
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  1. manometry
    wire that measures of pressures in the esophagus and LES. Evaluation of peristalsis
  2. imaging tests for esophagus
    CT and endoscopic ultrasound. defining esophageal wall thickening, submucosal lesions, extent of malignancy
  3. Achalasia (general definition)
    Lower esophageal sphincter (LES) pressure is elevated (incr resting tone), esophageal aperistalsis. incomplete relaxation of lower esophageal sphincter in response to swallowing --> functional obstruction of esophagus.
  4. primary achalasia pathphysio
    loss of intrinsic inhibitory innervation of lower esophageal sphincter and smooth muscle segment of the esophageal body. Myenteric ganglia usually absent. Most common.
  5. secondary achalasia pathogenesis
    • Chagas caused by Trypanosoma cruzi, which causes destruction of myenteric plexus
    • Esophageal cancer
    • Scleroderma may manifest with hypomotility esophageal wall becomes fibrotic. Minimal LES tone
  6. Achalasia presentations
    Most commonly occur in 3rd to 5th decade. dysphagia, nocturnal regurg, may manifest in young adults, chest fullness. progressive dilation of esophagus above lower esophageal sphincter. Bird's beak deformity on esophagram.
  7. Possible complication of achalasia
    esophageal squamous cell carcinoma
  8. GERD presentation
    bitter taste in mouth, heartburn related to food, posture, anxiety.
  9. GERD etiology
    Low LES pressure*, Increased gastric refluxate, Transient LES Relaxation (TLESR)
  10. GERD risk factors
    Hiatal hernia, Widened crural diaphragm and proximally displaced gastroesophageal junction, smoking, mint, chocolate, coffee, alcohol, carbonated drinks, tomato juice, citrus juices
  11. GERD prevention also involves
    avoid eating w/in 3 hrs of bedtime, sleep on left side, lose weight, Elevate head of your bed 4-6 inches by placing bricks under headboard
  12. possible complications of GERD
    Hemorrhage, Peptic strictures, *Barrett’s esophagus, Precursor to esophageal adenocarcinoma
  13. Zenker diverticulum
    Hypopharyngeal. incomplete or uncoordinated UES relaxation.
  14. Zenker diverticulum presensation
    halitosis (bad breath), regurgitation of undigested material, dysphagia
  15. Definition of diverticulum
    outpouching of mucosa, submucosa, muscular layers
  16. Midesophageal diverticulae
    traction from lymph nodes due to TB, cancer
  17. Pseudodiverticula
    • only mucosa and submucosa herniate. Outer longitudinal muscle fibers form teniae.
    • Increased elastin in teniae. NO hypertrophy or hyperplasia. Change in collagen
  18. Myochosis, Prediverticular state
    thickening of the circular muscle layer, shortening of teniae, luminal narrowing
  19. Diverticulum surgical staging
    • Stage I -- Pericolic abscess or phlegmon
    • Stage II -- Pelvic, intra-abdominal, or retroperitoneal abscess
    • Stage III -- Generalized purulent peritonitis
    • Stage IV -- Generalized fecal peritonitis
  20. Boerhave's syndrome
    (transmural): spontaneous rupture of esophagus, usually associated w/ incr in intraluminal pressures and rupture of esophageal wall. Pt presents w// crepitus (crackling sound) in neck, alcoholics
  21. Mallory-Weiss syndrome
    nontransmural): Frequent cause of upper GI bleeding, assoc w/ retching (longitudinal tear at GE junction) and abrupt changes in pressures. Bleeding after vomiting, hematemesis.
  22. Mallory-Weiss syndrome seen common in...
    hiatal hernia, chronic alcoholic w/ severe vomiting, coughing
  23. Mallory-Weiss syndrome complications
    Infection, inflammatory ulcer, mediastinitis
  24. Esophagitis
    Usually related to reflux. CNS depressants, NSAIDs, radiation, tetracyclines, alcohol or tobacco exposure may be some of the contributing causes. More common in Iran and China.
  25. uncomplicated reflux esophagitis
    eosinophils w/ or w/o neutrophils in epithelial layer. basal zone hyperplasia and elongation of lamina propria papillae. Intraepithelial neutrophilic infiltration indicates severe injury
  26. Infectious causes of esophagitis
    Candida (tan yellow plaques in lower esophagus, mucosal hyperemia), CMV, herpes
  27. strictures
    • benign or malignant.
    • Peptic induced (erosive esophagitis, esophageal ulcers) most common.
    • Can also be due to caustic injury (after alkaline or strong acid ingestion in suicidal attempts)
  28. Schatzki’s ring
    Mucosa and submucosa. seen in distal esophagus, intermittent dysphagia to solids. “steakhouse syndrome”.
  29. Plummer-Vinson syndrome (cervical webs)
    mucosa and submucosa involved. iron deficiency anemia involved. Often in Swedish women.
  30. squamous cell carcinoma of esophagus
    90% of esophageal cancers (except in US). smoking and alcohol excesses risk factors, also risk factors include nitrosamine containing food products, hx of achalasia. More frequent in China and Africa. Common in middle 1/3 esophagus
  31. sx of esophageal carcinoma
    dysphagia, odynophagia, weight loss, fatigue, anorexia. Age >50
  32. stages of squamous cell carcinoma of esophagus
    • polypoid exophytic masses that protrude into lumen
    • necrotizing cancerous ulcerations that extend deeply and sometimes erode into resp tree, aorta, or elsewhere
    • diffuse infiltrative neoplasms that cause thickening and rigidity of the wall and narrowing of the lumen.
  33. Adenocarcinoma in esophagus
    more common in whites, M>F, assoc w/ Barrette's esophagus, distal 1/3 esophagus, large nodular masses or show deeply ulcerative or diffusely infiltrative features
  34. Barrett esophagus
    replacement of normal distal stratified squamous mucosa by columnar epithelium containing goblet cells. Complication of long-standing gastroesophageal reflux. M>F, whites > blacks.
  35. complications of barrett esophagus
    ulceration and stricture. adenocarcinoma
  36. all endoscopic views are ____ above GE junction
    3cm. Polypoid lesions after 5 yrs would be detected at this level.
  37. Behcet’s dz
    • Severe recurrent aphthous ulcers (canker sores).
    • Tends to be familial in the Middle East. Strep may be involved
  38. herpetic stomatitis
    HSV1 cold sores. intranuclear acidophilic viral inclusions.Form giant cells known as multinucleated polykaryons. Tzanck test.
  39. Pseudomembranous candidiasis
    • (thrush, moniliasis) is most common, particularly among persons w/ diabetes mellitus, anemia, antibiotic or glucocorticoid therapy, immunodeficiency, or debilitating illnesses such as disseminated cancer.
    • Pseudohyphae seen
  40. leukoplakia
    • whitish, well-defined mucosal patch or plaque caused by epidermal thickening or hyperkeratosis. strong link to tobacco, alcohol, HPV.
    • Can transform to squamous cell carcinoma esp if lesion is red.
  41. oral cancer dominant sites and causes/risk factors
    vermilion border of lateral margins of lower lip, floor of mouth, & lateral borders of tongue. HPV 16 + 18, leukoplakia/erythroplakia, tobacco abuse, alcohol abuse
  42. Mumps
    paramyxovirus (- strand ssRNA), parotid gland inflammation, orchitis, pancreatitis
  43. Bacterial sialadenitis
    usually by Staph aureus or strep viridans
  44. sialolithiasis
    ductal obstruction via stone
  45. Chronic sialadenitis
    dominant cause is autoimmune (bilateral). Seen in Sjögren syndrome. Linked to other connective tissue dz: rheumatoid arthritis, SLE, scleroderma
  46. Pleomorphic adenoma
    usually in superficial parotid glands, well demarcated, encapsulated, most common benign, saliva contains epidermal growth factors, painless swelling, 6/7th decade
  47. Pleomorphic adenoma major histo feature
    Heterogeneity: tumor cells form ducts, acini, tubules, strands, or sheets of cells
  48. Warthin tumor
    papillary cystadenoma lymphomatosum. parotid glands, less common benign, swelling at angle of jaw.
  49. most malignant tumor of salivary glands
    • mucoepidermoid carcinoma. malignant mixed. malignancy less in parotid gland, more in submandibular.
  50. malignant mixed salivary gland tumor
    When primary or recurrent benign tumors are present for many (10-20) years and malignancy transformation occurs. Assoc w/ mucoepidermoid carcinoma
  51. hiatal hernia
    separation of diaphragmatic crura & widening of space btwn muscular crura & esophageal wall permits a dilated segment of stomach to protrude above diaphragm. Incr incidence w/ age
  52. sliding hernia
    • 95% of hiatal hernias. Heartburn, regurg. those w/ severe reflux esophagitis are likely to have a sliding hiatal hernia. Other complications include mucosal ulceration, bleeding, and even perforation.
    • Many go on to develop Barrett esophagus
  53. esophageal varices
    Caused by portal hypertension (most often secondary to cirrhosis) May cause massive bleeding into lumen or hematemesis
  54. Ulcer-like dyspepsia
    epigastric pain relieved by food or antacids, periodic or nocturnal pain, pain before meals or when hungry
  55. Dysmotility-like dyspepia
    nausea or vomiting, bloating and distention, anorexia or weight loss, pain aggravated by food or after meals
  56. delayed gastric emptying - gastroparesis
    common in longstanding type I diabetes. Nausea, vomiting, early satiety. Cause is autonomic neuropathy causing delayed emptying of gastric contents
  57. Dumping syndrome
    early satiety nausea & vomiting, sweats, syncope, diarrhea and flushing. Rapid emptying causes distension and release of gut hormones (serotonin) which contributes to symptoms
  58. Peptic ulcer
    1st part of duodenum or stomach lesser curvature. NOT precursor for malignancy. Recurs, most in middle aged to older pts. M>F. Punched-out mucosal defect, penetrates gastric or intestinal wall deeper than muscularis mucosa. Small lesions, margins not elevated
  59. Major risk factors for peptic ulcer
    smoking, corticosteroids, NSAIDs
  60. Duodenal ulcer
    Epigastric pain 1-3 hours after eating, pain relief with food. more frequent in persons with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism (hypercalcemia).
  61. Peptic ulcers can also be caused by
    Excess production of gastrin from a (pancreatic) tumor in individuals w/ Zollinger-Ellison syndrome --> HCl secretion -- > multiple peptic ulcerations in stomach, duodenum, and even jejunum.
  62. Peptic ulcer sx
    Epigastric burning pain tends to be worse at night & occurs usually 1 to 3 hours after meals during day. Nausea, vomiting, bloating, belching, and significant weight loss. Bleeding is chief complication.

    Obstruction from edema or fibrotic scarring
  63. Gastric ulcer
    may be aggravated by food
  64. Erosion
    Mucosal defect not deeper than the muscularis mucosa
  65. In older pts w/ sudden onset of ulcer (H pylori associated), needs to check for
    lymphoma or adenocarcinoma
  66. Gastritis
    assoc w/ peptic ulcer. H pylori tends to attack antrum of stomach & induce prox duodenal ulcers. Epithelial injury is by vacuolating toxin called VacA, regulated by cytotoxin-associ gene A (CagA). Secretes urease & phospholipases that breaks down urea to form toxic compounds such as ammonium chlorid
  67. In chronic, open peptic ulcer, 4 zones can be distinguished
    Superficial to deep: Necrotic zone, inflammatory zone, granulation tissue, fibrosis.
  68. complication of gastritis
    • Gastric metaplasia of the duodenum occurs in response to protect epithelium by making mucus --> Colonization
    • of metaplastic epithelium by H. pylori, which then makes the epithelium susceptible to ulceration
  69. acute gastritis
    • Hemorrhagic, erosive, stress gastritis, Epigastric pain, nausea, vomiting, bleeding
    • Mucosal edema and congestion. May see hemorrhage, neutrophils.
    • Etiology: toxins, drugs, alcohol, spices, systemic dz, opportunistic infections.
  70. Chronic gastritis - autoimmune (type A)
    Uncommon. Abs against acid-producing parietal cells, and intrinsic factor (IF) leading to mucosal atrophy (chronic atrophic gastritis) loss of acid production (hypochorhydria). Pernacious anemia. Associated w/ other autoimmune disorders. Lymphocytes, plasma cells, intestinal metaplasia (incr likelihood of gastric carcinoma)
  71. Chronic antral gastritis (type B)
    More common. Due to H. pylori. Most severe in antrum. infiltrate of lymphocytes, plasma cells and neutrophils with eventual intestinal metaplasia. Linked with gastric adenocarcinoma and MALT lymphoma. End result of both types A and B is chronic atrophic gastritis
  72. hyperplastic gastric polyps
    most common gastric polyp. Mucosal overgrowth secondary to chronic inflammation. Dilated and cystic gastric pits, lined by bland mucous cells
  73. adenomatous gastric polyps
    Precursers to gastric carcinomas. Found in older patients with chronic gastritis and intestinal metaplasia
  74. gastric [adeno]carcinoma
    higher incidence in Japan, most common malignancy in stomach, dysphagia, Linitus plastica- diffusely infiltrative (rigid thickened stomach wall- “leather bottle”) - advanced beyond submucosa, poor outcome. mostly involves pylorus, antrum, and lesser curvature of stomach
  75. gastric [adeno]carcinoma risk factors
    H pylori, smoking, genetics (HER2 NEU), chronic atrophic gastritis, nitrosamines.
  76. exophytic growth of gastric adenocarcinoma
    fungating, polypoid. protrusion of tumor mass into lumen; flat or depressed, in which there is no obvious tumor mass within the mucosa
  77. types of gastric adenocarcinoma
    exophytic, superficial spreading (limited to mucosa and submucosa), and excavating (most common)
  78. intestinal type adenocarcinoma
    gastric mucous cells that have undergone intestinal metaplasia in setting of chronic gastritis (H pylori). M>F. incr risk w/ blood group A for chronic gastritis w/ intestinal metaplasia (H pylori)
  79. virchow node
    earliest lymph node spread (of gastric carcinoma) that goes to supraclavicular lymph node
  80. Krukenberg tumor
    gastric carcinoma that spreads intraperitoneal to ovaries in females
  81. histo features of diffuse varient gastric adenocarcinoma
    • gastric-type mucous cells that generally do not form glands but rather permeate mucosa & wall as scattered individual "signet-ring" cells or small clusters in an "infiltrative" growth pattern
    • cells are filled with mucin vacuoles that push the nucleus to one side
  82. diffuse variant type gastric carcinoma
    arise de novo from native gastric mucous cells, mutations in E-cadherin, not assoc w/ chronic gastritis or H pylori infection, and poorly differentiated. Early age w/ female predominance.
  83. gastric lymphoma
    most assoc w/ H pylori (setting chronic gastritis), B cell origin, t(11,18) translocation is common, Celiac dz is associated w/ higher risk of intestinal T-cell lymphomas
  84. Zollinger Ellison (gastrinoma)
    tumor in pancreas, sometimes stomach and duodenum. Releases excessive gastrin. Diarrhea due to large volume of gastric acid and malabsorbtion secondary to inactivation of pancreatic enzymes by low pH.
  85. gastric carcinoids
    Derived from enterochromaffin-like cells of fundus/body or gastrin-producing cells of antrum. potentially malignant. Elevated levels of 5-HT, hepatic dysfxn. Show markers for chromogranin A, synaptophysin, and neuron-specific enolase
  86. gastric carcinoids
    excessive gastrin release similar to ZE syndrome, Cushing syndrome, hyperinsulin (hypoglycemia)
  87. most common site for gut carcinoid tumors
    appendix. rectal and appendiceal carcinoids almost never metastasizes. solid, yellow-tan appearance on transection. Tumors are exceedingly firm cuz of desmoplasia
  88. GI stromal tumors
    • derived from interstitial cells of Cajal (pacemaker cells) w/in muscle layers. Contain KIT antigen. smooth
    • muscle tumors, either benign leiomyomas or malignant leiomyosarcomas
  89. Gastric heterotopia
    congenital. a nidus of gastric mucosa in the esophagus or small intestine ("ectopic rest")
  90. chronic gastritis sx.
    heartburn, epigastric pain, nausea, vomiting, hematemesis (coffee grounds appearance of vomit), melana. Or no sx
  91. H pylori staining
    Steiner silver stain
  92. Stomach acid releases...
    Vit B12. Achlorhydria pts will also show pernacious anemia.
  93. signs of VitB12 anemia/aplastic anemia
  94. chronic gastritis features
    lymphocytic infiltration, plasma cells. development of peptic ulcer and gastric carcinoma
  95. causes of acute gastritis
    • heavy use of NSAIDs, particularly aspirin. Excessive alcohol, Heavy smoking, chemotherapeutic drugs,
    • Uremia, Systemic infections, Severe stress , Ischemia and shock, Suicide attempts with acids and alkali, mechanical trauma, Reflux of bilious material after distal gastrectomy
  96. acute gastritis can present as
    hematemesis, melena, epigastric pain, nausea, vomiting, and potentially fatal blood loss. Major causes of hematemesis, particularly in alcoholics.
  97. acute gastric ulceration signs/sx
    Severe trauma, sepsis, shock, or grave illness of any type, Chronic exposure to NSAIDs & corticosteroids, Extensive burns (Curling ulcers) , CNS injuries or intracerebral hemorrhage (called Cushing ulcers) can all be causes
  98. acute gastric ulcerations are found...
    anywhere in stomach, multiple lesions, small and circular. Doesn’t affect adjacent mucosa
  99. Duodenal adenoma
    rare, May occur at ampulla causing obstructive jaundice or bleeding, Pts with familial adenomatous polyposis (FAP) at increased risk
  100. duodenal adenocarcinomas
    rare, incr incidence in celiac dz, May also *present with obstructive jaundice or bleeding
  101. Peutz-Jeghers syndrome
    multiple Hamartomatous Polyps in GI tract, non dysplastic. uncommon, usually in cecum.
  102. Familial polyposis syndromes
    autosomal dominant. FAP accounts for most (APC gene, tubular adenomas, risk of colonic cancer is virtually 100% by midlife). Peutz-Jeghers polyps and Cowden syndrome both involve hamartomatous polyps
  103. Duodenal lymphoma
    • almost exclusively non-Hodgkin lymphoma, 7th decade, Ab pain, wt loss, and small bowel obstruction.
    • Increased incidence in celiac sprue.
  104. focal nodular hyperplasia. F>M. Not linked to oral contraceptives