Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
A

normal esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A

normal esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

layers of normal esophagus

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
A

esophageal mucosa: stratified squamous epithelium with papillae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

symptoms of esophageal disorders

A

dysphagia

odynophagia - pain upon swallowing

heartburn - retrosternal chest pain

hematemesis - vomiting of blood

melena - blood in stools

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

esophagitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

symptoms of infectious esophagitis

A

patients usually present with odynophagia

more common in immunosuppressed and elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
A

punched out ulcers from HSV infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the 3 Ms and what are they associated with

A

Multinucleation

Margination

Molding

HSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
A

punched out ulcers seen in CMV or HSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
A

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

CMV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
A

CMV in gastric pyloric glands with classic Owl eye nuclear inclusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the most common cause of infectious esophagitis

A

candida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
A

candida esophagitis

top arrow - distal esophagus

middle arrow - white plaques

bottom arrow - erythematous mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
A

candida esophagitis

superficial squamous mucosa with neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
A

candida esophagitis

Gomori methamine silver stain highlighting fungal hyphae

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
non infectious causes of esophagitis
reflux eosinophilic pill esophagitis toxins/chemicals
26
clinical symptoms and sequelae of reflux esophagitis
clinical - heartburn, regurgitation and chest pain sequelae - bleeding, strictures and barrets esophagus
27
pathogenesis of reflux esophagitis
multifactorial, incompetent LES, hiatal hernia, increased gastric volume, obesity, alcohol, tobacco, CNS depressants, pregnancy
28
reflux esophagitis gross appearance and histo
gross - redness, erosions histo - elongation of papillae, basal cell hyperplasia, intraepithelial eosinophils and neutrophils
29
normal esophagus
30
reflux esophagus
31
normal esophagus
32
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
33
numerous intraepithelial eosinophils reflux esophagitis
34
what are symptoms of eosinophilic esophagitis and treatment
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
35
gross and histo appearance of eosinophilic esophagitis
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
36
trachealization or felinzation of esophagus seen in EoE
37
EoE Some eosinophilic microabcsesses and mostly superficial location
38
what is barretts esophagus
probably complication of longstanding reflux more common in middle aged white males replacement of normal distal stratified squamous mucosa with intestinal type glandular mucosa
39
pathogenesis of barrets esophagus
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
40
gross and histo appearance of barretts esophagus
gross - irregular band **dark pink, velvety mucosa** extending upwards as tongues of mucosa, may be very patchy histo - metaplastic columnar epithelium with **goblet cells**
41
barrets esophagus endoscopically the gastroesophageal junction has tongues of velvety red tongues of metaplastic mucosa extending upward with adjacent pale squamous mucosa
42
barretts esophagus
43
higher power view of abundant intestinal metaplasia in esophagus barrets esophagus goblet cells - arrows
44
barrets esophagus sequelae
ulceration bleeding stricture dysplasia
45
name the layers
46
name the cell types
47
body/fundus of stomach with pairetal and chief cells
48
antrum with mucous cells
49
what is gastritis and what are the types
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
what is gastropathy
when inflammatory cells are absent or rare diverse set of disorders marked by injury or dysfunction NSAIDs, alcohol, bile, stress induced injury
51
what is acute gastritis
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
gross and micro path of acute gastritis
gross - hemorrhage, erosions, edema micro - inflammation, neutrophilic\>chronic focal or diffuse superficial or full thickness
53
what is chronic gastritis
often asymptomatic, pain, nausea, vomiting defined as a chronic inflammatory process which may lead to: ulceration atrophy metaplasia --\> dysplasia --\> carcinoma lymphoma (Helicobacter)
54
etiology of chronic gastritis
H pylori autoimmune chemical/reactive (NSAIDs, bile reflux, alcohol) other - uremia, radiation
55
what is H. pylori
non invasive spirillar gram negative rod (spirochete) producing urease and other toxins highly prevalent esp in developing countries risk factors are socioeconomic
56
reservoir/transmission and gross appearance of H. pylori
humans/water fecal-oral, oral oral, not really known increased risk of carcinoma and lymphoma gross - normal usually, may see erythema, nodularity, ulcers
57
H pylori gastritis
58
h pylori gastritis
59
h pylori gastritis
60
chronic HP associated gastritis histo
dense lamina propria lymphoplasmacytic infiltrate +/- neutrophils infiltrating glands HP may be found in mucus layer (NOT within cells) antrum \> body
61
what can HP gastritis lead to
atrophy, metaplasia, dysplasia
62
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
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
h pylori gastritis
65
complications of h pylori gastritis
peptic ulcer disease atrophic antral gastritis leading to intestinal metaplasia adenocarcinoma lymphoma
66
treatment of HP gastritis
**triple therapy** **proton pump inhibitor (omeprazole) and 2 antibiotics**
67
atrophy with IM, complication of h pylori
68
clinical features of peptic ulcer disease
dyspepsia, epigastric pain, melena, hematemisis, anemia
69
pathogenesis of peptic ulcer disease
h pylori infection most common hyperacidity - zollinger ellison syndrome NSAIDs
70
where is peptic ulcer disease found and how is it treated
98% in antrum and duodenal bulb lesser curvature of stomach clean base and smooth edge responsive to antibiotics biopsy
71
what is AMAG
autoimmune metaplastic atrophic gastritis
72
describe AMAG
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
what is pernicious anemia
from loss of B12, a complication of AMAG
74
gross appearance, histo of AMAG
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
lab tests for AMAG
high gastrin, anti parietal or anti intrinsic factor antibody; microcytic anemia at first but then changes to macrocytic anemia
76
treatment of AMAG
B12 supplementation (shots)
77
AMAG atrophy with intestinal metaplasia (goblet cells)
78
shows IF anti parietal cell Ab in AMAG
79
compare and contrast HP and AMAG
80
what part of the GI system does celiacs affect
small bowel
81
small bowel mucosa comprised of epithelium and lamina propria in a villous architecture. epithelium is columnar, single layer, with goblet cells
82
what is celiacs disease presenation, gross/micro appearance
malabsorption, diarrhea (light colored, foul smelling) gross - cracked earth appearance micro - blunting of villi, increased intraepithelial lymphocytes
83
treatment of celiacs
gluten free diet
84
celiac disease
85
celiac - left; blunted villi and increased intraepithelial lymphocytes normal - right
86
normal colon mucosal lining similar to small bowel but no villli formation
87
normal colon - equal parts epithelium and lamina propria, organized and regular test tume like crypts
88
what are ulcerative colitis and crohns disease
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
what test can you do to look for ulcerative colitis that sets it apart
pANCA - 60-80%+
90
presentation of inflammatory bowel disease
chronic diarrhea crohns may have upper GI symptoms or present with bowel obstruction symptoms
91
endoscopy and histo of IBD
endoscopy - erythema and friability of mucosa; ulcerations histo - chronic colitis; crypt architecture distortion basal lamina propria lymphoplasmacytosis active disease has neutrophils
92
chronic colitis - crypt distortion
93
crypt distortion typical of IBD branching crypts, no longer test tube shaped green arrow - basal lymphoplasmacytosis
94
chronic active colitis crypt abscesses
95
UC prognosis/treatment
no cure treatment - anti-inflammatory and immunosuppressive drugs; surgery if not responsive
96
crohns therapy and prognosis
no cure treatment - anti inflammatory and immunosuppressive drugs, monoclonal TNA alpha ab surgery for complications increased risk of adenocarcinoma (UC as well)
97
microscopic colitis pathogenesis and presentation
presentation - chronic, watery diarrhea in middle aged to elderly patients pathegenesis - incompletely understood, thought to be autoimmune
98
gross/endoscopy apperance, histo, treatment of microscopic colitis
gross - normal histo - surface epithelium attenuation, lymphocytic, collagenous treatment - symptom management, anti inflammatories
99
lymphocytic colitis (microscopic)
100
collagenous colitis (microscopic)
101
symptoms of ischemic colitis
acute onset, bloody diarrhea, abdominal pain, usually elderly
102
pathogenesis of ischemic colitis
atherosclerotic CVD hypercoagulability global ischemia
103
gross appearance of ischemic colitis
dark red/hyperemic abrupt transition to normal mucosa; watershed areas affected more often (splenic flexure, sigmoid colon) can have patchy psudomembranes
104
microscopic apprearance of ischemic colitis
attenuation of epithelium beginning at surface, can lead to crypt drop out **(withered crypts)** necrosis if severe hyalinization of lamina propria chronic
105
treatment of ischemic colitis
supportive correct cause may need surgical resection
106
ischemic colitis normal colon on left, transitioning to crypt epithelial attenuation at arrow. Also note deep pink color of lamina propria - hyalinization
107
ischemic colitis surface epithelial attenuation and pink hyalinization of lamina propria
108
differential for ischemic colitis
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions