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Pathomorph - CREDIT 5 > Oral cavity and GI tract - DONE > Flashcards

Oral cavity and GI tract - DONE Flashcards

1
Q

Salivary glands general description:

A
  • Capsule
  • Tubuloalveolar
  • Exocrine function
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2
Q

Parotid gland:

A

predominantly serous

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3
Q

Submandibular gland:

A

mucous

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4
Q

Minor salivary glands location:

A

numerous (hundreds) in lips, in the submucosa of oral cavity

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5
Q

Salivary glands % of all tumors:

A
  • Parotid -> 65-80% of all tumors
  • Submandibular - > 10% of all tumors
  • Minor salivary glands -> remainder
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6
Q

Salivary glands % of tumors are malignant:

A
  • Parotid -> 15-30%
  • Submandibular - > 40%
  • Minor salivary glands -> 50% (70-90% of sublingual)
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7
Q

Who usually get Salivary gland tumors?

A

F > M (Wärthin in males)

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8
Q

When does the Salivary gland tumors appear?

A
  • Benign appear in 5th-7th decade
  • Malignant later

Parotid: swelling in front and below the ear

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9
Q

How are the Salivary gland tumors upon diagnosis?

A

4-6 cm in diameter, mobile in palpation (exception: neglected malignant)
- Generally malignant grow faster

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10
Q

Mixed tumor =

A

Pleomorphic adenoma

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11
Q

Where does most of the Pleomorphic adenoma (Mixed tumor) appear?

A

60% of tumors in the parotid

* Rare in minor salivary glands

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12
Q

What increases the risk of Pleomorphic adenoma (Mixed tumor)?

A

Radiation increases the risk

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13
Q

Pleomorphic adenoma (Mixed tumor) - Macroscopically:

A
  • Rounded, well-demarcated, firm mass
  • <6 cm in greatest dimension
  • Encapsulated (in small salivary glands capsule not fully developed)
  • Expansile growth with small protrusions into surroundings -> enucleation difficult
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14
Q

Pleomorphic adenoma (Mixed tumor) - Microscopically:

A
  • Mixture of ductal (epithelial) and myoepithelial cells, (both epithelial and mesenchymal differentiation)
  • Epithelial elements dispersed throughout the matrix along with varying degrees of myxoid, hyaline, chondroid (cartilaginous), and even osseous tissue
  • In some tumors the epithelial elements predominate; in others they are present only in widely dispersed foci
  • Islands of well-differentiated squamous epithelium may also be present
  • No difference in biologic behavior between the tumors composed largely of epithelial elements and those composed largely of seemingly mesenchymal elements
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15
Q

Warthin tumor =

A

Adenolymphoma

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16
Q

Where does the Adenolymphoma (Warthin tumor) occur?

A

Almost exclusively in the parotid gland

  • 10% are multifocal
  • 10% bilateral
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17
Q

What is the 2nd most common salivary gland neoplasm?

A

Adenolymphoma (Warthin tumor)

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18
Q

Risk factors of Adenolymphoma (Warthin tumor):

A

Smokers have eight times the risk of nonsmokers for developing these tumors

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19
Q

Adenolymphoma (Warthin tumor) - Macroscopically:

A
  • Round to oval, encapsulated, pale gray mass
  • Narrow cystic spaces filled with a mucinous/serous secretion
  • 2 to 5 cm in diameter
  • Usually arising in the superficial parotid gland (palpable)
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20
Q

Adenolymphoma (Warthin tumor) - Microscopically:

A
  • Spaces lined by a double layer of neoplastic epithelial cells resting on a dense lymphoid stroma (sometimes germinal centers)
  • Polypoid projections of the lymphoepithelial elements
  • Surface palisade of columnar cells having an oncocytic appearance; Deep layer of cuboidal to polygonal cells
  • Sometimes foci of squamous metaplasia
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21
Q

Where can Warthin tumors arise?

A

Warthin tumors can arise within cervical lymph nodes - a finding that should not be mistaken for metastases.

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22
Q

Recurrence rates of Warthin tumors after resection?

A

Recurrence rates of only 2% after resection

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23
Q

Who usually gets Esophageal squamous cell carcinoma?

A
  • In adults over age 45

- M:F = 4:1

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24
Q

What are the risk factors of Esophageal squamous cell carcinoma?

A
  • alcohol and tobacco use
  • poverty
  • caustic esophageal injury
  • achalasia, tylosis (95% in age of 70)
  • Plummer Vinson syndrome
  • frequent consumption of very hot beverages
  • previous radiation
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25
Q

When do people usually get Esophageal squamous cell carcinoma?

A

50% of ESCC occur in the middle third

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26
Q

How does Esophageal squamous cell carcinoma begin?

A

Begins as an in situ lesion termed squamous dysplasia

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27
Q

What does the early lesions of Esophageal squamous cell carcinoma appear like?

A

Early lesions appear as small, gray-white, plaque-like thickenings

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28
Q

What is the level of differentiation of Esophageal squamous cell carcinoma?

A

Most squamous cell carcinomas are moderately to

well-differentiated

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29
Q

Describe the symptomatic tumors of Esophageal squamous cell carcinoma?

A

Symptomatic tumors are generally very large at diagnosis and have already invaded the esophageal wall

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30
Q

Esophageal squamous cell carcinoma - Clinical features

A
  • Dysphagia, odynophagia (pain on swallowing), and obstruction
  • Progressively increasing obstruction by altering patients diet from solid to liquid foods -> extreme weight loss and debilitation
  • Hemorrhage and sepsis may accompany tumor ulceration
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31
Q

What is the survival rate of Esophageal squamous cell carcinoma?

A

Overall 5-year survival: 9%

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32
Q

What causes the first symptoms of Esophageal squamous cell carcinoma

A

Occasionally, the first symptoms are caused by aspiration of food via a tracheoesophageal fistula

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33
Q

What is the lifetime risk of getting Chronic gastric ulcer, peptic ulcer disease

A

Lifetime risk: 10% males, 4% females

34
Q

What causes Chronic gastric ulcer, peptic ulcer disease?

A

Develops on the basis of chronic gastitis

35
Q

What are the main risk factors of Chronic gastric ulcer, peptic ulcer disease?

A
  • Helicobacter pylori infection:
    • 85-100% of duodenal ulcers
    • 65% of gastric ulcers
  • NSAIDs (aspirin, ibuprofen)
36
Q

What are the other risk factors of Chronic gastric ulcer, peptic ulcer disease?

A
  • Zollinger-Ellison syndrome
  • cigarette smoking
  • high-dose corticosteroids
  • alcoholic cirrhosis
  • chronic obstructive pulmonary disease
  • chronic renal failure
  • hyperparathyroidism (hypercalcemia: ↑gastrin)
37
Q

Where is the localization of Chronic gastric ulcer, peptic ulcer disease?

A
  • 95-98% proximal duodenum and stomach (3-4:1)
    • Duodenum: bulb
    • Stomach: lesser curvature (interface of body and antrum)
38
Q

Is the Chronic gastric ulcer, peptic ulcer disease solitary or not?

A

80% solitary

39
Q

Describe the classic peptic ulcer:

A

The classic peptic ulcer is a round to oval, sharply punched-out defect (heaped-up margins: cancers)

40
Q

Chronic gastric ulcer, peptic ulcer disease (alot)

A
  • The base of peptic ulcers is smooth and clean as a result of peptic digestion of exudate (blood vessels may be evident)
  • In active ulcers the base may have a thin layer of fibrinoid debris underlaid by a predominantly neutrophilic inflammatory infiltrate
  • Beneath this, active granulation tissue infiltrated with mononuclear leukocytes and a fibrous or collagenous scar forms the ulcer base
  • Vessel walls within the scarred area are typically thickened and are occasionally thrombosed
  • Scarring may involve the entire thickness of the wall and pucker the surrounding mucosa into folds that radiate outward
41
Q

Chronic gastric ulcer, peptic ulcer disease - Clinical features (alot)

A
  • Epigastric burning or aching pain
  • The pain tends to occur 1 to 3 hours after meals during the day, is worse at night, and is relieved by alkali or food
  • Iron deficiency anemia
  • Nausea, vomiting, bloating, and significant weight loss
  • Penetrating ulcers: the pain is occasionally referred to the back, the left upper quadrant, or the chest (may be misinterpreted as cardiac!)
42
Q

Chronic gastric ulcer, peptic ulcer disease - Complications:

A
  • Hemorrhage (15-20%)
    • In almost 1/3 of patients a first sign
  • Perforation (5-10%)
  • Obstruction
  • Cancer ???
43
Q

What comprises over 90% of all gastric cancers?

A

Adenocarcinoma

44
Q

Gastric cancer / Carcinoma ventriculi - symptoms:

A 
Early symptoms resemble those of chronic gastritis
including:
- dyspepsia
- dysphagia
- nausea which leads to late diagnosis
45
Q

Gastric cancer / Carcinoma ventriculi - symptoms:

A 
Early symptoms resemble those of chronic gastritis
including:
- dyspepsia
- dysphagia
- nausea which leads to late diagnosis
46
Q

Gastric cancer / Carcinoma ventriculi - survival:

A

The overall 5-year survival is less than 30%

47
Q

Gastric cancer - types:

A
  • Diffuse (M:F=1:1, incidence similar in different countries)
  • Intestinal (M:F=2:1, 2nd most common cancer death cause worldwide)
48
Q

Diffuse type of stomach cancer - risk factors?

A
  • Germline mutationsin CDH1, which encodes Ecadherin, a protein that contributes to epithelial intercellular adhesion
  • BRCA2 (breast cancer type 2 susceptibility gene) mutations
49
Q

Intestinal type of gastric cancer - risk factors:

A
  • Helicobacter pylori infection
  • Smoking
  • Alcohol consumption
  • Autoimmune atrophic gastitis
  • Genetic factors (FAP, others)
  • Partial gastrectomies
50
Q

Gastric adenocarcinomas classification depends on:

A
  • most importantly, gross and histologic morphology

- location in the stomach

51
Q

Most gastric adenocarcinomas involve…….

A
  • the gastric antrum

- lesser curvature > greater curvature

52
Q

Intestinal type:

A
  • bulky tumors (exophytic mass or an ulcerated)

- glandular structures

53
Q

Diffuse type:

A
  • diffuse infiltrative growth pattern
  • signet-ring cells
  • desmoplastic reaction (thickened wall - linitis plastica)
54
Q

Ileitis terminalis Crohn

A

Inflammatory bowel disease

- Crohn disease and ulcerative colitis

55
Q

Ileitis terminalis Crohn - Pathogenesis:

A
  • Genetic factors. (family members; in Crohn disease the concordance rate for monozygotic twins is approximately 50%)
  • Mucosal immune responses. Immunosuppression - basic IBD therapy
  • Epithelial defects
  • Microbiota: metronidazole can be helpful in management of Crohn disease
56
Q

What has:

  • skip lesions
  • transmural inflammation
  • ulcerations
  • fissures
A

Crohns disease

57
Q

What has:

  • continous colonic involvment, beginning in rectum
  • pseudopolyp, ulcer
A

Ulcerative colitis

58
Q

TABLE PAGE 7

A

difference between CD and UC

59
Q

What causes CD and UC?

A

CD and UC result probably from a combination of defects in host interactions with intestinal microbiota, intestinal epithelial dysfunction, and aberrant mucosal immune responses

60
Q

CD =

A

Crohns disease

61
Q

UC =

A

Ulcerative colitis

62
Q

Crohns disease - Clinical features:

A
  • Clinical manifestations – extremely variable
  • Most patients: mild diarrhea, fever, abdominal pain (20% pain in lower right quadrant – mimics appendicitis)
  • Active disease – asymptomatic periods of weeks months
  • Reactivation – stress, dietary change, smoking (strong association of onset, but cessation does not cause remission)
  • Anemia, protein loss, vitamin B12 malabsorption
  • Perforations, fistulas
63
Q

Ulcerative colitis - Clinical features:

A
  • Extra-intestinal manifestation
  • Uveitis, polyarthritis, ankylosing spondylitis, erythrema nodosum, clubbing of fingertips (may develop before disease is recognized)
  • Pericholangitis, primary sclerosing cholangitis (more commonly associated with UC)
  • Increased risk of colonic adenocarcinoma
64
Q

Which one of CD and UC has an increased risk of colonic adenocarcinoma?

A

Ulcerative colitis (UC)

65
Q

Crohn disease:

A
  • Terminal ileum, ileocecal valve, cecum
  • Fissures, thickenning of wall, mesenteric fat extends on serosal surface (creeping fat)
  • Ulcerations, Paneth cell metaplasia
  • Noncaseating granulomas (35%)
66
Q

Crohn disease - earliest lesion:

A

Earliest lesion: aphthous lesion

67
Q

Crohn disease - appearance:

A

Patchy distribution: cobblestone appearance

68
Q

Crohn disease - Microcopic feature of active process:

A

Microcopic feature of active process:

abundant neutrophils in crypts epithelium (crypt abscesses)

69
Q

What has a cobblestone appearance?

A

Crohn disease

70
Q

What has aphthous lesion in early lesions?

A

Crohn disease

71
Q

What is the 2nd cause of cancer related death in western countries?

A

Colonic adenocarcinoma

72
Q

Colonic adenocarcinoma - Risk factors - diet:

A
  • Low fiber intake, high carbohydrates and fat intake
73
Q

Who usually gets Colonic adenocarcinoma (risk factors)?

A

M slightly higher incidence than F

74
Q

Colonic adenocarcinoma - Risk factors:

A
  • Genetic disorders (~5%) : familial adenomatous polyposis –all patients develop colon cancer), hereditary non-polyposis colorectal cancer (Lynch syndrome)
  • Inflammatory bowel disease
75
Q

Sporadic colon cancers (90-95%) (alot):

A
  • APC/WNT/β-katenin pathway: left side of colon. Tubular, villous adenoma -> typical adenocarcinoma
  • MSH2,MLH1 pathway: right side of colon. Sessile serrated adenoma -> mucinous carcinoma (poorer prognosis)
76
Q

Location for colon cancer:

A
  • Rectosigmoid (50% of cases)
  • Ascending colon (15% of cases)
  • Descending colon (15% of cases)
  • Transverse colon and cecum (each 10%)
77
Q

Screening tests for colon cancer:

A
  • Fecal occult blood test (NOT very sensitive or specific)
  • colonoscopy
  • Serum carcinoembryonic antigen (CEA) – used to detect recurrences
78
Q

Which screening tests is used to detect recurrences?

A

Serum carcinoembryonic antigen (CEA)

79
Q

Clinical findings in colon cancer (Left-sided):

A

Left-sided: change in bowel habits; constipation or diarrhea with or without bleeding

80
Q

Clinical findings in colon cancer (Right-sided):

A

Right-sided: tend to bleed; blood in the stool and iron deficiency ANEMIA are more likely

81
Q

Clinical findings in colon cancer (Sites of metastasis):

A

Sites of metastasis: liver and lungs or bone

Pathomorph - CREDIT 5 (2 decks)

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