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Gen Path > Exam 3 - GI Pathology > Flashcards

Exam 3 - GI Pathology Flashcards

1
Q

Oral manifestations of GI disease can:

A

precede the onset of lower GI disease
be present during the disease process and be similar to lower GI lesions
persist even after disease has resolved
reflect systemic alterations secondary to GI disease (malabsorption)

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2
Q

Describe the secretions of each salivary gland.

A

Parotid - serous
Sublingual - mucous
Submandibular - mixed
Minor gland - mixed

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3
Q

What conditions result in inflammatory salivary gland lesions?

A

Sialoliths (stones)
Mumps
Sarcoidosis
Sjogren Syndrome

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4
Q

What are symptoms of inflammatory lesions in the salivary gland?

A

dry mouth
swelling
pain

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5
Q

What are characteristics of Sjogren Syndrome?

A

Autoimmune disease
More common in females 4th-5th decades
dry mouth, dry eyes, keratoconjunctivitis sicca
intense lymphocytic infiltrate in salivary glands
increased risk for lymphoma (40x)
Parotid enlargement (unilateral/bilateral)
Can be primary or secondary

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6
Q

Describe primary Sjogren Syndrome.

A

People just develop the disease.

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7
Q

Describe secondary Sjogren Syndrome.

A

Occurs when the person has another autoimmune disease (rheumatoid arthritis, Lupus)

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8
Q

Which salivary gland is most frequently affected by tumors?

A

parotid - 75% –> and 75% of those are benign

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9
Q

What are the two types of benign salivary gland tumors we are focusing on?

A 
Pleomorphic adenoma (mixed tumor)
Warthin Tumor
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10
Q

What is the type of malignant salivary gland tumor we are focusing on?

A

Mucoepidermoid carcinoma

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11
Q

What are some increased risks of oral disease of someone with Sjogren syndrome?

A

increase caries risk (esp root caries)

increased candidiasis risk

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12
Q

What are some characteristics of pleomorphic adenoma?

A 
most common neoplasm
60% occur in parotid gland
lobulated, firm on palpation
variably encapsulated
10% recurrence
may undergo malignant transformation
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13
Q

Describe characteristics of Warthin tumor.

A

occurs in the parotid gland
more common in males
10% are bilateral

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14
Q

Describe mucoepidermoid carcinoma.

A

most common malignant salivary gland tumor
affects parotid and minor salivary glands
May look bluish in color b/c mucin and cystic growth pattern

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15
Q

Is mucoepidermoid carcinoma aggressive?

A

not usually, but can be if it occurs in the parotid

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16
Q

What is the normal epithelium of the esophagus?

A

light keratinized stratified squamous epithelium

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17
Q

What can cause the esophagus to be obstructed?

A

mechanical or functional issues

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18
Q

What are examples of mechanical esophageal obstructions?

A

post-inflammatory fibrosis/stenosis

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19
Q

What are examples of functional esophageal obstructions?

A

discoordinated muscular contractions/spasms
diverticula
achalasia (lower sphincter doesn’t open)

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20
Q

What is a vascular disease of the esophagus?

A

esophageal varices

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21
Q

Describe esophageal varices.

A

arise from portal hypertension
seen in 40% of cirrhotic pts (hepatitis or alcohol)
often asymptomatic

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22
Q

What occurs if an esophageal varice ruptures?

A

massive hemorrhage or death

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23
Q

What is esophagitis?

A

inflammation of the esophagus

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24
Q

What extrinsic agents cause esophagitis?

A 
chemicals
iatrogenic (caused by medical tx)
infections
trauma
heavy smoking
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25
Q

What are intrinsic agents that cause esophagitis?

A

GERD/reflux

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26
Q

What are iatrogenic agents?

A

caused by medical procedures: chemo, radiation, graft versus host disease

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27
Q

What type of people is esophagitis more likely to occur?

A

immunosuppressed pts

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28
Q

If someone had GERD/reflux, what are some oral signs/symptoms?

A

enamel erosion on lingual/palatal surfaces

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29
Q

What is Barret Esophagus?

A

alteration/intestinal metaplasia within the esophagus squamous mucosa (associated with GERD)

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30
Q

If someone had GERD, they are at increased risk for ______.

A

adenocarcinoma

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31
Q

Do patients with Barret Esophagus develop tumors?

A

No

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32
Q

What diagnostic features does someone with Barret Esophagus have?

A

extension of abnormal mucosa above the gastro-esophageal junction
demonstration of squamous metaplasia

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33
Q

Barret Esophagus can be in short segments or longer segments. Which is associated with more risk?

A

long segment

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34
Q

Name the two types of benign esophageal neoplasms/tumors we are focusing on.

A

Leiomyoma (tumors of smooth muscle)

Mucosal polyps

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35
Q

What are the two types of malignant esophageal tumors/neoplasms we are focusing on?

A

adenocarcinoma

squamous cell carcinoma

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36
Q

What percent of esophageal neoplasms are malignant?

A

8%

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37
Q

Describe esophageal squamous cell carcinoma.

A

caused by smoking and alcohol use
more common in males (esp African American)
9% 5 yr survival (poor prognosis)

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38
Q

What region of the esophagus does squamous cell carcinoma occur?

A

middle 1/3 of the esophagus

most common worldwide

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39
Q

What are regional variations of squamous cell carcinoma due to?

A

diet (minerals, vitamins, nitrates, fungal contamination)
environment
genetics

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40
Q

What disease can result from squamous cell carcinoma in the esophagus?

A

Plummer Vinson (iron deficiency anemia)
achalasia
esophagitis

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41
Q

Describe esophageal adenocarcinoma

A

Not as widespread as squamous cell carcinoma
results from Barret esophagus
more common in white males

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42
Q

What portion of the esophagus does esophageal adenocarcinoma occur?

A

distal 1/3 of the esophagus

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43
Q

What are some symptoms of esophageal adenocarcinoma?

A

dysphagia (difficulty swallowing), chest pain, weight loss

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44
Q

What is gastritis, and what are the different types?

A

inflammation of the stomach
acute
chronic
autoimmune

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45
Q

Describe acute gastritis.

A

abrupt, transient

asymptomatic, epigastric pain, hemorrhage

46
Q

What is the pathogenesis of acute gastritis?

A

cigarettes, alcohol, stress, ischemia, NSAIDs, aspirin, infection

47
Q

Pathology of acute gastritis.

A

punctate hemorrhage
erosion
edema
acute inflammation

48
Q

What is the pathogenesis of chronic gastritis?

A

Helicobacter pylori (90% of cases)
autoimmune (pernicious anemia)
acquired in childhood
present in 85-100% of duodenal ulcers

49
Q

Pathology of chronic gastritis

A

atrophic epithelium
chronic inflammation
intestinal metaplasia
ulcerations

50
Q

How do you treat chronic gastritis?

A

antibiotics

proton pump inhibitors

51
Q

Why can chronic gastritis be autoimmune? What occurs?

A

Pernicoious anemia.

The body develops antibodies to intrinsic factors –> parietal cells

52
Q

Is H. pylori gram negative or gram positive?

A

gram negative, curved

53
Q

What contributes to peptic ulcer disease?

A

H. pylori
NSAID use
smoking

54
Q

Pathology of peptic ulcer disease.

A

Gastric hyperacidity

recurrent ulcers w/ intermittent healing

55
Q

Where do peptic ulcers typically occur in the body?

A

98% duodenum or

stomach

56
Q

True or False:

If someone has peptic ulcer disease they are 10% (males) 4% (females) more likely to have lifetime risk of cancer.

A

True

57
Q

What are some complications from peptic ulcers?

A 
intractable pain
hemorrhage
perforation
obstruction-edema
fibrosis
58
Q

What is an important structure contained in the small intestine?

A

Villi - increase surface area for absorption

59
Q

What diseases are associated with small intestine malabsorptive diarrhea?

A 
Celiac disease (gluten allergy)
Tropical sprue (aerobic bacteria)
Lactase deficiency
abetalipoproteinemia (mono & triglycerides)
60
Q

How common is Celiac disease?

A

1:100-200 people

61
Q

What protein group do Celiac patients have hypersensitivity to?

A

gliadin

62
Q

What occurs histologically in a Celiac patient?

A

Villi are blunted leading do decreased absorption

63
Q

Treatment of Celiac disease.

A

Withdrawal of wheat gliadin and related proteins from diet

64
Q

What might you see clinically in malabsorption?

A

anemia (B12, folate, Vit K deficiency)

Osteopenia, tetany, amenorrhea, infertility

65
Q

If you have osteopenia/tetany what are you deficient in?

A

calcium
magnesium
vitamin D
protein absorption

66
Q

If you have deficiencies in vitamin A or B12 what occurs?

A

peripheral neuropathy

nyctalopia (difficult to see at night)

67
Q

What are some oral manifestations if you have malabsorption?

A

atrophic glossitis (bald, red tongue)
patchy dorsum
overt tongue lesions - usually tender
glossopyrosis (burning sensation)

68
Q

Are there any villi in the colon?

A

No villi

69
Q

What other histology do you find in the colon?

A

tubular crypts
surface absorptive cells
goblet, endocrine
occasionally paneth cells in cecum and ascending colon

70
Q

What is a polyp?

A

an extension into the lumen

71
Q

What are the different types of colon polyps?

A

hyperplastic ( increase number of cells)
inflammatory
harmartomatous (increase in tissue normally at this site)
adenomatous (neoplastic, tumor)

72
Q

What is the most important predictor of malignant change in colon adenomas?

A

size; larger is more likely to be malignant

73
Q

What shape can colon adenomas take?

A

tubular
tubulo-villous
villous

74
Q

What gene is mutated in familial adenomatous polyposis?

A

APC gene

75
Q

What is the percentage of penetrance for adenomas in FAP (familial adenomatous polyposis)?

A

90%

76
Q

What types of extracolonic tumors is a person with FAP at risk of developing?

A 
upper GI
desmoid (connective tissue)
osteoma
thyroid
brain, etc.
77
Q

What feature in FAP may be present early on, in children?

A

CHRPE

congenital hypertrophy of retinal pigment epithelium

78
Q

If FAP goes untreated what percentage ends with cancer?

A

100%

79
Q

What is Gardner Syndrome?

A

It is just like FAP, but with additional head and neck features

80
Q

What types of extraintestinal features are noted in Gardner Syndrome?

A

epidermoid cysts
jaw osteomas
supernumerary and unerupted teeth
increased odontomas

81
Q

What is the second most common polyposis syndrome?

A

Peutz-Jeghers Syndrome

82
Q

What is different about the polyps in Peutz Jeghers?

A

the polyps are not precancerous, but the patient is at increased risk for GI adenocarcinoma

83
Q

What are some key features of Peutz-Jegher Syndrome?

A

perioral pigmentation
non-sun dependent freckling around the lips/vermilion zone
melanin deposits around nose, lips, buccal mucosa

84
Q

What type of GI polyps are found in Peutz-Jeghers Syndrome?

A

harmartomatous polyps which can cause intussusception (strangling of the bowel)

85
Q

What surfaces does ulcerative colitis affect?

A

It is contiguous, non-transmural, and is limited to the rectosigmoid area and extends proximally.

86
Q

What are the two types of ulcerative inflammatory diseases of the colon we are focusing on?

A

Crohn disease

ulcerative colitis

87
Q

What surfaces does Crohn disease affect?

A

It is segmental (“skip lesions”), transmural, and involved in any portion of the GI tract.

88
Q

Is ulcerative colitis often found in the oral cavity?

A

No, oral manifestations are rare

89
Q

Are oral manifestations common with Crohn disease?

A

Yes they are frequently seen

90
Q

What is the most common place to fine Crohn disease?

A

terminal ileum

91
Q

What are some other pathological findings in Crohn disease?

A

thickened bowl wall
“cobblestone” oral mucosal ulcer
noncaseating granulomas

92
Q

What are some pathological findings in ulcerative colitis?

A

mucosal ulceration

continuous pseudo-polyps

93
Q

What is the pathology of oral lesions if they are seen with ulcerative colitis?

A

scattered, arc-shapped pustules on erythematous mucosa

94
Q

What is the pathology of oral manifestation if seen with Crohn disease?

A

hyperplastic gingivitis
contiguous ulcerations
cobblestone mucosal ulcers
granular lesions

95
Q

What is the term used for the arc-shaped pustules on erythematous mucosa found in the oral cavity associated with ulcerative colitis?

A

Pyostomatitis Vegetans

96
Q

What percentage of patients with ulcerative colitis develop arthritis in the TMJ?

A

10%

97
Q

What is pseudomembranous colitis associated with?

A

C. difficile

98
Q

What types of benign tumors of the stomach are we focusing on?

A

inflammatory
reactive
Leiomyomas

99
Q

What areas of the stomach do leiomyomas affect?

A

smooth muscle

100
Q

What malignant tumors of the stomach are we focusing on?

A

adenocarcinoma
lymphoma
carcinoid (neuroendocrine tumor)
spindle cell tumors

101
Q

What are the risks for gastric carcinoma?

A

diet
genetics
adenoma
chronic gastritis

102
Q

What determines the prognosis of gastric carcinoma?

A

depth of invasion and metastasis

103
Q

Where can gastric carcinoma metastasize?

A 
liver
lung
ovaries
supraclavicular
lymph node (Virchow's node)
104
Q

What type of cells are present in gastric cancers?

A

signet ring cells

105
Q

What are some small intestine tumors?

A

Benign: adenoma, leiomyoma
Malignant: adenocarcinoma, carcinoid, lymphoma, sarcoma

106
Q

What is the most common type of malignancy in the GI tract?

A

Colon adenocarcinoma

107
Q

What are important indicators for prognosis of colon adenocarcinoma?

A

depth of invasion

lymph node metastases

108
Q

What percentage of all cancer deaths is colon adenocarcinoma responsible for in the USA?

A

15%

109
Q

What are risk factors for colorectal cancers?

A 
high fat, low fiber diet
over age 50
family hx of colorectal carcinomas
IBD
FAP family hx
personal hx of adenoma/colorectal carcinomas
110
Q

What classification system is used for colon cancers?

A

TMN classification

111
Q

What does TMN stand for?

A 
T - depth of tumor invastion
* 1. submucosa
*2. muscularis propria
*3. subserosa or pericolic fat
*4. contiguous structures
N - lymph nodes
M - metastasis

Higher stage = lower survival

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