Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology Pt. 3 > GI 1 > Flashcards

GI 1 Flashcards

1
Q

What is the fancy word for “Canker Sore?”

A

Aphthous ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Are aphthous ulcers found or keratinized, or non-keratinized epithelium?

A

Non-keratinized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What four things can trigger aphthous ulcers?

A
  1. Stress
  2. Fever
  3. Indigestion
  4. IBD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Are aphthous ulcers usually self-limiting and heal without scarring?

A

Yeah.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which viruses causes herpetic stomatitis?

A

HSV1 or HSV2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

____% of the population becomes infected by the HSV1 virus by midlife.

A

75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Are oral infection rates of HSV2 rising?

A

Yeah

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name eight things that can activate the herpex simplex virus.

A
  1. Fever
  2. Sun
  3. Cold exposure
  4. Respiratory tract infection
  5. Allergies
  6. Immunosuppression
  7. Pregnancy
  8. Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Do herpes lesions often rupture?

A

Yeah

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name three cellular changes seen in a herpes lesion.

A
  1. Ballooning degeneration of infected cells.
  2. Intranuclear acidophilic viral inclusions.
  3. Multinucleated polykaryons (fusion of cells).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Herpetic gingivostomatitis and lymphadenopathy may develop in herpes-infected patients who are __________.

A

immunocompromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name six conditions that can put a person at risk for oral candidiasis/thrush.

A
  1. DM
  2. Anemia
  3. Antibiotic or steroid therapy.
  4. HIV infection
  5. Metastatic cancer
  6. Infants can get it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the gross appearance of a thrush lesion.

A

White, curd-like circumscribed plaque in the oral cavity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Oral candidiasis may spread to the _________ and is life-threatening if it continues to spread.

A

esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why is candidiasis referred to as PSEUDOmembranous?

A

The pseudomembrane can be scraped off.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Is leukoplakia cancer?

A

No, its a preneoplastic lesion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which habits predispose people to leukoplakia?

A

Use of tobacco, especially pipe smoking and chewing tobacco.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is buccal mucosa?

A

The inside lining of the cheeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Do aphthous ulcers often occur in the same exact locations repeatedly?

A

Yeah

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Can leukoplakia vary from simple hyperkeratosis without underlying dysplasia to severe dysplasia bordering on carcinoma in situ?

A

Yeah

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the frequency of malignant transformation from leukoplakia to squamous cell carcinoma?

A

5 to 25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is erythroplakia? Is it precancerous?

A

Much like leukoplakia, except red. Also is precancerous.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What percentage of erythroplakia lesions undergo malignant transformation?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the morphological changes of erythroplakia.

A

Red, granular, circumscribed, may or may not be elevated, poorly defined and irregular boundaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

In which disease do keratin pearls form? What are they?

A

Squamous cell cancer only. When keratin sheds off from endophytic cancer cells (cells that have invaded inwards) and become trapped.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Name the disease: Mumps, enlargement of all three major salivary glands, especially the parotid.

A

Sialadenitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What infectious agents cause sialadenitis?

A

Paramyxovirus.

Also bacterial (usually secondary to duct obstruction): Staph aureus, Strep viridans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

In which populations is sialadenitis most problematic? What are three potential complications?

A

Adults - can lead to pancreatitis, orchitis, or sterility.

Not too bad in children.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What type of cancer are 95% of all head and neck cancers? Where exactly do they most commonly arise?

A

Squamous cell carcinomas, most commonly in the oral cavity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

At what age are oral and tongue cancers most common?

A

40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the prognosis for oral and tongue cancers?

A

50% die in five years because they metastasize by the time they are detected.

40
Q

Name six factors that increase risk for oral cancer.

A
  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
Q

Where are oral/tongue squamous cell carcinomas usually found?

A

Found in lateral margin of lower lip, floor of mouth, lateral borders of tongue

42
Q

Describe the progression of a squamous cell carcinoma lesion in the oral cavity.

A

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
Q

Can squamous cell carcinomas invade the underlying CT BEFORE they progress to a full thickness dysplasia (carcinoma in situ)?

A

Yeah!

44
Q

Who has a better prognosis: A person with HPV+ squamous cell carconima or HPV-?

A

HPV+

45
Q

Which oral squamous cell carcinomas have spread to regional lymph nodes at the time of Dx? Which ones don’t?

A

60% of floor cancers, 50% of tongue cancers. Lip cancer doesn’t.

46
Q

What is sialadenitis? In whom is it most commonly seen?

A

Inflammation of the salivary gland. Most commonly seen in children and older folks.

47
Q

What is a mucocele/sialadenitis? What often causes it?

A

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
Q

Describe the clinical presentation of a patient with sialadenitis. How is it treated?

A

Swelling of the lower lip that is movable and compressible. Treatment is excision of the cyst along with the minor salivary gland.

49
Q

Describe the histologic changes that occur in sialadenitis.

A

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
Q

Which virus can cause sialadenitis? What other clinical features occur? What are the complications?

A

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
Q

Describe how bacteria can cause sialadenitis and name which organisms specifically usually do it.

A

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
Q

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.

A

Sjogren

53
Q

What histologic changes are seen in the glands of a person with Sjogren syndrome? Name a gross change.

A

Lymphocytic infiltration, fibrosis, and epithelial hyperplasia of the lacrimal and salivary glands. Glands become enlarged.

54
Q

What is the most common tumor of the salivary glands, especially in the parotid gland?

A

Pleomorphic ademona (benign salivary gland tumor)

55
Q

What is the major complication that may occur from a pleomorphic adenoma? Describe the complication.

A

A malignant mixed tumor can arise. They are the most aggressive of all salivary gland malignant tumors. 30-50% mortality in 5 years.

56
Q

What is the most common form of primary MALIGNANT tumor of the salivary glands?

A

Mucoepidermoid carcinoma.

57
Q

What cell types are found in a mucoepidermoid carcinoma?

A

Neoplastic epidermal cells, mucus-secreting cells, and epithelial cells.

58
Q

From where do mucoepidermoid carcinomas originate?

A

From ductal epithelium

59
Q

What is the prognosis associated with mucoepidermoid carcinomas?

A

Degree of differentiation; clinical course depends on the grade.

60
Q

What histologic changes are common in mucoepidermoid carcinomas?

A

“Nests” composed of squamous cells as well as clear vacuolated cells with mucin

61
Q

In which population is Barrett’s esophagus most common?

A

White males

62
Q

What causes Barrett’s esophagus?

A

Chronic GERD

63
Q

Where in the esophagus does Barrett’s esophagus occur?

A

The lower third

64
Q

What histologic changes occur with Barrett’s esophagus?

A

SSNKE –> columnar epithelium (goblet cells and foveolar cells but NO absorptive cells)

65
Q

Barrett’s esophagus increses risk for which cancer type? By how much is risk increased?

A

Esophogeal adenocarcinoma by 30-100x

66
Q

What causes esophogeal varices (2)?

A

Cirrhosis and portal hypertension, often due to alcohol abuse. Hepatic schistosomiasis is the second most common cause of varices

67
Q

Esophogeal varices greater than ___mm are prone to rupture, leading to life-threatening hemorrhage.

A

5

68
Q

Where in the esophagus do adenocarcinomas occur?

Where do squamous cell carcinomas of the esophagus occur?

A

adenocarcinoma: distal end

squamous cell carcinoma: middle third

69
Q

Fresh fruits and veggies lowers risk for which esophogeal cancer?

A

Adenocarcinoma

70
Q

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.

A

Adenocarcinoma of the esophagus.

71
Q

In which US population are squamous cell carcinomas of the esophagus most common?

A

Males over 45

72
Q

Do risk factors for esophogeal adenocarcinoma include dysplasia, tobacco use, obesity, and radiation therapy?

A

Yeah

73
Q

What increases risk for squamous cell carcinomas of the esophagus (6)?

A
  1. Alcohol
  2. Tobacco
  3. GERD
  4. Achalasia (failure of sphincter to relax)
  5. Previous radiation
  6. Frequent consumption of very hot beverages.
74
Q

Squamous cell carcinomas of the esophagus begin as squamous ________ and progress to cancer.

A

dysplasia

75
Q

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.

A

pearls

dysphagia

76
Q

What causes acute gastritis?

A

Disruption of mucus layer and stimulation of acid secretion –> epithelial damage.

77
Q

What 6 factors increase risk for acute gastritis?

A
  1. NSAIDs
  2. Aspirin
  3. Alcohol
  4. Smoking
  5. Chemo
  6. Ischemic injury
78
Q

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.

A

concurrent erosion and hemorrhage

mucosal edema

infiltrate of neutrophils

79
Q

What infectious agent causes chronic gastritis?

A

H. pylori

80
Q

Chronic inflammatory changes from H. pylori are due to an imbalance between mucosal defenses and damaging forces that results in mucosal _____ and epithelial ______.

A

mucosal atrophy and epithelial metaplasia

81
Q

Describe the cellular composition involved in chronic gastritis.

A

Intraepithelial neutrophils and subepithelial plasma cells.

82
Q

B-cells may expand to fight H- pylori infection, potentially resulting in which type of cancer?

A

MALT lymphoma

83
Q

How is chronic gastritis treated?

A

Antibiotics and proton pump inhibitors.

84
Q

What are the usual causes of peptic ulcer disease (2)?

A

H. pylori and NSAIDs

85
Q

Where in the GI tract do most ulcers occur?

A

Duodenum (4x more common than stomach)

86
Q

Describe the gross changes seen in a peptic ulcer.

A

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
Q

Peptic ulcers are solitary in ____% of cases.

A

80

88
Q

Describe the histologic changes seen in a peptic ulcer (3).

A
  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
Q

What are two complications of a peptic ulcer?

A

Bleeding, perforation. Potentially life threatening.

90
Q

What is the most common malignancy of the stomach (90%)?

A

Gastric adenocarcinoma

91
Q

Rates of gastric INTESTINAL TYPE adenocarcinomas are declining in some countries, suggesting that ________ and _______ factors are associated with the disease.

A

environmental and dietary

92
Q

The loss of ________ function is a key step in the development of gastric adenocarcinoma.

A

E-cadherin

93
Q

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 ____%.

A

30%

94
Q

What are the two types of gastric adenocarcinomas?

A

Intestinal type, Diffuse (infiltrating) type

95
Q

Name three characteristics of an intestinal-type adenocarcinoma.

A
  1. Bulky, glandular.
  2. Elevated mass with heaped-up borders and central ulcerations.
  3. Develops from precursor lesions.
96
Q

Name four characteristics of a diffuse (infiltrating) type adenocarcinoma.

A
  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.”

Pathology Pt. 3 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions