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Gen Path Final > Gastrointestinal Pathology > Flashcards

Gastrointestinal Pathology Flashcards

1
Q

A. Inflammatory Lesions - Sialadenitis

1. Symptoms:

A

Dry mouth and/or gland swelling with pain

2. Sarcoidosis, mumps and salivary duct stones with obstruction

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2
Q

A. Inflammatory Lesions - Sialadenitis

3. Sjogren’s Disease

A

a. Autoimmune
b. Females, 4th-5th decades
c. Dry mouth (xerostomia), dry eyes (xerophthalmia, kerato-conjunctivitis sicca)
d. Intense lymphocytic infiltrate in salivary glands
e. Increased risk for lymphoma (40x)
d. Parotid enlargement; uni/bilateral
f. Primary SS (sicca syndrome)
g. Secondary SS (60%) occurs in setting of other autoimmune diseases (rheumatoid arthritis, SLE)

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3
Q

B. Salivary gland tumors

The parotid gland is the

A

most frequently involved (75% of total, 75% benign). Tumors present with enlargement of the gland and if malignant may involve the facial nerve with subsequent pain, paralysis, numbing.

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4
Q

B. Salivary gland tumors

1. Benign

A

a. Pleomorphic adenoma (mixed tumor)

b. Warthin tumor (papillary cystadenoma lymphomatosum)

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5
Q

a. Pleomorphic adenoma (mixed tumor)

A
  1. Most common neoplasm, 60% occur in parotid
    2. Lobulated, firm on palpation
    3. Variably encapsulated
    4. Epithelial and myoepithelial components
    5. 10% recurrences
    6. May undergo malignant transformation
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6
Q

b. Warthin tumor (papillary cystadenoma lymphomatosum)

A
  1. Primarily affects parotid gland
    2. Cystic neoplasm with papillary infoldings and lymphoid tissue
    3. 10% bilateral
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7
Q

Salivary gland tumors

2. Malignant

A

a. Mucoepidermoid carcinoma: squamous and mucous cells
1. Most common SG malignancy
2. Parotid and minor glands
3. May note bluish color due to mucin and cystic growth pattern
b. Other carcinomas, which include Adenoid cystic and Acinic cell

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8
Q

Esophagus:

Obstruction
1. Mechanical:

A

Post-inflammatory fibrosis/stenosis

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9
Q

Esophagus
obstruction:
2. Functional:

A

Discoordinated muscular contractions or spasms, diverticula may result;
achalasia (inability of lower esophageal sphincter to relax) difficulty in swallowing

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10
Q

Esophageal varices

1. Arise due to

A

portal hypertension

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11
Q

Esophageal varices:

2. Seen in

A

90% of cirrhotic patients

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12
Q

Esophageal varices:

3. Often asymptomatic, but

A

rupture can result in massive hemorrhage/death

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13
Q

Esophagitis:

  1. Extrinsic agents:
A

acids, Alkalis, Pill lodging, Chemical, Trauma, Heavy Smoking

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14
Q

Esophagitis:

2. Iatrogenic causes:

A

Chemotherapy, Radiation, Graft versus host disease

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15
Q

Esophagitis:

3. Infectious agents:

A

More common in immune-suppressed patients, include fungal and viral (CMV, HSV)

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16
Q

Esophagitis:

4. Intrinsic:

A

Reflux esophagitis-reflux of gastric juices-central to GERD (gastroesophageal reflux disorder) associated mucosal injury
a. Symptoms: dysphagia, heartburn, regurgitation gastric contents. Odynophagia = pain on swallowing.

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17
Q

Esophagitis:

5. Oral manifestations of GI Reflux:

A

a. Gastric acid enamel erosion may be seen in patients with chronic gastric reflux (e.g. GERD, hiatal hernia, chronic alcoholism and bulimia)
b. Enamel loss often affects lingual/palatal surfaces
c. Extent of loss may reflect reflux duration or frequency

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18
Q

Barrett Esophagus

A
  1. Intestinal metaplasia within the esophagus squamous mucosa
  2. Complication of GERD with increased risk of adenocarcinoma.
    NOTE: despite risk, most persons with Barrett esophagus do not develop esophageal tumors.
  3. Diagnostic features for Barrett esophagus: 1) extension abnormal mucosa above gastro-esophageal junction, 2) demonstration of squamous metaplasia (intestinal metaplasia).
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19
Q

E. Esophagus-benign and malignant tumors

  1. Benign lesions:
A

Leiomyomas (tumors of smooth muscle), mucosal polyps, squamous papillomas, Lipomas (tumor of fat)

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20
Q

E. Esophagus-benign and malignant tumors:

  1. Malignant lesions: 8 % of all GI cancer
    a. Esophageal adenocarcinoma:
A
  • Worldwide rate < SCCa or esophagus
  • Usually affect the distal third of the esophagus
  • Associated with long-standing GERD or Barrett change
  • Increased in Caucasians
  • Increased in males over females (7:1)
  • Dysphagia, “Chest Pain”, weight loss
  • Often detected at late stage: 25% 5yr survival.
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21
Q

E. Esophagus-benign and malignant tumors b. Squamous cell carcinoma (SCC) of the esophagus:

A
  • Adults
  • > 45 yo
  • Males > females (4:1)
  • Esp. African-American males (6:1 vs white men)
  • Risk factors: EtOH, tobacco use, very hot beverages, caustic esophageal injury, vitamin/trace metal deficiencies, fungal contamination of food, nitrates and nitrosamines
  • Occurs primarily in the middle third of the esophagus
  • Most common esophageal malignancy worldwide, but regional variation recognized (Diet, environment, genetics, most common variant in China, Brazil, South Africa)
  • Plummer Vinson, Achalasia, Esophagitis
  • Very poor prognosis (9% 5 yr survival)
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22
Q

Acute gastritis

A
  • Abrupt, transient
  • Pathogenesis: Cigarettes, Alcohol, Stress, Ischemia, NSAID’s, aspirin, infection
  • May range from asymptomatic to pain, nausea and vomiting. May develop erosion and/or hemorrhage.
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23
Q

Acute gastritis:

• Pathology:

A

Punctate hemorrhage, erosion, edema, acute inflammation

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24
Q

Chronic gastritis

• Primarily caused by

A

infection with Helicobacter pylori in patients with H. pylori (spiral or curved bacilli): 90% of cases.

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25
Q

Chronic gastritis:

• Often acquire the infection in

A

childhood.

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26
Q

Chronic gastritis:

• Helicobacter pylori present in

A

65 % of gastric ulcers, 85-100 % of duodenal ulcers

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27
Q

Chronic gastritis:

• Treatment with

A

antibiotics and proton pump inhibitors.

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28
Q

Chronic gastritis:

• Autoimmune-gastritis

A

: 10 % of cases (E.g. Pernicious Anemia

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29
Q

Chronic gastritis:

• Pathology:

A

atrophic epithelium, chronic inflammation, intestinal metaplasia

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30
Q

Chronic gastritis:

• Clinical course:

A

Ulceration, cancer risk 2-4% (intestinal metaplasia)

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31
Q
  1. Peptic ulcer disease
A
  • H. pylori, NSAID use
  • Gastric hyperacidity, recurrent ulcers with intermittent healing
  • 98 % duodenum or stomach
  • Lifetime risk about 10 % for males, 4 % females
  • Peptic ulcer complications: Intractable pain, hemorrhage, perforation (5 %), obstruction-edema, fibrosis (2 %)
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32
Q

B. Stomach neoplasia:

Benign:

A
  • Hyperplastic, fundic gland polyps, adenomas & inflammatory polyps
  • Approximately 75% of gastric polyps are inflammatory or hyperplastic.
  • Leiomyomas
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33
Q

B. Stomach neoplasia

Gastric adenomas:
• Increased in

A

Familial adenosis polyposis (FAP) patients and most frequently arise in a background of atrophy and intestinal metaplasia.

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34
Q

B. Stomach neoplasia
3. Gastric adenocarcinoma:
• 90-95 % of gastric cancers are

A

adenocarcinomas

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35
Q

B. Stomach neoplasia
3. Gastric adenocarcinoma:
• Other malignant tumors of the stomach include:

A

Lymphoma (4 %), Carcinoid (3 %), Spindle cell tumors (2 %)

36
Q

B. Stomach neoplasia
3. Gastric adenocarcinoma::
• =—– of all cancer deaths
•

A

3 %

37
Q

B. Stomach neoplasia
3. Gastric adenocarcinoma:
Overall marked decrease in U.S. due to reduced use of

A

smoked and salt-cured meat. There is an association with GERD-due to increased rates for cancer of gastric cardia. Linitis plastica “leather bottle appearance” markedly thickened stomach wall, reactive to diffusely-infiltrative, aggressive form of stomach cancer.

38
Q

B. Stomach neoplasia
3. Gastric adenocarcinoma:
• Risk factors for development of gastric adenocarcinomas

A

: Hereditary factors, consumption of smoked and salt cured meat (Nitrites), GERD, Pernicious anemia (B12deficiency), atrophic gastritis (intestinal metaplasia), Chronic gastritis (H. pylori), A pre-existing adenomatous polyp
• 5 year survival < 10 % (advanced)

39
Q

B. Stomach neoplasia
3. Gastric adenocarcinoma:
• Prognosis: Dependent on

A

depth of invasion, metastasis

40
Q

B. Stomach neoplasia
3. Gastric adenocarcinoma:
• Metastasis:

A

Liver, lung, ovaries, supraclavicular lymph node (Virchow’s node)

41
Q

a. Ulcerative colitis-

A

severe ulcerating inflammatory disease that is limited to the colon and rectum-extends only to mucosa and submucosa.

42
Q

b. Crohn disease-

A

regional enteritis-may involve any area of the GI tract; frequently transmural. “Skip lesions”, non-caseating granulomas.

43
Q

c. Both UC and Crohn are more frequent in

A

women, teens and early 20s for presentation.

44
Q

Both UC and crohn are

A

idiopathic disorders-not autoimmune, per se. Felt these 2 diseases result from a combination of deficits entailing host interactions and GI microflora, intestinal epithelial dysfunction and aberrant mucosal immune responses.

45
Q

e. UC related to Crohn, but UC is limited to the

A

colon and always involves the rectum. May also note hybrid “Indeterminant Colitis”.

46
Q

f. Increased risk of neoplasia, particularly with

A

UC.

47
Q

A. Small Intestine-reactive, non-neoplastic conditions

A
  1. Small intestine malabsorptive diarrhea
  2. Celiac disease
  3. Infectious enterocolitis e.g. Vibrio cholerae, Campylobacter jejuni-acute, self-limited colitis “traveler’s diarrhea”.
  4. Viral gastroenteritis and parasitic enterocolitis
  5. Inflammatory Bowel Disease-arises from inappropriate mucosal immune activation. See Section III. Crohn Disease and ulcerative colitis.
48
Q

a. Ulcerative colitis-

A

severe ulcerating inflammatory disease that is limited to the colon and rectum-extends only to mucosa and submucosa.

49
Q
  1. Small intestine malabsorptive diarrhea
A

• Celiac disease (Gluten allergen), Tropical sprue (Aerobic bacteria), Lactase (disaccharidase) deficiency, Abetalipoproteinemia (Transepithelial transport defect, mono- and triglycerides)

50
Q

. Celiac disease

A
  • Gluten-sensitive enteropathy
  • Caucasians; 1:100-200
  • Hypersensitivity to gliadin
  • Morphology: Blunted villi, Inflammatory infiltrate
  • Dramatically improves with withdrawal of wheat gliadin and related grain proteins from the diet
51
Q

c. Both UC and Crohn’s-are

A

more frequent in women, teens and early 20s for presentation.

d. Both are idiopathic disorders-not autoimmune, per se. Felt these 2 diseases result from a combination of deficits entailing host interactions and GI microflora, intestinal epithelial dysfunction and aberrant mucosal immune responses.
e. UC related to Crohn-but UC is limited to the colon-and UC always involved the rectum. May also note hybrid “Indeterminant Colitis”.
f. Increased risk for neoplasia

52
Q

Clinical aspects of malabsorption:

A
  1. Anemia: Iron, Pyridoxine, Folate, or B12 deficiency, bleeding from Vitamin K deficiency
  2. Osteopenia, tetany: Defective Ca, Mg, Vitamin D and protein absorption
  3. Amenorrhea, impotence and infertility: Generalized malnutrition
  4. Deficiencies in Vitamin A and B12: Peripheral neuropathy, nyctalopia (↓ Vitamin A)
  5. Oral manifestations of Malabsorption: Iron malabsorption → Iron deficiency, anemia, Vitamin B12 malabsorption, pernicious anemia. If severe, initial oral sign can be atrophic glossitis (bald, reddish tongue). Patchy or involvement of entire dorsum surface of tongue. Overt tongue lesions are usually tender. Burning sensation (glossopyrosis) is a common complaint.
53
Q

Tumors of the Small Intestine

1. Accounts for less than

A

6% of all GI tumors

54
Q

Tumors of the small intestine:

2. Benign:

A

Adenoma, leiomyoma

55
Q

Tumors of the small intestine:

3. Malignant:

A

Adenocarcinomas, carcinoid tumors (often associated with hormone production), lymphoma, sarcoma.

56
Q

Colon histology:

A
  • No villi
  • Tubular crypts
  • Surface absorptive cells
  • Goblet, endocrine, undifferenciated
  • Occasional Paneth cells in cecum and ascending colon
57
Q

A. Colon polyps

A

• Extensions into the colonic lumen

a. Hyperplastic: ↑ number of cells
b. Inflammatory
c. Hamartomatous: ↑ in tissue normally at this site
d. Adenomatous: Neoplastic, tumor

58
Q

B. Adenoma

A
  • Neoplastic
  • Dysplastic
  • Shape: Tubular, tubulo-villous, Villous
  • Size: Most important predictor of malignant change
59
Q

. TNM Classification

A 
T: Depth of tumor invasion
    1.	Submucosa
    2.	Muscularis propria
    3.	Subserosa or pericolic fat
    4.	Contiguous structures
N: Lymph nodes
M: Metastasis
60
Q

C. Adenocarcinoma of the Colon:

• Most common

A

malignancy of GI tract

61
Q

C. Adenocarcinoma of the Colon:

• Most common malignancy of the GI tract. Although the small intestine comprises 75% of the length of the GI tract,

A

colon is site of many more tumors. Overall, the GI tract is an uncommon site for neoplasia.

62
Q

C. Adenocarcinoma of the Colon:

• In the U.S.-colorectal CA is responsible for

A

causing 15% of all CA deaths, and is second only to lung cancer in cancer deaths.

63
Q

C. Adenocarcinoma of the Colon:

• Dietary factors are implicated-

A

especially low intake of unabsorbable vegetable fiber and high intake of refined carbohydrates and fat.

64
Q

C. Adenocarcinoma of the Colon:

• Genetic component:

A

increased incidence in FAP patients.

65
Q

C. Adenocarcinoma of the Colon:

• Most cancers arise within

A

pre-existing adenomas, and colonoscopies are effective screening tools.

66
Q

Adenocarcinoma of the colon:

• Other risk factors:

A

Age > 50 years, family history of colorectal carcinoma, inflammatory bowel disease, personal history of adenoma/colorectal carcinoma

67
Q

Adenocarcinoma of the Colon:

• Most important prognostic indicators:

A

Depth of invasion and lymph node metastases

68
Q

A. Familial Adenomatous Polyposis

• Entails mutations of

A

APC gene. Most common polyposis syndrome of the gastrointestinal tract

69
Q

A. Familial Adenomatous Polyposis:

• Estimated penetrance for adenomas

A

> 90 %: Adenomas throughout colorectum (average onset 16 yo)

70
Q

A. Familial Adenomatous Polyposis:

• Rsk of \

A 
extracolonic tumors (upper GI, desmoid, osteoma, thyroid, brain, other)
•	Risk of affected patients developing colon cancer approaches 100%
71
Q

A. Familial Adenomatous Polyposis:

• Require

A

> or equal to 100 polyps to diagnose FAP

72
Q
  1. Gardner’s syndrome:
A

FAP + Extraintestinal lesions

73
Q

Gardner’s syndrome:

• Oral manifestions of Gardner syndrome:

A

Unerupted teeth, supernumerary teeth, dentigerous and mandibular cysts, increased risk for odontomas, delayed tooth eruption. Also develop benign skin lesions. Congenital hypertrophy of retinal pigment epithelium (CHRPE).

74
Q

Gardner’s syndrome:

• Oral manifestations can contribute to

A

early recognition of the condition and allow for appropriate screening for bowel disease and other neoplasms

75
Q

B. Peutz Jegher Syndrome

• Second most common

A

polyposis syndrome

more common after 45 yo.

76
Q

B. Peutz Jegher Syndrome:

• ——– and pigmented ——– of mucous membranes and skin.

A

Gastrointestinal hamartomatous polyps (Intussusception)

macules

77
Q

B. Peutz Jegher Syndrome:

• Melanin deposits around

A

nose, lips, buccal mucosa, hands and feet, genitalia and perianal region. Develop in early childhood

78
Q

B. Peutz Jegher Syndrome:

• ———— skin around the lips and the vermilion zone of the lips – Common feature.

A

Non-sun dependant freckling of the

79
Q

B. Peutz Jegher Syndrome:

• Average age at diagnosis:

A

23 -26 yo

80
Q

Peutz jegher syndrome:

• 0—————- cancer

A

Gastrointestinal and non gastrointestinal

81
Q

A. Crohn Disease:

1.  	Clinical manifestations
A
  • Chronic intermittent diarrhea +/- blood, colicky abdominal pain
  • Presents in young adulthood
82
Q

A. Crohn Disease:

Pathology

A
  • Segmental transmural inflammation of bowel, particularly ileum (distal small bowel) and colon. Any portion of the GI tract → Oral involvement frequently seen
  • Frequently spares the rectum
  • Ulcerations, granulomas, thickened bowel wall, stenotic, with fat wrapping, fissure and fistula formation, Noncaseating granulomas
  • Distribution: Often note “skip lesions”
83
Q

A. Crohn Disease:

Oral manifestations:

A

a. Multifocal, linear, nodular, polypoid or diffuse mucosal thickening with predilection for labial and buccal mucosa and mucosal folds –Can be confused with aphthous ulcers.
b. Mucosal ulcer “cobblestone” Diseased tissue lower than normal tissue
c. Subepithelial, noncaseating granulomatous inflammation identical to those seen in the bowel. Infections (fungal, TB) should be ruled out.
d. Typically persistent and remit and relapse over the years.

84
Q

B. Ulcerative Colitis:

Clinical:

A
  • Diarrhea, tenesmus, colicky lower abdominal pain

* Risk for development of carcinoma

85
Q

B. Ulcerative Colitis:

Pathology:

A
  • Begins in rectosigmoid area and extends proximally. Not transmural
  • Continuous (diffuse) involvement (pseudo-polyps), not patchy
  • Small to large ulcerations, crypt abscesses
  • Greater risk of dysplasia and adenocarcinoma
  • Association with primary sclerosing cholangitis (PSC
86
Q

B. Ulcerative Colitis:

Oral manifestations:

A

a. Rare, less common than in Crohn disease
a. Scattered, clumped or linearly oriented arc-shaped pustules on an erythematous mucosa at multiple oral sites with variable severity, “snail-track” (Pyostomatitis Vegetans), but may also be seen in Crohn patients
b. Long-standing lesions may become granular, polypoid or fissured and mimic Crohn disease
c. 10% of patients develop arthritis of temporo-mandibular joints.
d. Lesions mimic the crypt abscesses of colonic lesions with no evidence of granulomas. Rule out candidiasis, benign migratory glossitis, and pemphigus vegetans.

Gen Path Final (18 decks)

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