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11-7 (1,2) esophagus non-neoplastic


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Gi histology layers
-lamina propria
-muscularis mucosa
the rest:
-muscularis propria
-auerbach's plexus
-muscularis propria
common in the vasculature of the submucosa layer
-superficial necrosis
-Involves only mucosa.
-Heals by regeneration i.e. without fibrosis/scar
-deeper necrosis
Involves mucosa + deeper layers.
-Heals with : granulation tissue → fibrosis/scar
Neoplastic basics
in the epithelium:
a. squamous epith. → Squamous CA
b. columnar/glandular epith. → AdenoCA
c. metaplasia: intestinal → AdenoCA
GI stenosis, 2 types
-circumfrential lesion = stricture
-focal lesion
GI stenosis etiologies
2.Fibrosis/scar(contracts) → stricture
3.Neoplasms – benign/malignant
GI stenosis presentation
-Obstructs movement of GI lumen contents.
-Esophagus → dysphagia
Esophagus anatamy
-thick stratified squamous epith(white)
-25cm long
-connects pharynx to stomach
-GE junction: rich lymphatics
-behind: heart, trachea, aortic arch
-near nerves: recurent laryngeal, vagus
Muscularis propria
inner: circular muscle, thicker
outer: longitudenal thinner
Proximal 1/3: skel muscle(swallowing)
dist 2/3: SM (peristalsis)
Esophageal sphincters
-LES-angle of His ->"pinch cock"
-normal LESP=10-40mmHg
-tLESR = transient LES relaxation occurs on it's own->vents stomach
Herpetic Esophagitis Gross
-superficial vesicles
-superficial ulcers
Herpetic Esophagitis Histopathology
-Infects epithelial cells (keratinocytes)
-Replicated viral material collects in nucleus
→ nuclear inclusions = ground glass
→ pushes chromatin to edges = margination
- Some cells are multinucleated with nuclear molding (SEE ON TZANCK SMEAR)
esophageal peristalsis
-primary peristalsis=w/ swallowing
-Normal amplitude of wave=30-180 mmHg, mean=70
Normal speed=4 cm/sec
mucosal barrier defenses
-Tight junctions
-Enhanced mucosal bicarbonate production
-Increased blood flow to aid cell repair and provide bicarbonate
-Transmembrane pumps Na/H+, Cl/Bicarbonate
-Salivary Bicarb aids in neutralizing pH
Pill (Drug) Esophagitis
pill gets caught(on arch of aorta)->Localized inflammation in MUCOSA +/- ulceration (circular lesion)

Bad in women
NSAIDS, erythromycin, iron supplements
2ndary to:
-esophageal dysmotility
-esophageal stricture
-nature of medicine (sticky, dry)
-little accompanying food, H2O
Chemical (Corrosive) Esophagitis Epidemiology & Etiology
Children-accidental ingestion
Ingestion of:
-strong alkaline agents (lye)
-strong acids (sulfuric or HCL)
Hiatal hernia basics
-stomach into thorax
-sliding(95%) vs. rolling(5%)
Natural History:
-can cause incompetent LES->GERD
Hiatal hernia etiology
-usually accuired, not congenital
-messes up angle of HIS->GERD
-2ndary to:
1.esoph disease->PULL stomach up
2.abdominal condition->PUSH stomach up
3.weak hiatal openning
Chemical (Corrosive) Esophagitis Pathogenisis
-Alkaline solutions worse than > acids worse than > alkaline solids
-Alkali->inflammation->liquefactive necrosis(absolute cell death)
-Acids->coagulative necrosis(cells don't go away) forms protective eschar
-in the mucosa
-itis = inflimation
-infectious or inflamatory inflimation
Chemical (Corrosive) Esophagitis Severity
1st degree: injury to mucosa/submucosa → mucosa may slough
2nd degree: injury to submucosa/muscularis propria →ulceration, granulation tissue, fibrosis +/- stricture
3rd degree: full thickness necrosis
Esophagitis Causes
GERD Deffinition/pathogenisis
-GastroEsophageal Reflux Disease
- movement of gastric contents(acid, pepsin, +/- bile) into esophagus causing either tissue damage or symptoms(can be non-erosive GERD)
-*It's NOT too much acid, It's acid in the wrong place
esophagitis pathogenisis
Mucosal necrosis-> ulceration-> fibrosis +/- stricture
mucosal necrosis-> erosion-> regenerative healing
GERD Gross
Gross: Erythema(reddening), +/-complications:erosions(ulcers->fibrosis->strictures)
Etiology of infectious Esophagitis
-Most common = immunocompromised (CA chemo, transplants, AIDS)
-Other predisposing conditions include: DM, ETOH, ↑ age, systemic antibiotics
Esophageal Candidiasis basics/pathogenisis
-most common esophageal pathogen
-Normal oral flora + predisposing conditions → overgrowth of fungus Candida
GERD Histopathology
Epithelial changes:
-inflammation(eosinophils, PMN)
-basal zone hyperplasia
-edema = spongiosis(intracellular spacing and bridging)
Esophageal Candidiasis Gross path
-Superficial white plaques = pseudomembranes(mouth & esophagus)
-Hyperemic borders(bloody)
Esophageal Candidiasis Histopathology
Pseudomembranes composed of:
-Candida pseudohyphae-SEE ON PAS STAIN(red rods)
-inflammatory cells (PMN)
-necrotic debris
CMV esophagitis gross & pathogenisis
Gross: superficial ulcers
acquired: sexual, organ transplant, etc.
CMV esophagitis histopathology
-"Owl Eye" cells
-Infects lamina propria cells (including endothelial cells, fibroblasts)
-Replicated viral material collects in infected cells:
→ nuclear and cyto--megaly
→ nuclear inclusions
GERD clinical presentation (esophageal Sx's)
1.Heartburn(most common)-substernal chest burning
-often w/ regurgitation, belching or dysphagia
-Specific, not sensitive (SPIN)
2.rarely - dyspepsia(belly pain)
GERD clinical presentation (extra esophageal, atypical Sx's)
Less common
3.chronic cough
7.erosion of dental enamel
GERD epidemiology
-40% of americans = heartburn(monthly or more)
-20% of adults = dysphagia
-Risk goes up w/ AGE, MALES
GERD epidemiology Risk Factors
(Age, Males)
4.Collagen Vasc Dz
5.EtOH use
6.Hiatal Hernia
GERD Pathophysiology
Potential contributors to pathophysiology:
1.Loose LES
2.Too many/too prolonged tLESR’s
3.Poor/Incomplete Peristalsis
4.Decreased gastric emptying
5.Weakened epithelial resistance
GERD Complications
Erosive Esophagitis
-10-40% of people w/ reflux
1.chest pain
3.occ. odynophagia
1.hatal hernias
2.increased amts of acid, pepsin, & maybe bile(duodenal)
increase chance of:
2.Barrett's Esophagus
Esophageal Stricture formation
-Repeated/severe circumferential mucosal damage causes it
-Composed of circular bands of scar tissue underlying mucosa
-Presents as dysphagia
-treat w/ dilatation w/ balloon endoscopically
Barrett's Esophagus Definition
metaplasia of normal esophageal stratified SQUAMOUS epithelium to intestinal COLUMNAR epithelium.
-2ndary to GERD(symptoms may get better b/c it protects from the reflux)
Barrett's Esophagus
-occurs in 10% of people w/ GERD
-can lead to adeno CA of esophagus(risk is low)
Barrett's Esophagus Pathogenisis/histology
-Chronic reflux → chronic injury → metaplasia of epithelium
-stratified squamous turns to intestinal simple columnar(SEE GOBLET CELLS)
Other GERD complications
1.Loss of Dental Enamel
2.Laryngeal Cancer
3.Aspiration Pneumonia
4.Pulmonary Fibrosis
5.Chronic Asthma(could be 25% of asthma)
6.Vocal Cord Granulomas
7.Chronic Sinusitis
GERD Testing
Classic Symptoms:
-Test=give treatment and see if it helps them
Alarm Symptoms:
-Test=do Upper endoscopy(EGD) Or Barium swallow Or 24 nose probe
GERD Alarm symptoms
1.Weight loss
4.early satiety
GERD Testing EGD specifics
-good for seeing complications disease (stricture, BE, esophagitis)
-but bad test for looking for GERD itself
-Misses non-erosive reflux disease (NERD)
Non-Erosive Reflux Disease
-half of patients w/ GERD actually are NERDs
-Test for it w/ 24 probe
Non-pharm GERD therapy
1.Elevate the head of the bed 6⬝ on blocks
2.Stop smoking
3.Stop EtOH
4.Reduce dietary fat
5.Lose weight (if overweight)
6.Avoid chocolate, peppermint, caffeine, citrus, tomato-based foods
therapy for mild to stronger (non-errosive) GERD
1.occasional/mild or non-erosive treatment with:
-baking soda
-OTC antacids
-H2 blockers ok(can't really over dose them
2.More severe disease:
-bid(2x daily) H2 blockers at doses up to 3 times the recommended dose may be used
GERD testing Ba Swallow specifics
-Good for dysphagia
-Bad to Dx GERD(neither sensitive or specific)
Therapy for sever or Erosive Esophagitis from GERD
PPI (-azole, nexium, prilosec)
-irreversibly block the H/K ATPase (proton pump)
-Most potent acid suppressing agents
-Heal 90+% of erosive esophagitis
-Safe for longterm use
GERD testing 24 hr pH probe specifics
-through nose into esophagus
-can correlate reflux events w/ symptoms(like coughing)
-"functional test"
-tells how much acid is coming up and how high
Surgical GERD therapy
Nissen procedure(laparoscopically): Fix hiat hern, and wrap stomach around the bottom of the esophagus->tightens LES
-for those who are:
1.refractory to therapy
2.regurgitating food
3.unable/unwilling to take longterm, high dose PPI
GERD outcomes
-doesn't usually kill, But Terrible for Quality of Life
-complications occur early in reflux life(first 5yrs) if at all
-if get BE and cancer->prognosis is dismal

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