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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
microscopic appearance of candida esophagitis
neutrophils at surface of epithelium basal cell hyperplasia fungal hyphae on silver stain
26
clinical presentation of reflux esophagitis
heartburn, regurgitation and chest pain
27
sequelae of reflux esophagitis
bleeding, strictures, Barrett's esophagus
28
reflux pathogenesis
multifactorial, incompetent LES, sphincter, hiatal hernia, increased gastric volume, obesity, alcohol, tobacco, CNS depressants, pregnancy
29
gross appearance of reflux esophagitis
redness, erosions
30
histology of reflux esophagitis
elongation of papillae basal cell hyperplasia intraepithelial eosinophils and neutrophils
31
treatment for reflux esophagitis
proton pump inhibitor
32
who gets eosinophilic esophagitis?
children and adults, mainly atopic
33
symptoms of eosinophilic esophagitis
food impaction, dysphagia, GERD like symptoms in kids
34
treatment of eosinophilic esophagitis
``` dietary restriction (six food elimination diet) steroid inhalation ```
35
gross findings of eosinophilic esophagitis
furrowed esophagus | trachealized esophagus
36
histology of eosinophilic esophagitis
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
what is barrett's esophagus
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
pathogenesis of barrett's
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
gross findings of barrett's esophagus
irregular band of dark pink, velvety mucosa extending upwards as tongues of mucosa may be patchy
40
histology of barretts
metaplastic columnar epithelium with goblet cells
41
barrett's esophagus sequelae
ulceration bleeding stricture dysplasia > adenocarcinoma
42
layers of stomach wall
``` mucosa muscularis mucosa submucosa muscularis propria subserosa ```
43
fundus histology
mucin clumps on surface epithelial cells | bright pink parietal cells, dark purple chief cells
44
antrum histology
mucin cells, but no parietal cells
45
gastritis definition
inflammation of gastric mucosa caused by a variety of agents, chemical, infectious, and autoimmune
46
acute gastritis
transient, self-limiting hemorrhagic erosive
47
chronic gastritis causes
environmental - h.pylori autoimmune chemical/reactive
48
what is chronic gastritis
often asymptomatic, pain, nausea, vomiting | defined as a chronic inflammatory process which may lead to: ulceration, atrophy, metaplasia, cancer
49
what is h.pylori
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
gross appearance of h.pylori gastritis
often appears normal | may see erythema, nodularity, ulcers (common cause of PUD)
51
chronic h.pylori associated gastritis histopathology
dense lamina propria lymphoplasmacytic infiltrate +/- neutrophils infiltrating glands HP may be found in mucus layers antrum > body may lead to atrophy, metaplasia, dysplasia
52
complications of HP gastritis
peptic ulcer disease atrophic antral gastritis leading to intestinal metaplasia dysplasia leading to adenocarcinoma lymphoma
53
treatment of HP gastritis
triple therapy | PPI and 2 antibiotics
54
what is autoimmune metaplastic atrophic gastritis (AMAG)
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
gross appearance of AMAG
flattened/atrophic gastric mucosa
56
histology of AMAG
biopsy of body/fundus shows a lack of parietal cells | normal cells are replaced by mucous cells or intestinal metaplasia (goblet cells)
57
lab test findings in AMAG
high gastrin anti-parietal or anti-IF antibodies microcytic anemia at first, but then changes to macrocytic
58
treatment of AMAG
B12 supplementation | surveillance
59
normal small bowel histology
columnar epithelium with goblet cells | villous projections and crypts
60
presentation of celiacs
malabsorption (weight loss, edema, muscle wasting) | diarrhea (light colored, foul smelling)
61
gross appearance of celiacs
cracked earth appearance
62
microscopic appearance of celiac
blunting of villi increased intraepithelial lymphocytes enlongated crypts
63
normal colon histology
columnar epithelium test tube shaped crypts many goblet cells 50/50 epithelium/ lamina propria
64
2 types of inflammatory bowel disease
ulcerative colitis | crohn's disease
65
location of UC
confined to colon | distribution usually confluent and starts at left side/rectum
66
location of Crohns
can involve entire GI tract | skip lesions, granulomas and deep ulcers with strictures are hallmarks
67
presentation of IBD
can be similar for both-chronic diarrhea | Crohn's may have upper GI symptoms or present with symptoms of bowel obstruction
68
endoscopy of IBD
erythema and friability of mucosa | ulcerations
69
histology of IDB (chronic colitis)
crypt architectural distortion basal lamina propria lymphoplasmacytosis active disease has neutrophils (cryptitis and crypt abscess)
70
prognosis for UC
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
prognosis for Crohns
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
microscopic colitis pathogenesis
incompletely understood, thought to be autoimmune
73
presentation of microscopic colitis
chronic, watery diarrhea in middle aged to elderly patients
74
gross/endoscopic presentation of microscopic colitis
normal
75
histology of microscopic colitis
surface epithelial attenuation -lymphocytic = increased surface lymphocytes -collagenous = increased collagen layer under surface epithelium no distortion
76
treatment of microscopic colitis
symptom management | anti inflammatories
77
ischemic colitis pathogenesis
decreased blood flow - atherosclerotic cardiovascular disease - hypercoagulability - global ischemia
78
symptoms of ischemic colitis
acute onset bloody diarrhea abdominal pain usually elderly
79
gross/endoscopic presentation of ischemic colitis
dark red/hyperemic, abrupt transition to normal mucosa watershed areas affected more often (splenic flexure, sigmoid colon) patchy psuedomembranes
80
microscopic presentation of ischemic colitis
attenuation of epithelium beginning at surface can lead to crypt drop out ("withered crypts") necrosis if severe enough hyalinization of lamina propria
81
treatment of ischemic colitis
supportive correct cause of ischemia may need surgical resection

GIR Test 1 (24 decks)

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