GI 1 Flashcards
1
Q
What is the fancy word for “Canker Sore?”
A
Aphthous ulcer
2
Q
Are aphthous ulcers found or keratinized, or non-keratinized epithelium?
A
Non-keratinized
3
Q
What four things can trigger aphthous ulcers?
A
- Stress
- Fever
- Indigestion
- IBD
4
Q
What two types of inflammatory cells are found in an aphthous ulcer? Name two other characteristics.
A
Monocytes and polys. The lesions have a red (erythematous) rim and gray-white exudate.
5
Q
Name the condition: Shallow ulcer of the oral cavity covered by fibrinopurulent exudate with underlying infiltrate composed of monocytes and polymorphs.
A
Aphthous ulcer
6
Q
Are aphthous ulcers usually self-limiting and heal without scarring?
A
Yeah.
7
Q
Which viruses causes herpetic stomatitis?
A
HSV1 or HSV2
8
Q
____% of the population becomes infected by the HSV1 virus by midlife.
A
75%
9
Q
Primary infection with herpes simplex virus is ___________ and the virus persists in a _________ state within ganglia around the mouth.
A
asymptomatic, persists in a dormant state
10
Q
Are oral infection rates of HSV2 rising?
A
Yeah
11
Q
Name eight things that can activate the herpex simplex virus.
A
- Fever
- Sun
- Cold exposure
- Respiratory tract infection
- Allergies
- Immunosuppression
- Pregnancy
- Trauma
12
Q
Describe herpes lesions (size, what they’re filled with, where they occur).
A
Small (<5mm dia), single or multiple, filled with clear exudate on lips and around nasal orifices.
13
Q
Do herpes lesions often rupture?
A
Yeah
14
Q
Name three cellular changes seen in a herpes lesion.
A
- Ballooning degeneration of infected cells.
- Intranuclear acidophilic viral inclusions.
- Multinucleated polykaryons (fusion of cells).
15
Q
What is the Tzanck test? Name one infection that yields a positive Tzanck test.
A
Looking at vesicle fluid (from a blister) under the microscope and seeing acidophilic viral inclusions and polykaryons. Typical of Herpes infection.
16
Q
Herpetic gingivostomatitis and lymphadenopathy may develop in herpes-infected patients who are __________.
A
immunocompromised
17
Q
Which infectious agent causes pseudomembranous candidiasis/thrush? Where is this agent found?
A
Caused by the yeast Candida albicans which is part of the normal oral biota.
18
Q
Name six conditions that can put a person at risk for oral candidiasis/thrush.
A
- DM
- Anemia
- Antibiotic or steroid therapy.
- HIV infection
- Metastatic cancer
- Infants can get it
19
Q
Describe the gross appearance of a thrush lesion.
A
White, curd-like circumscribed plaque in the oral cavity.
20
Q
Oral candidiasis may spread to the _________ and is life-threatening if it continues to spread.
A
esophagus
21
Q
Why is candidiasis referred to as PSEUDOmembranous?
A
The pseudomembrane can be scraped off.
22
Q
What is found in the pseudomembrane of a thrush plaque?
A
Fungal organisms in the fibrous pus (fibrinosupperative exudate) which are superficially attached to the underlying granular erythematous inflammatory mucosa.
23
Q
What is the WHO definition of leukoplakia?
A
A white patch or plaque that CAN’T BE SCRAPED OFF and can’t be classified as any other disease.
24
Q
Is leukoplakia cancer?
A
No, its a preneoplastic lesion.
25
Which habits predispose people to leukoplakia?
Use of tobacco, especially pipe smoking and chewing tobacco.
26
What is buccal mucosa?
The inside lining of the cheeks
27
Do aphthous ulcers often occur in the same exact locations repeatedly?
Yeah
28
Can leukoplakia vary from simple hyperkeratosis without underlying dysplasia to severe dysplasia bordering on carcinoma in situ?
Yeah
29
What is the frequency of malignant transformation from leukoplakia to squamous cell carcinoma?
5 to 25%
30
What is erythroplakia? Is it precancerous?
Much like leukoplakia, except red. Also is precancerous.
31
What percentage of erythroplakia lesions undergo malignant transformation?
50%
32
Describe the morphological changes of erythroplakia.
Red, granular, circumscribed, may or may not be elevated, poorly defined and irregular boundaries.
33
In which disease do keratin pearls form? What are they?
Squamous cell cancer only. When keratin sheds off from endophytic cancer cells (cells that have invaded inwards) and become trapped.
34
Name the disease: Mumps, enlargement of all three major salivary glands, especially the parotid.
Sialadenitis.
35
What infectious agents cause sialadenitis?
Paramyxovirus.
Also bacterial (usually secondary to duct obstruction): Staph aureus, Strep viridans
36
In which populations is sialadenitis most problematic? What are three potential complications?
Adults - can lead to pancreatitis, orchitis, or sterility.
Not too bad in children.
37
What type of cancer are 95% of all head and neck cancers? Where exactly do they most commonly arise?
Squamous cell carcinomas, most commonly in the oral cavity.
38
At what age are oral and tongue cancers most common?
40
39
What is the prognosis for oral and tongue cancers?
50% die in five years because they metastasize by the time they are detected.
40
Name six factors that increase risk for oral cancer.
1. Leukoplakia
2. Erythroplakia
3. Tobacco use (pipe and smokeless especially).
4. Alcohol abuse
5. HPV 16 and 18
6. Betel quid and paan
41
Where are oral/tongue squamous cell carcinomas usually found?
Found in lateral margin of lower lip, floor of mouth, lateral borders of tongue
42
Describe the progression of a squamous cell carcinoma lesion in the oral cavity.
They look like leukoplakias early on, then they grow outwards (exophytic fashion). They can later become fungating (necrotic and ulcerated). Later they may grow inwards (endophytic) and become invasive with a region of central necrosis.
43
Can squamous cell carcinomas invade the underlying CT BEFORE they progress to a full thickness dysplasia (carcinoma in situ)?
Yeah!
44
Who has a better prognosis: A person with HPV+ squamous cell carconima or HPV-?
HPV+
45
Which oral squamous cell carcinomas have spread to regional lymph nodes at the time of Dx? Which ones don't?
60% of floor cancers, 50% of tongue cancers. Lip cancer doesn't.
46
What is sialadenitis? In whom is it most commonly seen?
Inflammation of the salivary gland. Most commonly seen in children and older folks.
47
What is a mucocele/sialadenitis? What often causes it?
The most common lesion of the salivary gland resulting from blockage or rupture of a gland duct with leakage of saliva into surrounding tissues. Often caused by trauma.
48
Describe the clinical presentation of a patient with sialadenitis. How is it treated?
Swelling of the lower lip that is movable and compressible. Treatment is excision of the cyst along with the minor salivary gland.
49
Describe the histologic changes that occur in sialadenitis.
Cystic space lined by inflammatory granulation tissue, filled with mucin, and inflammatory cells, particularly macrophages. Supperative necrosis and abcess can occur in bacterial infection.
50
Which virus can cause sialadenitis? What other clinical features occur? What are the complications?
Paramyxovirus can cause. Mumps, enlargement of all three salivary glands, esp. the parotid occurs. Complications occur in adults (not children) and include pancreatitis, orchitis, or sterility.
51
Describe how bacteria can cause sialadenitis and name which organisms specifically usually do it.
Secondary to ductal obstruction from a stone or retrograde entry of bacteria from the oral cavity, esp. in dehydration. Generally S. aureus or S. viridans.
52
A chronic autoimmune disease characterized by dry eyes (keratoconjunctivitis) and dry mouth (xenostomia) resulting from immune destruction of the lacrimal and salivary glands is known as _________ syndrome.
Sjogren
53
What histologic changes are seen in the glands of a person with Sjogren syndrome? Name a gross change.
Lymphocytic infiltration, fibrosis, and epithelial hyperplasia of the lacrimal and salivary glands. Glands become enlarged.
54
What is the most common tumor of the salivary glands, especially in the parotid gland?
Pleomorphic ademona (benign salivary gland tumor)
55
What is the major complication that may occur from a pleomorphic adenoma? Describe the complication.
A malignant mixed tumor can arise. They are the most aggressive of all salivary gland malignant tumors. 30-50% mortality in 5 years.
56
What is the most common form of primary MALIGNANT tumor of the salivary glands?
Mucoepidermoid carcinoma.
57
What cell types are found in a mucoepidermoid carcinoma?
Neoplastic epidermal cells, mucus-secreting cells, and epithelial cells.
58
From where do mucoepidermoid carcinomas originate?
From ductal epithelium
59
What is the prognosis associated with mucoepidermoid carcinomas?
Degree of differentiation; clinical course depends on the grade.
60
What histologic changes are common in mucoepidermoid carcinomas?
“Nests” composed of squamous cells as well as clear vacuolated cells with mucin
61
In which population is Barrett's esophagus most common?
White males
62
What causes Barrett's esophagus?
Chronic GERD
63
Where in the esophagus does Barrett's esophagus occur?
The lower third
64
What histologic changes occur with Barrett's esophagus?
SSNKE --> columnar epithelium (goblet cells and foveolar cells but NO absorptive cells)
65
Barrett's esophagus increses risk for which cancer type? By how much is risk increased?
Esophogeal adenocarcinoma by 30-100x
66
What causes esophogeal varices (2)?
Cirrhosis and portal hypertension, often due to alcohol abuse. Hepatic schistosomiasis is the second most common cause of varices
67
Esophogeal varices greater than ___mm are prone to rupture, leading to life-threatening hemorrhage.
5
68
Where in the esophagus do adenocarcinomas occur?
Where do squamous cell carcinomas of the esophagus occur?
adenocarcinoma: distal end
squamous cell carcinoma: middle third
69
Fresh fruits and veggies lowers risk for which esophogeal cancer?
Adenocarcinoma
70
Name the disease: Pain while swallowing, progressive weight loss, hematemesis (vomiting blood), chest pain. Often spread to lymphatics by the time symptoms appear. 5 year survival rate is 25% if spread and 85% if limited to mucosa or submucosa.
Adenocarcinoma of the esophagus.
71
In which US population are squamous cell carcinomas of the esophagus most common?
Males over 45
72
Do risk factors for esophogeal adenocarcinoma include dysplasia, tobacco use, obesity, and radiation therapy?
Yeah
73
What increases risk for squamous cell carcinomas of the esophagus (6)?
1. Alcohol
2. Tobacco
3. GERD
4. Achalasia (failure of sphincter to relax)
5. Previous radiation
6. Frequent consumption of very hot beverages.
74
Squamous cell carcinomas of the esophagus begin as squamous ________ and progress to cancer.
dysplasia
75
Squamous cell carcinomas of the esophagus range from well differentiated with epithelial ______ to poorly differentiated tumors. Presents with _______, but by time of discovery, tumors are unresectable.
pearls
dysphagia
76
What causes acute gastritis?
Disruption of mucus layer and stimulation of acid secretion --> epithelial damage.
77
What 6 factors increase risk for acute gastritis?
1. NSAIDs
2. Aspirin
3. Alcohol
4. Smoking
5. Chemo
6. Ischemic injury
78
The morphology of acute gastritis is characterized by localized or diffuse superficial inflammation with concurrent _______ and hemorrhage. There is mucosal _______ and inflammatory infiltrate of _______ and chronic inflammatory cells.
concurrent erosion and hemorrhage
mucosal edema
infiltrate of neutrophils
79
What infectious agent causes chronic gastritis?
H. pylori
80
Chronic inflammatory changes from H. pylori are due to an imbalance between mucosal defenses and damaging forces that results in mucosal _____ and epithelial ______.
mucosal atrophy and epithelial metaplasia
81
Describe the cellular composition involved in chronic gastritis.
Intraepithelial neutrophils and subepithelial plasma cells.
82
B-cells may expand to fight H- pylori infection, potentially resulting in which type of cancer?
MALT lymphoma
83
How is chronic gastritis treated?
Antibiotics and proton pump inhibitors.
84
What are the usual causes of peptic ulcer disease (2)?
H. pylori and NSAIDs
85
Where in the GI tract do most ulcers occur?
Duodenum (4x more common than stomach)
86
Describe the gross changes seen in a peptic ulcer.
Round to oval “punched-out” defect. Mucosal margin is level with surrounding mucosa. Base of ulcer smooth and clean. Blood vessels may be evident.
87
Peptic ulcers are solitary in ____% of cases.
80
88
Describe the histologic changes seen in a peptic ulcer (3).
1. Thin layer of fibrinoid debris with neutrophil infiltrate.
2. Granulation tissue infiltrated with monocytes and fibrous/collagenous scarring.
3. Vessel walls in the scar are thickened and thrombosed.
89
What are two complications of a peptic ulcer?
Bleeding, perforation. Potentially life threatening.
90
What is the most common malignancy of the stomach (90%)?
Gastric adenocarcinoma
91
Rates of gastric INTESTINAL TYPE adenocarcinomas are declining in some countries, suggesting that ________ and _______ factors are associated with the disease.
environmental and dietary
92
The loss of ________ function is a key step in the development of gastric adenocarcinoma.
E-cadherin
93
By the time gastric adenocarcinomas are detected most have penetrated the submucosa into the muscularis propria. Therefore the 5 year survival rate is less than ____%.
30%
94
What are the two types of gastric adenocarcinomas?
Intestinal type, Diffuse (infiltrating) type
95
Name three characteristics of an intestinal-type adenocarcinoma.
1. Bulky, glandular.
2. Elevated mass with heaped-up borders and central ulcerations.
3. Develops from precursor lesions.
96
Name four characteristics of a diffuse (infiltrating) type adenocarcinoma.
1. No true tumor seen.
2. Do NOT form glands
3. Large mucin vacuoles that expand and push the nucleus to the outer edge (called a signet ring).
4. Desmoplastic reaction (fibroblast proliferation) that stiffens the gastric wall --> "Litinis plastica appearance."
