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

B5.019 Non-Neoplastic GI Pathology Flashcards

1
Q

inflammatory esophagus conditions

A

reflux

eosinophilic esophagitis

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2
Q

inflammatory stomach conditions

A

autoimmune gastritis

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3
Q

inflammatory small bowel condition

A

celiacs

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4
Q

inflammatory colon conditions

A

inflammatory bowel disease (UC, Crohn’s)

microscopic colitis, diverticulitis/segmental colitis, diversion colitis, ischemic colitis

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5
Q

infectious esophagus conditions

A

CMV, HSV, Candida

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6
Q

infectious stomach conditions

A

H. pylori

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7
Q

layers of the esophageal wall

A

mucosa
muscularis mucosa
submucosa
muscularis propria

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8
Q

esophageal epithelium

A

stratified squamous epithelium

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9
Q

symptoms that present with esophageal disorders

A 
dysphagia- difficulty swallowing
odynophagia- pain upon swallowing
heartburn- retrosternal chest pain
hematemesis- vomiting of blood
melena- blood in stools
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10
Q

esophagitis

A

an inflammatory process of the esophagus caused by biochemical, infectious, inflammatory, or chemical agents

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11
Q

typical presentation of infectious esophagitis

A

usually present with odynophagia

more common in immunosuppressed and elderly

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12
Q

causative organisms of infectious esophagitis

A

HSV and CMV

candida

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13
Q

source of HSC and CMV esophagitis

A

reactivation of latent viruses in laryngeal and superior cervical nerves

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14
Q

source of candida esophagitis

A

normal oral flora

colonization due to stricture of obstruction

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15
Q

course of HSV esophagitis

A

usually an opportunistic infection in immunosuppressed patients
self limited in healthy patients
may cause esophageal perforation or disseminate in immunocompromised patients

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16
Q

gross appearance of HSV esophagitis

A

shallow vesicles and ulcers

may coalesce into extensive areas of erosion

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17
Q

micro appearance of HSV esophagitis

A

viral inclusions present in multinucleated squamous cells at margin of ulcer
inclusions usually Cowdry type A (dense eosinophilic and intranuclear)
thickened nuclear membrane and clear halo
ground glass inclusions

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18
Q

what gives cells a ground glass appearance

A

condensed DNA in one side of the nucleus

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19
Q

3 primary histo characteristics of HSV esophagitis

A

multinucleation
margination (DNA shifted to one side)
molding (funky shaped nuclei)

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20
Q

gross appearance of CMV esophagitis

A

punched out mucosal ulcers similar to HSV

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21
Q

micro appearance of CMV esophagitis

A

virus present in endothelium and enlarged stromal cells at ulcer base
inclusions are intranuclear surrounded by clear halo
course intracytoplasmic granules

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22
Q

nuclear inclusions of CMV on histo

A

single nucleus, bright pink

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23
Q

characterize candida esophagitis

A

most common infectious cause

associated with antibiotic use in non-immunocompromised

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24
Q

endoscopic appearance 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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25
Q

microscopic appearance of candida esophagitis

A

neutrophils at surface of epithelium
basal cell hyperplasia
fungal hyphae on silver stain

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26
Q

clinical presentation of reflux esophagitis

A

heartburn, regurgitation and chest pain

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27
Q

sequelae of reflux esophagitis

A

bleeding, strictures, Barrett’s esophagus

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28
Q

reflux pathogenesis

A

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

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29
Q

gross appearance of reflux esophagitis

A

redness, erosions

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30
Q

histology of reflux esophagitis

A

elongation of papillae
basal cell hyperplasia
intraepithelial eosinophils and neutrophils

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31
Q

treatment for reflux esophagitis

A

proton pump inhibitor

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32
Q

who gets eosinophilic esophagitis?

A

children and adults, mainly atopic

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33
Q

symptoms of eosinophilic esophagitis

A

food impaction, dysphagia, GERD like symptoms in kids

34
Q

treatment of eosinophilic esophagitis

A 
dietary restriction (six food elimination diet)
steroid inhalation
35
Q

gross findings of eosinophilic esophagitis

A

furrowed esophagus

trachealized esophagus

36
Q

histology of eosinophilic esophagitis

A

similar to reflux
papillary hyperplasia, basal hyperplasia, eosinophils
superficial clustering, degranulation of eosinophils
20 eosinophils per high power field
not confined to distal esophagus

37
Q

what is barrett’s esophagus

A

probable complication of longstanding reflux
more common in middle aged white males
replacement of normal distal stratified squamous mucosa with intestinal type glandular mucosa

38
Q

pathogenesis of barrett’s

A

reflux induces inflammation and mucosal injury
healing occurs by ingrowth of stem cells and re-epithelialization
cells differentiate into abnormal intestinal mucosa that may be more injury resistant

39
Q

gross findings of barrett’s esophagus

A

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

40
Q

histology of barretts

A

metaplastic columnar epithelium with goblet cells

41
Q

barrett’s esophagus sequelae

A

ulceration
bleeding
stricture
dysplasia > adenocarcinoma

42
Q

layers of stomach wall

A 
mucosa
muscularis mucosa
submucosa
muscularis propria
subserosa
43
Q

fundus histology

A

mucin clumps on surface epithelial cells

bright pink parietal cells, dark purple chief cells

44
Q

antrum histology

A

mucin cells, but no parietal cells

45
Q

gastritis definition

A

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

46
Q

acute gastritis

A

transient, self-limiting
hemorrhagic
erosive

47
Q

chronic gastritis causes

A

environmental - h.pylori
autoimmune
chemical/reactive

48
Q

what is chronic gastritis

A

often asymptomatic, pain, nausea, vomiting

defined as a chronic inflammatory process which may lead to: ulceration, atrophy, metaplasia, cancer

49
Q

what is h.pylori

A

noninvasive spirillar gram negative rod (spirochete) producing urease and other toxins
highly prevalent especially in developing countries, risk factors primarily socioeconomic
increased risk of carcinoma and lymphoma

50
Q

gross appearance of h.pylori gastritis

A

often appears normal

may see erythema, nodularity, ulcers (common cause of PUD)

51
Q

chronic h.pylori associated gastritis histopathology

A

dense lamina propria lymphoplasmacytic infiltrate
+/- neutrophils infiltrating glands
HP may be found in mucus layers
antrum > body
may lead to atrophy, metaplasia, dysplasia

52
Q

complications of HP gastritis

A

peptic ulcer disease
atrophic antral gastritis leading to intestinal metaplasia
dysplasia leading to adenocarcinoma
lymphoma

53
Q

treatment of HP gastritis

A

triple therapy

PPI and 2 antibiotics

54
Q

what is autoimmune metaplastic atrophic gastritis (AMAG)

A

10% of all chronic gastritis
anti-parietal cell and anti intrinsic factor antibodies present
affects parietal cells, (decreased parietal cells and decreased acid..increased gastrin to compensate)
leads to decreased B12 absorption = pernicious anemia

55
Q

gross appearance of AMAG

A

flattened/atrophic gastric mucosa

56
Q

histology of AMAG

A

biopsy of body/fundus shows a lack of parietal cells

normal cells are replaced by mucous cells or intestinal metaplasia (goblet cells)

57
Q

lab test findings in AMAG

A

high gastrin
anti-parietal or anti-IF antibodies
microcytic anemia at first, but then changes to macrocytic

58
Q

treatment of AMAG

A

B12 supplementation

surveillance

59
Q

normal small bowel histology

A

columnar epithelium with goblet cells

villous projections and crypts

60
Q

presentation of celiacs

A

malabsorption (weight loss, edema, muscle wasting)

diarrhea (light colored, foul smelling)

61
Q

gross appearance of celiacs

A

cracked earth appearance

62
Q

microscopic appearance of celiac

A

blunting of villi
increased intraepithelial lymphocytes
enlongated crypts

63
Q

normal colon histology

A

columnar epithelium
test tube shaped crypts
many goblet cells
50/50 epithelium/ lamina propria

64
Q

2 types of inflammatory bowel disease

A

ulcerative colitis

crohn’s disease

65
Q

location of UC

A

confined to colon

distribution usually confluent and starts at left side/rectum

66
Q

location of Crohns

A

can involve entire GI tract

skip lesions, granulomas and deep ulcers with strictures are hallmarks

67
Q

presentation of IBD

A

can be similar for both-chronic diarrhea

Crohn’s may have upper GI symptoms or present with symptoms of bowel obstruction

68
Q

endoscopy of IBD

A

erythema and friability of mucosa

ulcerations

69
Q

histology of IDB (chronic colitis)

A

crypt architectural distortion
basal lamina propria lymphoplasmacytosis
active disease has neutrophils (cryptitis and crypt abscess)

70
Q

prognosis for UC

A

no cure
low mortality, high morbidity
treat w anti inflammatory and immunosuppressive drugs
increased risk of adenocarcinoma
surveillance for dysplasia annually after 8 years

71
Q

prognosis for Crohns

A

no cure
low mortality, high morbidity
treat w anti inflammatory and immunosuppressive drugs, monoclonal TNFa ab
surgery only for complications or if not responsive to medical therapy

72
Q

microscopic colitis pathogenesis

A

incompletely understood, thought to be autoimmune

73
Q

presentation of microscopic colitis

A

chronic, watery diarrhea in middle aged to elderly patients

74
Q

gross/endoscopic presentation of microscopic colitis

A

normal

75
Q

histology of microscopic colitis

A

surface epithelial attenuation
-lymphocytic = increased surface lymphocytes
-collagenous = increased collagen layer under surface epithelium
no distortion

76
Q

treatment of microscopic colitis

A

symptom management

anti inflammatories

77
Q

ischemic colitis pathogenesis

A

decreased blood flow

  • atherosclerotic cardiovascular disease
  • hypercoagulability
  • global ischemia
78
Q

symptoms of ischemic colitis

A

acute onset bloody diarrhea
abdominal pain
usually elderly

79
Q

gross/endoscopic presentation of ischemic colitis

A

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

80
Q

microscopic presentation of ischemic colitis

A

attenuation of epithelium beginning at surface
can lead to crypt drop out (“withered crypts”)
necrosis if severe enough
hyalinization of lamina propria

81
Q

treatment of ischemic colitis

A

supportive
correct cause of ischemia
may need surgical resection

GIR Test 1 (24 decks)

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