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GIR Test 1 > B5.019 - Non-Neoplastic GI Pathology Histo COPY > Flashcards

B5.019 - Non-Neoplastic GI Pathology Histo COPY Flashcards

1
Q

cell types in the esophagus and stomach

A

esophagus - squamous

stomach - columnar

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2
Q
A

normal esophagus

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3
Q
A

normal esophagus

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4
Q

layers of normal esophagus

A
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5
Q
A

esophageal mucosa: stratified squamous epithelium with papillae

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6
Q

symptoms of esophageal disorders

A

dysphagia

odynophagia - pain upon swallowing

heartburn - retrosternal chest pain

hematemesis - vomiting of blood

melena - blood in stools

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7
Q

esophagitis

A

an inlammatory process of the esophagus cuased by biochemical acid reflux, infectious, inflammatory or chemical agents

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8
Q

symptoms of infectious esophagitis

A

patients usually present with odynophagia

more common in immunosuppressed and elderly

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9
Q

most common causes of infectious esophagitis

A

HSV and CMV - reactivation of latent virus in laryngeal or superior cervical nerves

Candida - normal flora, colonzation due to structure or obstruction

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10
Q

describe epidemiology of HSV and gross/micro

A

usually opportunistic/immunosuppressed paitients. Self limited in healthy

gross: shallow vesicles and ulcers
micro: viral inclusions present and mulitnucleated squamous cells at margin of ulcer with thickened nuclear membrane and ground glass inclusions that fill nuclei

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11
Q
A

punched out ulcers from HSV infection

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12
Q
A

shallow ulcer with granulation tissue and superficial necrosis (L) and squamous mucosa (R) seen in HSV

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13
Q
A

high power of rim/edge of ulcer demonstrating pahtognomic cytologic featurs of HSV

red arrow - multinucleation, nuclear molding and

yellow arrow - nuclear margination

in squamous epithelium

HSV

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14
Q

what are the 3 Ms and what are they associated with

A

Multinucleation

Margination

Molding

HSV

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15
Q

describe the epidemiology of CMV and gross/micro appearance

A

immunocompromised patients

gross: punched out mucosal ulcers similar to herpes
micro: virus present in endothelium and enlarged stroma cells at ulcer base; inclusions are intranuclear surround by clear halo, often with coarse intracytoplasmic granules

owl eye inclusions

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16
Q
A

punched out ulcers seen in CMV or HSV

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17
Q
A

granulatino tissue in bed of ulcer (infecting endothelial and stromal cells) with nuclear and cytoplasmic inclusions

CMV

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18
Q
A

CMV in gastric pyloric glands with classic Owl eye nuclear inclusions

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19
Q

what is the most common cause of infectious esophagitis

A

candida

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20
Q

describe candida esophagitis

A

associated with antibiotc use in non immunocompromised

usually due to candida albicans

fungal invasion a requirement for dx since its normal flora in GI tract

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21
Q

endoscopy findings of candida esophagitis

A

gray white pseudomembrane or plaques in mid to distal esophagus; mucosa is erythematous, edematous, ulcerated or friable.

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22
Q
A

candida esophagitis

top arrow - distal esophagus

middle arrow - white plaques

bottom arrow - erythematous mucosa

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23
Q
A

candida esophagitis

superficial squamous mucosa with neutrophils

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24
Q
A

candida esophagitis

Gomori methamine silver stain highlighting fungal hyphae

note: it has to be invaded otherwise it could be normal flora

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25
Q

non infectious causes of esophagitis

A

reflux

eosinophilic

pill esophagitis

toxins/chemicals

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26
Q

clinical symptoms and sequelae of reflux esophagitis

A

clinical - heartburn, regurgitation and chest pain

sequelae - bleeding, strictures and barrets esophagus

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27
Q

pathogenesis of reflux esophagitis

A

multifactorial, incompetent LES, hiatal hernia, increased gastric volume, obesity, alcohol, tobacco, CNS depressants, pregnancy

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28
Q

reflux esophagitis gross appearance and histo

A

gross - redness, erosions

histo - elongation of papillae, basal cell hyperplasia, intraepithelial eosinophils and neutrophils

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29
Q
A

normal esophagus

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30
Q
A

reflux esophagus

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31
Q
A

normal esophagus

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32
Q
A

reflux esophagitis

Note the basal cell hyperplasia and papillary elongation. Maturation of the epithelium is decreased with more immature cells present above the normal 1-2 cell thickness. Also note the elongation of the lamina propria papilla extending to upper third of epithelium

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33
Q
A

numerous intraepithelial eosinophils

reflux esophagitis

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34
Q

what are symptoms of eosinophilic esophagitis and treatment

A

most atopic

symptoms - food impactions, dysphagia, GERD like in children

treatment - diatary restriction (six food elimination diet SFED: milk, egg, soy, wheat, peanuts/tree nuts, fish/shellfish, other)

steroid inhalation

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35
Q

gross and histo appearance of eosinophilic esophagitis

A

furrowed esophagus, trachealized esophagus (felinzation)

Histo - similar to reflux, papillary hyperplasia, basal hyperplasia, eosiophils; also superficial clustering, degranulation of eosinophils

note: the eosninophils are not confined to distal esophagus

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36
Q
A

trachealization or felinzation of esophagus seen in EoE

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37
Q
A

EoE

Some eosinophilic microabcsesses and mostly superficial location

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38
Q

what is barretts esophagus

A

probably complication of longstanding reflux

more common in middle aged white males

replacement of normal distal stratified squamous mucosa with intestinal type glandular mucosa

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39
Q

pathogenesis of barrets esophagus

A

reflex induces inflammation and mucosal injury

healing occurs by ingrowth of stem cells and re-epithelialization

cells differentiatin into abnormal inestinal mucosa that may be more injury resistant

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40
Q

gross and histo appearance of barretts esophagus

A

gross - irregular band dark pink, velvety mucosa extending upwards as tongues of mucosa, may be very patchy

histo - metaplastic columnar epithelium with goblet cells

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41
Q
A

barrets esophagus

endoscopically the gastroesophageal junction has tongues of velvety red tongues of metaplastic mucosa extending upward with adjacent pale squamous mucosa

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42
Q
A

barretts esophagus

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43
Q
A

higher power view of abundant intestinal metaplasia in esophagus

barrets esophagus

goblet cells - arrows

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44
Q

barrets esophagus sequelae

A

ulceration

bleeding

stricture

dysplasia

45
Q

name the layers

A
46
Q

name the cell types

A
47
Q
A

body/fundus of stomach with pairetal and chief cells

48
Q
A

antrum with mucous cells

49
Q

what is gastritis and what are the types

A

inflammation of gastric mucosa caused by a variety of agents, chemical, infectious, autoimmune

acute - transient and self limiting, hemorrhagic, erosive

chronic - environmental - H. pylori, autoimmune

50
Q

what is gastropathy

A

when inflammatory cells are absent or rare

diverse set of disorders marked by injury or dysfunction

NSAIDs, alcohol, bile, stress induced injury

51
Q

what is acute gastritis

A

common mucosal acute inflammatory process

often transiet

can be accompanied by erosions, hemorrhage

severity ranges from mild to massive

usually resolves if stimulus is removed

52
Q

gross and micro path of acute gastritis

A

gross - hemorrhage, erosions, edema

micro - inflammation, neutrophilic>chronic

focal or diffuse

superficial or full thickness

53
Q

what is chronic gastritis

A

often asymptomatic, pain, nausea, vomiting

defined as a chronic inflammatory process which may lead to:

ulceration

atrophy

metaplasia –> dysplasia –> carcinoma

lymphoma (Helicobacter)

54
Q

etiology of chronic gastritis

A

H pylori

autoimmune

chemical/reactive (NSAIDs, bile reflux, alcohol)

other - uremia, radiation

55
Q

what is H. pylori

A

non invasive spirillar gram negative rod (spirochete) producing urease and other toxins

highly prevalent esp in developing countries

risk factors are socioeconomic

56
Q

reservoir/transmission and gross appearance of H. pylori

A

humans/water

fecal-oral, oral oral, not really known

increased risk of carcinoma and lymphoma

gross - normal usually, may see erythema, nodularity, ulcers

57
Q
A

H pylori gastritis

58
Q
A

h pylori gastritis

59
Q
A

h pylori gastritis

60
Q

chronic HP associated gastritis histo

A

dense lamina propria lymphoplasmacytic infiltrate

+/- neutrophils infiltrating glands

HP may be found in mucus layer (NOT within cells)

antrum > body

61
Q

what can HP gastritis lead to

A

atrophy, metaplasia, dysplasia

62
Q
A

low power view of antral type mucosa with expansion of lamina propria by chronic inflammatory cells, including lymphoid aggregate and active inflammation.

H pylori gastritis

inset shows helicobacter pylori immunostain with organisms in mucin between cells NOT WITHIN CELLS

63
Q
A

H pylori gastritis

chronic active gastritis with active inflammation with neutrophils in epithelium and expanded lamina propria with predominantly plasma cells

intraepithelial neutrophils and subepithelial plasma cells are characteristic of H pylori

64
Q
A

h pylori gastritis

65
Q

complications of h pylori gastritis

A

peptic ulcer disease

atrophic antral gastritis leading to intestinal metaplasia

adenocarcinoma

lymphoma

66
Q

treatment of HP gastritis

A

triple therapy

proton pump inhibitor (omeprazole) and 2 antibiotics

67
Q
A

atrophy with IM, complication of h pylori

68
Q

clinical features of peptic ulcer disease

A

dyspepsia, epigastric pain, melena, hematemisis, anemia

69
Q

pathogenesis of peptic ulcer disease

A

h pylori infection most common

hyperacidity - zollinger ellison syndrome

NSAIDs

70
Q

where is peptic ulcer disease found and how is it treated

A

98% in antrum and duodenal bulb

lesser curvature of stomach

clean base and smooth edge

responsive to antibiotics

biopsy

71
Q

what is AMAG

A

autoimmune metaplastic atrophic gastritis

72
Q

describe AMAG

A

antibodies are present - antiparietal cell antibody

anti-intrinsic factor antibody

affects parital cells, decreased parietal cells and decreased acid production

leads to decreased B12 absorption

73
Q

what is pernicious anemia

A

from loss of B12, a complication of AMAG

74
Q

gross appearance, histo of AMAG

A

flattened/atrophic gastric mucosa

histo - biopsy of the body/fundus shows lack of parietal cells; normal cells replaced by mucous cells (looks like antrum) or intestinal metaplasia

75
Q

lab tests for AMAG

A

high gastrin, anti parietal or anti intrinsic factor antibody; microcytic anemia at first but then changes to macrocytic anemia

76
Q

treatment of AMAG

A

B12 supplementation (shots)

77
Q
A

AMAG

atrophy with intestinal metaplasia (goblet cells)

78
Q
A

shows IF anti parietal cell Ab in AMAG

79
Q

compare and contrast HP and AMAG

A
80
Q

what part of the GI system does celiacs affect

A

small bowel

81
Q
A

small bowel

mucosa comprised of epithelium and lamina propria in a villous architecture. epithelium is columnar, single layer, with goblet cells

82
Q

what is celiacs disease presenation, gross/micro appearance

A

malabsorption, diarrhea (light colored, foul smelling)

gross - cracked earth appearance

micro - blunting of villi, increased intraepithelial lymphocytes

83
Q

treatment of celiacs

A

gluten free diet

84
Q
A

celiac disease

85
Q
A

celiac - left; blunted villi and increased intraepithelial lymphocytes

normal - right

86
Q
A

normal colon

mucosal lining similar to small bowel but no villli formation

87
Q
A

normal colon - equal parts epithelium and lamina propria, organized and regular test tume like crypts

88
Q

what are ulcerative colitis and crohns disease

A

UC - confined to colon, distribution usually confluent and starts at left side/rectum

crohns - can involve entire GI, skip lesions, granulomas and deep ulcers with stricture are hallmarks

89
Q

what test can you do to look for ulcerative colitis that sets it apart

A

pANCA - 60-80%+

90
Q

presentation of inflammatory bowel disease

A

chronic diarrhea

crohns may have upper GI symptoms or present with bowel obstruction symptoms

91
Q

endoscopy and histo of IBD

A

endoscopy - erythema and friability of mucosa; ulcerations

histo - chronic colitis; crypt architecture distortion

basal lamina propria lymphoplasmacytosis

active disease has neutrophils

92
Q
A

chronic colitis - crypt distortion

93
Q
A

crypt distortion typical of IBD

branching crypts, no longer test tube shaped

green arrow - basal lymphoplasmacytosis

94
Q
A

chronic active colitis

crypt abscesses

95
Q

UC prognosis/treatment

A

no cure

treatment - anti-inflammatory and immunosuppressive drugs; surgery if not responsive

96
Q

crohns therapy and prognosis

A

no cure

treatment - anti inflammatory and immunosuppressive drugs, monoclonal TNA alpha ab

surgery for complications

increased risk of adenocarcinoma (UC as well)

97
Q

microscopic colitis pathogenesis and presentation

A

presentation - chronic, watery diarrhea in middle aged to elderly patients

pathegenesis - incompletely understood, thought to be autoimmune

98
Q

gross/endoscopy apperance, histo, treatment of microscopic colitis

A

gross - normal

histo - surface epithelium attenuation, lymphocytic, collagenous

treatment - symptom management, anti inflammatories

99
Q
A

lymphocytic colitis (microscopic)

100
Q
A

collagenous colitis (microscopic)

101
Q

symptoms of ischemic colitis

A

acute onset, bloody diarrhea, abdominal pain, usually elderly

102
Q

pathogenesis of ischemic colitis

A

atherosclerotic CVD

hypercoagulability

global ischemia

103
Q

gross appearance of ischemic colitis

A

dark red/hyperemic abrupt transition to normal mucosa; watershed areas affected more often (splenic flexure, sigmoid colon) can have patchy psudomembranes

104
Q

microscopic apprearance of ischemic colitis

A

attenuation of epithelium beginning at surface, can lead to crypt drop out (withered crypts)

necrosis if severe

hyalinization of lamina propria chronic

105
Q

treatment of ischemic colitis

A

supportive

correct cause

may need surgical resection

106
Q
A

ischemic colitis

normal colon on left, transitioning to crypt epithelial attenuation at arrow. Also note deep pink color of lamina propria - hyalinization

107
Q
A

ischemic colitis

surface epithelial attenuation and pink hyalinization of lamina propria

108
Q

differential for ischemic colitis

A

psudomembranous colitis - pathy pseudomembranes, hyanalized lamina propria and withered crypts favor ischemia

EHEC - right sided involvement and fibrin thrombi favor this

GIR Test 1 (15 decks)

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