Path Winter 2 Esophagous

Front 1

what is the wall of the esophagous made of (inside out)

Back 1

1. non kerat strat squam epithelium
2. lamina propria
3. submucosa
4. muscularis propria
5. adventitia

Front 2

what are the 2 high pressure areas in the esophagous

Back 2

1. upper esophageal sphincter
2. lower esophageal sphincter

Front 3

what are the sx that are common to all diseases of esophagous

Back 3

1. dysphagia
2. heartburn
3. pain
4. hematemesis

Front 4

what is the most common congenital tracheosophageal fistula?

what are the sx

Back 4

esophagous ends in blind end sac, there is a connection btwn distal esophagous and trachea

*immediate regurg after feeding, Aspiration, paroxysmal suffocation, pneumonia

Front 5

atresia

Back 5

atresia- a hole that shoule be open but it closed

fistula- a hole that should not be there

Front 6

what does this describe

a newborn is regurging right after feeding. you scope him and see that the esophagous ends in a blind pouch at the tracheal bifurcation. the distal esophagus is connected to teh stomach

Back 6

its a congenital tracheosephageal fistula (an opening that shoudlnt be there)

Front 7

whats a nutcracker esophagous

Back 7

esophageal dysmotilty: outer long SM layer contracts BEFORE inner circular layer

Front 8

what is the location and name for 3 esophageal diverticulum

Back 8

1. zenker- above UES. neck mass, food accumulation, no dysphagia, aspiration pneumonia
2. Traction- midpoint
3. Epiphrenic- above LES

**these are obstructions

Front 9

what is zenker diverticulum

Back 9

diverticulum (obstruction) just above the UES. it accululates food and gives you a neck mass

**food regurg WITHOUT dysphagia (no problem with the esophagous itself)

**risk for aspiration pneumonia

Front 10

mostly we have dysphagia with anything with the esophagous, do we get it with zenker diverticula

Back 10

NO, not a problem with esophagous so swallow is OK

Front 11

what is enlarged in esophageal stenosis

what does it look like

what can it cause

Back 11

thickened submucosa, atrophy of muscularis propria

**esophageal injury with inflammation and scarring bc of: GERD, irradiation, caustic injury

Causes dysphagia

Front 12

whats a mucosal web, who gets them

Back 12

ledgelike semicircumferential
protrusions of mucosa into lumen

women over 40. Upper web with iron deficiency anemia,
glossitis and chelosis

Front 13

whats a Schazki ring

Back 13

like a web but circumferential and thick

A ring at GE junction
B ring at squamocolumnar junction

Front 14

what is it called when there is a mass just above the UES

Back 14

zenker diverticula

Front 15

whats achalasia

Back 15

Esophageal dysmotility disorder

1. aperistalisis
2. partial/incomplete relaxation of LES with swallow
3. increased resting tone of LES

*caused by who knows what?!

Front 16

what are the 3 major abnormalities associated with achalasia

Back 16

Esophageal dysmotility disorder bc there is too high resting tone of LES, the LES wont fully relax and tehre is aperistalis

Front 17

what is it called when you cant swallow bc resting tone in LES is high, the LES wont fully relax and there is no peristalsis

Back 17

Achalasia

Front 18

tell me about a hiatal hernia

morph
sx
complication

Back 18

*the crura of diaphragm dont close tight so the stomach sneaks up

Sx: common. heart burn, LES incompetence. worse when laying on back or bending forward
Complicate: ulcerate, performation


**idiopathic:

Front 19

when are the sx (regurg, heartburn, LES incompetence) of hiatal hernia worse

what would really complicate things

Back 19

laying on back
bending forward

**complications: ulcerate, perforation

Front 20

what is mallory weiss syndrome

Back 20

Longitudinal tears in esophagus at esophagogastric junction

caused by: severe vomit, EtOH, also seen in ppl w/o these risk factors

Front 21

what is common in an EtOH who vomits

Back 21

mallory weiss tear

Longitudinal tear in esophagous at the esophagealgastraic junction

Front 22

is mallory weiss (long tear in esophagous where it meets stomach) common? how is it treated

Back 22

ya, esp in those who vomit or are EtOH (5-10% of upper GI bleeds)

*bleed is self limited but can treat with constrictors. balloon tamponade

can be associated with boerhaave syndrome- esophageal rupture with tears

Front 23

whats a varicie

what causes it? what are the clinical features and complications

Back 23

1. dilated tortous vessels in esophagous

2. Bc of portal HTN

3. Clinical: asx til rupture. rupture is a med emergency- ligate, balloon tamponade, thrombolytics

Front 24

what disease are varicies associated with

Back 24

alcoholic cirrhosis
hepatic schistosomiasis (2 most common)

**underlying cause is portal HTN- portal flow diverted to coronary stomach veins, then to plexus of esophagous, then submucosal veins --> dilated tortous varicies

Front 25

in pts with advanced cirrhosis what causes death in 1/2 the ppl.

Back 25

varicies- portal HTN

Front 26

___1______ is one of the most serious complications
of portal hypertension. ____2_____ are the
treatment of choice for prevention of the first bleeding
episode. Active bleeding is managed with octreotide and
endoscopic sclerotherapy. TIPS and shunt surgery are
reserved for those in whom octreotide and endoscopic
surgery have failed. Endoscopic g y p band ligation should be used
for prevention of recurrent bleeding. If endoscopic band
ligation fails, patients can be offered TIPS or surgical therapy;
they should be evaluated for liver transplantation

Back 26

1. Variceal hemorrhage
2. Nonselective beta blockers

Front 27

what are the final steps in the final common pathway for esophagitis

Back 27

esophagitis- inflammation. lots of causes: smoke, EtOH, hit liquids, fungus, etc

Final common path: severe acute inflammation, superficial necrosis and ulceration, granulation tissue, fibrosis

Front 28

describe esophagitis due to...
1. Candida
2. Herpes/CMV
3. Foerign Pill
what is the final common path in ALL

Back 28

1. candida- grey/white pseudomembrane, densly matted hyphea (fungal)

2. HSV/CMV- punched out ulcers

3. localized ulceration

ALL end with inflammation: acute, superficial necrosis and ulceration, granulation tissue, fibrosis

Front 29

in what form of esophagitis does the intima get thick

Back 29

irradiation, this makes the lumen seem narrow

Front 30

who gets esophagitis usually

Back 30

debilitated, immunosuppressed

HIV, preggo, BMT, steroids

Front 31

whats GERD

Back 31

reflux can lead to esophagitis

Front 32

what things decrease LES tone or increase abd pressure related to GERD

Back 32

EtOH
Obesity
Tobacco
CNS depressants
preggo
hiatal hernia

Front 33

wwhat are hte 3 morphologoical features of GERD

Back 33

1. inflammatory cells- eos, PMN
2. Basal Zone Hyperplasia-
3. Elongation of lamina propria papillae with congestion

Front 34

what are hte sx and complications of GERD

Back 34

dysphagia, heart burn, regurg

**bleeding, stricture, barret esophagous

**these sx dont always match the morphology of the esophagous

Front 35

what does GERD look like

Back 35

lots of inflamm cells- PMN eos
basal zone hyperplasia
elongation of lamina propria papillea with congestion

**sx (dynphagia, heartburn, regurg) dont always match up with morphology

Front 36

who gets GERD (reflux esophagitis)

Back 36

adult over 40, smoke and drink, fat and preggo, CNS depressants, hiatal hernia (decrease LES tone and increase abd pressure)

*dysphagia, heart burn, regurg. sx dont correspond with morphology

can develop: bleeding, stricture, barret esophagous

Front 37

barrett esophagous is a complication of what

Back 37

complication of long standing reflux!

**super important risk factor for esophageal adenocarcinoma

**squamous replaced by columnar epithelium, intestinal goblet cells present

**HAVE to have had GERD in order to have barrets, barretts is the result of prolonged reflux

Front 38

what does barrett esophagous look like

Back 38

squamous cells are replaced by columnar cells as a result of long term reflux- important risk factor for esophageal adenocarcinoma

**intestinal goblet cells

red mucosa btwn pale squamous mucosa, light brown/pink mucosa

*can be patches or bands

Front 39

what are the clinical features of barrett esophagous

Back 39

chronic reflux stim squamous metaplasia to columnar- risk for esophageal adenocarcinoma

40-60 yo male, sx of reflux esophagitis: dysphagia, heartburn, reflux

local ulceration with bleeding and stricture

can develop into adenocarcinoma

Front 40

what does barrett esophagous increase the risk of

Back 40

esophageal adenocarcinoma

**HAVE to have had GERD in order to have barrets, barretts is the result of prolonged reflux

Front 41

tell me the kinds of benign esophageal tumors

Back 41

1. leiomyoma: SM
2. polyps: fibrous, vascular, fat, inflamed granulation tissue- resemble malignant lesion

Front 42

what are the 2 main malignant tumors of the esophagous

Back 42

1. squamous
2. adenocarcinoma

Front 43

for both malignant tumors of the esophagous describe the risk factors, age sex and morph/clinical

Back 43

squamous: most common
risk: EtOH, TOB, diet, environment (carcinogen exposure), p53 loss
age: >45
sex: M
morph: white plaquelike thickening. protruded, flat, excavated. middle esophagous
clinical: insidious dysphagia, weight loss,

Adenocarcinoma:
risk: barrett esophagous
age: >40
sex: white men
morph: p53 changes. distal esophagous. flat becomes nodular, deep infiltrated-ulcerated
clinical: dysphagia, weight loss, bleed, chest pain, vomit

Front 44

tell me in general about squamous cell carcinoma of the esophagous and adenocarcinoma

Back 44

not common but deadly

*asx, discovered too late for cure
*arise from epithelium

Front 45

tell me about squamous cell carcinoma

Back 45

esophageal cancer is uncommon but this one is common amongst them.

malignant

affects males >45 who drink, smoke adn are otherwise exposed to carcinogens (diet, environment)

**nutritional deficit can be prototer
**loss of p53 tumor suppressor gene

Front 46

what type of malignant cancer is assoicated with diet, environment, EtOH and TOB

Back 46

squamous cell carcinoma of esophagous

**also have loss of p53 tumor suppressor

Front 47

whats the pathogensis of normal squamous epithelium to squamous cell carcinoma

Back 47

male over 45 with chronic exposure to carcinogens. increased epithelial cell turnover in a carcinogenic environment --> dysplasia --> carcinoma

Front 48

which malignant carcinoma of the esophagous begins as in situ lesions of squamous dysplasia in the middle section of esophagous. Lesions are wite grey and plaquelike, they eventually become tumor masses

Back 48

squamous cell carcinoma

**commonn in the middle of the esophagous

– Three patterns
• Protruded (60%) ‐ a polypoid exopyhtic lesion
• Flat (15%) ‐ a diffuse infiltrative form, tends to spread
within wall, thickened, rigid, narrow lumen
• Excavated (25%) ‐ a necrotic cancerous ulceration,
excavates deeply into surrounding structures
– May erode into respiratory tree ‐ fistula, pneumonia
– May erode into aorta ‐ exsanguination

Front 49

what are the 3 morphologies of the later squamous cell carcinoma lesions

Back 49

1. protruded
2. Flat- spreads within wall, narrowed lumen
3. Excavated- necrotic cancerous ulceration, digs deep into surrounding tissues. can erode into respiratory fistula and lead to pneumonia or erode into aorta as exanguination

Front 50

is the onset of squamous cell carcinoma abrupt or insidious

Back 50

insidious, dysphagia, obstruction

weight loss, solid to liquid diet

Front 51

tell me about esophageal adenocarcinoma

Back 51

most will have had gerd that developed into barrettes esophagous

metaplastic: overexpression of p53
dysplastic: point mutions in p53

**clonal prorgression of dysplasia leads to cancer

**common in distal esophagous (middle esophagous was squamous cell)

Front 52

ok so burkitts has progressed into adenocarcinoma, what does the lesion look like

Back 52

flat, raised patch initiall and then becomes a nodular mass, can deep infiltrate or ulcerate

**mucin producing glandular tumor with intestinal type features (recall barrett has intestinal goblet cells)

Front 53

in adenocarcinoma does dysplasia always mean cancer

Back 53

nope, can regress

Front 54

what is the clinical picture of a person with esophageal adenocarcinoma

Back 54

men over 40, Whites

dysphagia, weight loss, bleeding, chest pain, vomit

Front 55

describe all of the features of congenital hypertrophic pyloric stenosis

Back 55

common congenital defect of stomach

infnat boys more than girls
palpable olive- hypertrophy and hyperplasia of muscularis propria of pyloric
regurg and projective vomit til 2 weeks of life
visible peristalsis

**open it surgically

Front 56

what are some things that cause acute gastritis

Back 56

NSAIDS
Excess EtOH
TOB
cancer chemo
uremia, infection, stress, ischemia/shock etc

Front 57

acute gastritis

risks:
morphoogy:
clinical

Back 57

RIsks: nsaids, EtOH, TOB, chemo, ischemia etc

**mech: increased acid, decreased bicarb, decreased blood flow, --> damage to mucosa

Morph: PMN above BM, edema, vascular congestion etc. severe- erosion, hemorrhage. defect in mucosa, can get errosion or hemorrhage

Clinical: asx, epigastric pain, NV, hemorrhage, massive hmatemesis, melanin,

**common in EtOH and ppl taking daily asprin

Front 58

your old man pt comes in with epigastric pain and NV, there is some blood in vomit. he is a heavy drinker and takes asprin regularly, whats the deal

Back 58

acute gastritis

Front 59

what is chronic gastritis?
what is ti caused by

Back 59

chronic inflammation --> mucosal atrophy, epithelial metaplasia w/o errosion. can become dysplastic and become carcinoma

caused by chronic H pylori infectino, pernicious anemia, toxins, surgery, etc

Front 60

what is the important etiology of chronic gastritis

Back 60

H pylori

**seen w/poverty, croding, limited education, low SES, rural

Front 61

describe H pylori with respect to:

risk factors
morphology
associated disease

Back 61

Risk: chronic gastritis, duodenal ulcer, gastric ulcer.

Morph

Associated disease: ulcers, chronic gastritis. INCERASED RISK OF GASTRIC CANCER

Clinical: no sx, come in for gastritis

Front 62

risk for gastric cancer is increased by what

Back 62

h pylori infection

Front 63

what are the micro about H pylori

Back 63

gram -, rod
motile- flagella
urease
bacterial adhesions, toxins
lived in superficial epithelial layer


**associated with: chronic gastritis, peptic ulcer disease, gastric carcinoma,

Front 64

whats pan gastritis, what is it associated with

Back 64

mucosal atrophy
decreased acid secretion
increstinal metaplasia
increased risk of gastric cancer

**assoicated with H pylori

Front 65

where is h pylori, what is associated with it

Back 65

in duperficial mucosa, epiuthelium

PMN, plasma cells are characteristic

H pylori is NOT in regions of intestinal metaplasia

Front 66

how is H pylori dx

Back 66

serology for AB, bacteria in poo, urea breath test
gastric biopsy

Front 67

infection with H pylori causes chronic gastritis how

Back 67

H pylori --> urease, and other toxins, increased gastric acidity, peptic enxymes

leads to atrophy, intestinal metaplasia, PMN infiltrate, lymphoid aggregates

gastric adenocarcinoma is the m ost serious risk of H pylori infection

Front 68

what are hte clinical features of autoimmune gastritis

Back 68

less common

AB to parietal cells and IF (detected in serum)
*decreased pepsinogen I
endocrine cell hyperplasia
B12 deficit
achlorhydria (decrease acid secretion)

Front 69

compare:

autoimmune gastritis and H pylori

Back 69

Autoimmune gastritis: AB to parietal cells and IF --> B12 deficit, decreased acid --> gastrin secretion and large G cells

Front 70

what things are inhibited bc in autoimmune gastritis there are AB to parietal cells and IF

Back 70

Parietal cells --> decreased acid, decreased IF

Decreased acid --> sim gastrin release --> large G cells

IF --> B12 deficit

cheif cells damaged --> decreased pepsinogen

**tx with immunosuppression

Front 71

whats the morph of autoimmune gastritis

Back 71

diffuse damage to mucosa (damage to the body and fundus, where acid is made)

inflammatory infiltrate of lymphs, macro, plasma

intestinal metaplasia (this is NOT seen with H pylori) endocrine hyperplasia (this IS seen in H pylori)

Front 72

a 60 yo male tested + for AB to parietal cells 20 years ago, he now has some mucosal atrophy. is this normal

Back 72

yep, autoimmune gastritis

Front 73

what are the microscopic features of chronic gastritis

Back 73

1. regenerative change- proliforation
2. metaplasia- mucosa replaced by intestinal epithelium
3. atrophy
4. hyperplasia of gastrin producint cells (Bc of decreased acid production)
5. dysplasia

Front 74

for H pylori and autoimmune gastritis what is the

1. Location
2. Inflamm infiltrate
3. acid level
4. gastrin level
5. lesion
6. serology
7. sequelea
8. associateions

Back 74

1. Location: HP- antrum. AIG- body
2. Inflamm infiltrate: HP- PMN, plasma. AIG- lymphs, macro
3. acid level: HP- increased. AIG- decreased
4. gastrin level: HP- decreased. AIG- increased
5. lesion: HP- hyperplastic polyp. AIG- endocrine hyperplasia
6. serology: HP- AB to HP. AIG- AB to parietal cells, IF
7. sequelea: HP- peptic ulcer, adenocarcinoma. AIG- atrophy, PA, adenocarcinoma, carcinoid tumor
8. associateions: HP- low SES. AIG- AI disease, thyroiditis, DM, graves

Front 75

what is eosinophilic gastritis

Back 75

tissue damage bc of lots of eosionophiles

associated with peripheral eosinophilia, increased IgE

allergens: soy, cow milk, drugs

can occur with systemic collagen vascular disease

Front 76

tell me about lymphocytic gastritis

Back 76

women with celiac

aka carioform gastritic

thick folds with nodules w/central ulcerations

Front 77

tell me about granulomatous gastritis

Back 77

granulomas: chrons, sarcoid, mycobacteria, fungi, CMV, H pylori

Front 78

case

esophageal biopsy shows reflus with eosionophiles, squamous and glandular (columnar) epithelium present,

will there be dysplasia? what can it develop into

Back 78

barretts esophagous

yes dysplasia

develop into adenocarcinoma

Front 79

case 2

mass in esophagous, shows Squamous cell carcinoma (SCC)

Back 79

weird case presentation