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M2 GI > 6. Pathology of Mouth & Esophagus > Flashcards

6. Pathology of Mouth & Esophagus Flashcards

1
Q

Oral pathology: what problems did we cover?

A
  • infectious diseases
  • benign and malig lesions
  • salivary gland neoplasms
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2
Q

Esophageal pathology: what did we cover?

A
  • congenital and acquired conditions
  • Reflux esophagitis
  • Barrett esophagus
  • malignant tumors
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3
Q

what are the most common infections of the oral cavity?

A
  • Herpes (HSV1 and 2)
  • CMV
  • Fungal (candida, aspergillus, mucor)
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4
Q

Fungal infections of the oral cavity: which are superficial, which are deeper?

A

Candida is superficial

Aspergillus and Mucor are deep (they are angioinvasive)

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5
Q

what does a herpetic vesicle look like on histo?

A

edema, cells within the edematous space, disorganized

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6
Q

what does a herpetic ulcer look like on histo?

A

(ulcer = erupted herpetic vesicle)

granulation tissue (L side of pic) abutting squamous cell epithelial hyperplasia (R side of pic).

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7
Q

what are the 3 M’s of HSV infection on histo?

A

Multinucleation, Margination, nuclear Molding

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8
Q

what cells are infected by HSV?

A

epithelial cells

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9
Q

what do the 3 M’s actually mean (histo of HSV)?

A
  • Multinucleation: self-explanatory
  • Margination: the nuclear chromatin is pushed to the margin/edge of the nucleus
  • nuclear Molding: the nuclei are fitted together, squished together
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10
Q

HSV: the viral inclusions are where?

A

intra-nuclear

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11
Q

CMV: viral inclusions are where?

A

both intra-nuclear and cytoplasmic

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12
Q

CMV: what do the infected cells look like?

A

owl-eye cells, big in size (at least 2x RBCs), particles in cytoplasm

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13
Q

CMV: infects what types of cells?

A

epithelial and mesenchymal/stromal

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14
Q

Candida: what is unique about its presence in the mouth?

A

it can be scraped off, unlike leukoplakia

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15
Q

Candida: appearance on biopsy?

A

fungal pseudohyphae are perpendicular to squamous cell layer. image she gave looks like red confetti.

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16
Q

Candida infection ulceration: appearance of tongue scraping on histo?

A

lots of pink, can see budding yeast forms (linear) and also pseudohyphae

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17
Q

Oral candida is most likely to occur in what patients?

A

immunosuppressed (post-transplant, diabetes, HIV+)

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18
Q

Aspergillus: characteristics of the fungus? deep or superficial infection?

A

hyphal forms only

septate hyphae, 45 deg angle branching

deeper infection due to angioinvasion

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19
Q

Mucormycosis: characteristics of the fungus? deep or superficial infection?

A

hyphal forms only

broad, bulbous, non-septate hyphae, right angle branching

deeper infection due to angioinvasion

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20
Q

Pyogenic granuloma: wtf is it? what pts does it typically occur in?

A

lesion of the oral cavity. benign, may regress, may progress to fibroma. occurs in young, sometimes associated with pregnancy

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21
Q

pyogenic granuloma: how is it described pathologically? can it be resected?

A

description: lobular capillary hemangioma w surface ulceration.

looks edematous, can see surface breakage on histo

can be surg resected, won’t recur

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22
Q

what is an aphthous ulcer? what does it look like?

A

oral cavity lesion: donut/annular shaped, edematous ring with sunken center.

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23
Q

Aphthous ulcer: prognosis? sx? associated with what?

A

will resolve on its own, painful, occurs on lip/tongue most commonly. associated with stress

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24
Q

hairy leukoplakia: occurs in what patients?

A

immunocompromised: post-transplant, chemo, HIV+

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25
Q

hairy leukoplakia: occurs in what part of mouth? associated with what virus?

A

sides of tongue (cannot scrape off)

associated with EBV in HIV+

associated with immunocompromised state

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26
Q

hairy leukoplakia: appearance on histo?

A

hyperparakeratosis (thickened epit layer), acanthosis, “balloon” cells

hyperplasia but no dysplasia

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27
Q

leukoplakia: what is this? is it the same as hairy leukoplakia? tests needed?

A

-general term for plaque that cannot be scraped away.

5-25% are pre-malignant.

Pathoma says this often represents squamous cell dysplasia.

  • hairy leukoplakia is a benign subtype.
  • get a biopsy to rule out carcinoma
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28
Q

erythroplakia: how is this different from hairy leukoplakia? why?

A

red lesion of oral cavity. not necessarily on tongue, can be gumline.

more ominous because it is vascularized, inflamed. more concerning for cancer

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29
Q

squamous cell carcinoma of the oral cavity: accounts for what % of oral cancer? what are risk factors? what is mortality rate?

A

95% of oral cancer

associated with cigs, EtOH, HPV

50% mortality rate

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30
Q

squamous cell carcinoma of the oral cavity: what are some of the mutations?

A
  • p16
  • p53
  • CyclinD (cell becomes immortal -> lesion -> invasive SCC)
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31
Q

where can I find a good chart detailing the progression of SCC in the mouth?

A

Slide 21 of this lecture (or Robbins text) shows normal mucosa -> hyperplasia -> dysplasia -> SCC (both histo and gross)

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32
Q

neoplasms of the parotid, submandibular, sublingual glands: which have the highest % malignancy?

A

sublingual (80% are malignant)

(the smaller the gland, the greater the chance of malignancy)

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33
Q

which strains of HPV are highest risk for SCC?

A

Types 16, 18 SCC that is associated with HPV (rather than cigs, EtOH) have better prognosis

34
Q

two types of benign salivary gland tumors?

A
  • Pleomorphic adenoma (50% of these tumors)
  • Warthin tumor (5-10%)
35
Q

three types of malignant salivary gland tumors?

A
  • Mucoepidermoid carcinoma (15%)
  • Acinic cell carcinoma (5%)
  • Adenoid cystic carcinoma (5%)
36
Q

Salivary gland tissue made up of what kinds of glands? parotid has more of which? sublingual has more of which?

A

serous and mucinous parotid: more serous

sublingual: more mucinous.

(think that mucus is heavier -> stays on bottom/lower glands. also, 80% of sublingual neoplasms are malignant –> Malig/Mucinous)

37
Q

two types of benign salivary gland tumors?

A

Pleomorphic adenoma (50% of these tumors)

Warthin tumor (5-10%)

38
Q

three types of malignant salivary gland tumors?

A
  • Mucoepidermoid carcinoma (15%)
  • Acinic cell carcinoma (5%)
  • Adenoid cystic carcinoma (5%)
39
Q

Pleomorphic Adenoma: benign or malig? type of cells involved? most common in what glands? tx?

A

benign, with risk of transformation -> malig

biphasic: both ductal and myoepithelial cells

more common in parotid than subman/subling glands

Tx: excise completely given risk of malignancy

40
Q

Warthin tumor: benign or malig? type of cells involved? most common in what glands?

A
  • Benign
  • two components: epithelial (dense, eosin, granular) and lymphoid
  • almost always in parotid
41
Q

Warthin tumor: benign or malig? type of cells involved? most common in what glands? Most common in what pts?

A
  • Benign.
  • Epithelial & lymphoid cells
  • almost always in parotid
  • Males, usually due to smoking
42
Q

Pleomorphic Adenoma: appearance on histo?

A

duct structures should be visible, with scattered spindle-like cells and myoepithelial cells.

43
Q

define oncocytic

A

tumor composed of oncocytes (large, eosinophilic cells with round small nuclei and plentiful mitos) in the context of a Warthin Tumor, know that it is oncocytic and therefore eosinophilic.

44
Q

what gives a Warthin tumor its eosinoiphilic appearance?

A

oncocytes: abundant mitochondria in cytoplasm

45
Q

Warthin tumor: gross appearance?

A

cystic tumor. cystic fluid is motor-oil looking. black stuff within cysts is proteinaceous debris

46
Q

Mucoepidermoid Carcinoma: arises in which salivary gland? what might it invade?

A

Pathoma: mainly occurs in parotid. May invade the facial nerve.

47
Q

Mucoepidermoid Carcinoma: how do the 2 cell types stain differently?

A

-squamous cells stain as you would expect on H/E -mucinous cells stain orange with special stain

48
Q

Mucoepidermoid Carcinoma: can the 2 cell types help with prognosis?

A

Low grade: mucous cells predominate. 90% 5 yr survival High grade: squamous cells predominate. 50% 5 yr survival

49
Q

Mucoepidermoid Carcinoma: arises in which salivary gland? what might it invade?

A

Pathoma: mainly occurs in parotid. May invade the facial nerve.

50
Q

Adenoid Cystic Carcinoma: progression of the tumor? prognosis?

A

-slow growing, but high rate of recurrence and long term survival is low (30% surv at 10y)

51
Q

Adenoid Cystic Carcinoma: what is distinct about this tumor?

A

perineural invasion. there is a pic on slide 38.

52
Q

survival rate for which type of malignant salivary gland tumor is best at 20 yrs?

A

Mucoepidermoid carcinoma

53
Q

Congenital abnormalities of the esophagus: what are the two types?

A
  • Atresia: absence or malformation of esop
  • Fistula: connection between esop and trachea
54
Q

Congenital abnormalities of the esophagus: what is the most common variant?

A

proximal esophageal atresia, with distal esophagus arising from the trachea. incompatible with life.

55
Q

what is achalasia?

A

Pathoma: disorder of esop motility -> inability to relax lower esop sphincter

  • dysphagia (both solids and liqs)
  • bad breath
  • bird-beak sign on barium study
56
Q

what are a few acquired lesions of the esop?

A

-Achalasia -Esop webs -Esop rings -Mallory-Weiss tear -Boerhaave Syndrome -Esophageal Varices -Reflux Esophagitis

57
Q

what are esop webs? patients who typically present with this?

A

-thin protrusion of esop mucosa, usually in upper portion -women 40+ -may cause partial obstruction of esop -> dysphagia

58
Q

What is plummer-vinson syndrome?

A

-esop web -severe iron deficiency anemia -glossitis (beefy-red tongue) -cheilosis -risk for carcinoma of upper esop

59
Q

what are esop rings? how do they present?

A

-overgrowths of mucosa -“A” ring occurs in lower esop, above the gastroesophageal jct (GEJ) -“B” ring (Schatzki’s) occurs at the GEJ -present with episodic dysphagia

60
Q

what is a Mallory-Weiss tear? what causes it?

A

-longitudinal laceration at the GEJ -caused by forceful vomiting (alcoholism, bulimia) -painful hematemesis

61
Q

what is Boerhaave Syndrome? what causes it?

A

-rupture of esop leading to air in the mediastinum. catastrophic! -due to forceful vomiting (this is the extreme end of the Mallory-Weiss spectrum)

62
Q

what are esop varices? causes?

A

-dilated submucosal veins in lower esop -consequence of portal HTN secondary to cirrhosis -major cause of bleeding if rupture? Pathoma: these are asymptomatic but risk for rupture -> death

63
Q

what is reflux esophagitis?

A

acid reflux damages esop mucosa, leads to metaplasia and hyperplasia. characterized by eosinophil infiltration (can see on histo)

64
Q

esophageal carcinoma: squamous cell and adenocarcinoma: which is most prev worldwide? in US?

A

90% of esop cancer worldwide = SCC

Most prev in US is adenocarcinoma

65
Q

causes of squamous cell carcinoma of esop?

A

EtOH, cigs, fungus-derived carcinogens, nitrosamines

66
Q

causes of adenocarcinoma?

A

Barrett esophagus

67
Q

SCC: appearance on gross?

A

may appear as ulceration of esop, circumferential constriction, or longitudinal growth

68
Q

SCC: appearance on histo?

A

cord-like infiltrative cells

69
Q

criteria for dx of Barrett Esop?

A

-endoscopic evidence of columnar epithelium in the distal esophagus AND intestinal metaplasia (goblet cells) on a mucosal biopsy from here

70
Q

why does Barrett Esop occur?

A

reaction of lower esophageal cells to acidic stress

71
Q

what does Barrett Esop look like with endoscopy?

A

squamous cells are pale pink, columnar mucosa is darker red. normally the Z line is well-defined between these cell types. With BE, border is irregular, with darker columnar mucosa extending up into esop.

72
Q

what does Barrett Esop look like on histo?

A

presence of goblet cells/columnar mucosa in the esop

73
Q

once you have diagnosed BE, what should your followup be?

A

keep an eye out for dysplasia - need to biopsy regularly

74
Q

what does low grade dysplasia look like in BE?

A

immature cells rising to external layer. dark, stratified (still organized)

75
Q

what does high-grade dysplasia look like in BE?

A

N:C ratio increased, cells are disorganized all the way to the top of the layer. glands also disorganized - back to back, look inflated

76
Q

once BE progresses to cancer, what is prognosis?

A

high mortality

77
Q

regular endoscopy v chromoendoscopy?

A

chromoendoscopy = newer biopsy technique, can recognize dysplasia more easily. allows more targeted biopsying

78
Q

Treatment for esop adenocarcinoma?

A

esophagectomy is standard. take it out. newer tx: resection of part of the mucosa. more limited, can be used early in the course of the cancer.

79
Q

squamous cell carcinoma: more common in what portion of the esop?

A

mid-esop Pathoma says upper or middle third.

80
Q

adenocarcinoma: more common in what portion of the esop?

A

lower third.

M2 GI (41 decks)

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