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55 Cards in this Set
- Front
- Back
Gi histology layers
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Mucosa:
-epithelium -lamina propria -muscularis mucosa the rest: -submucosa -muscularis propria -auerbach's plexus -muscularis propria -serosa/adventitia |
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Varices
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common in the vasculature of the submucosa layer
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Erosion
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-superficial necrosis
-Involves only mucosa. -Heals by regeneration i.e. without fibrosis/scar |
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Ulceration
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-deeper necrosis
Involves mucosa + deeper layers. -Heals with : granulation tissue → fibrosis/scar |
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Neoplastic basics
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in the epithelium:
a. squamous epith. → Squamous CA b. columnar/glandular epith. → AdenoCA c. metaplasia: intestinal → AdenoCA |
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GI stenosis, 2 types
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-circumfrential lesion = stricture
-focal lesion |
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GI stenosis etiologies
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1.Congenital
2.Fibrosis/scar(contracts) → stricture 3.Neoplasms – benign/malignant |
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GI stenosis presentation
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-Obstructs movement of GI lumen contents.
-Esophagus → dysphagia |
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Esophagus anatamy
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-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 |
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Muscularis propria
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inner: circular muscle, thicker
outer: longitudenal thinner Proximal 1/3: skel muscle(swallowing) dist 2/3: SM (peristalsis) |
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Esophageal sphincters
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-UES
-LES-angle of His ->"pinch cock" -normal LESP=10-40mmHg -tLESR = transient LES relaxation occurs on it's own->vents stomach |
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Herpetic Esophagitis Gross
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-superficial vesicles
-superficial ulcers -plaques |
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Herpetic Esophagitis Histopathology
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-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) |
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esophageal peristalsis
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-primary peristalsis=w/ swallowing
-Normal amplitude of wave=30-180 mmHg, mean=70 Normal speed=4 cm/sec |
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mucosal barrier defenses
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-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 |
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Pill (Drug) Esophagitis
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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 -recumbent |
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Chemical (Corrosive) Esophagitis Epidemiology & Etiology
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Adults-suicide
Children-accidental ingestion Ingestion of: -strong alkaline agents (lye) -strong acids (sulfuric or HCL) |
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Hiatal hernia basics
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-stomach into thorax
-sliding(95%) vs. rolling(5%) Natural History: -can cause incompetent LES->GERD |
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Hiatal hernia etiology
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-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 |
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Chemical (Corrosive) Esophagitis Pathogenisis
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-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 |
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Esophagitis
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-in the mucosa
-itis = inflimation -infectious or inflamatory inflimation |
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Chemical (Corrosive) Esophagitis Severity
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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 |
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Esophagitis Causes
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-Infectious
1.Candida 2.herpes 3.CMV -Chemical -Drug -Reflux(GERD) -Barrett |
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GERD Deffinition/pathogenisis
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-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 |
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esophagitis pathogenisis
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Mucosal necrosis-> ulceration-> fibrosis +/- stricture
or mucosal necrosis-> erosion-> regenerative healing |
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GERD Gross
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Gross: Erythema(reddening), +/-complications:erosions(ulcers->fibrosis->strictures)
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Etiology of infectious Esophagitis
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-Most common = immunocompromised (CA chemo, transplants, AIDS)
-Other predisposing conditions include: DM, ETOH, ↑ age, systemic antibiotics |
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Esophageal Candidiasis basics/pathogenisis
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-most common esophageal pathogen
-Normal oral flora + predisposing conditions → overgrowth of fungus Candida |
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GERD Histopathology
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Epithelial changes:
-inflammation(eosinophils, PMN) -basal zone hyperplasia -edema = spongiosis(intracellular spacing and bridging) |
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Esophageal Candidiasis Gross path
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-Superficial white plaques = pseudomembranes(mouth & esophagus)
-Hyperemic borders(bloody) |
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Esophageal Candidiasis Histopathology
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Pseudomembranes composed of:
-Candida pseudohyphae-SEE ON PAS STAIN(red rods) -inflammatory cells (PMN) -squames -necrotic debris |
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CMV esophagitis gross & pathogenisis
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Gross: superficial ulcers
acquired: sexual, organ transplant, etc. |
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CMV esophagitis histopathology
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-"Owl Eye" cells
-Infects lamina propria cells (including endothelial cells, fibroblasts) -Replicated viral material collects in infected cells: → nuclear and cyto--megaly → nuclear inclusions |
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GERD clinical presentation (esophageal Sx's)
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1.Heartburn(most common)-substernal chest burning
-often w/ regurgitation, belching or dysphagia -Specific, not sensitive (SPIN) 2.rarely - dyspepsia(belly pain) |
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GERD clinical presentation (extra esophageal, atypical Sx's)
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Less common
1.hoarseness 2.asthma 3.chronic cough 4.sinusitis 5.bronchitis 6.bronchiectasis 7.erosion of dental enamel |
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GERD epidemiology
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-40% of americans = heartburn(monthly or more)
-20% of adults = dysphagia -Risk goes up w/ AGE, MALES |
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GERD epidemiology Risk Factors
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(Age, Males)
1.Obesity 2.Pregnancy 3.Smoking 4.Collagen Vasc Dz 5.EtOH use 6.Hiatal Hernia |
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GERD Pathophysiology
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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 |
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GERD Complications
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Erosive Esophagitis
-10-40% of people w/ reflux -Presentation: 1.chest pain 2.dysphagia 3.occ. odynophagia RF's: 1.hatal hernias 2.increased amts of acid, pepsin, & maybe bile(duodenal) increase chance of: 1.Strictures 2.Barrett's Esophagus |
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Esophageal Stricture formation
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-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 |
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Barrett's Esophagus Definition
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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) |
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Barrett's Esophagus
Epidemiology |
WHITE, MALES
-occurs in 10% of people w/ GERD -can lead to adeno CA of esophagus(risk is low) |
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Barrett's Esophagus Pathogenisis/histology
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-Chronic reflux → chronic injury → metaplasia of epithelium
-stratified squamous turns to intestinal simple columnar(SEE GOBLET CELLS) |
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Other GERD complications
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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 8.Bronchiectasis |
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GERD Testing
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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 |
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GERD Alarm symptoms
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1.Weight loss
2.dysphagia 3.anemia 4.early satiety 5.bleeding |
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GERD Testing EGD specifics
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EGD(endoscopy):
-good for seeing complications disease (stricture, BE, esophagitis) -but bad test for looking for GERD itself -Misses non-erosive reflux disease (NERD) |
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NERD
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Non-Erosive Reflux Disease
-half of patients w/ GERD actually are NERDs -Test for it w/ 24 probe |
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Non-pharm GERD therapy
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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 |
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therapy for mild to stronger (non-errosive) GERD
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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 |
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GERD testing Ba Swallow specifics
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-Good for dysphagia
-Bad to Dx GERD(neither sensitive or specific) |
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Therapy for sever or Erosive Esophagitis from GERD
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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 -Expensive!! |
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GERD testing 24 hr pH probe specifics
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-through nose into esophagus
-can correlate reflux events w/ symptoms(like coughing) -"functional test" -tells how much acid is coming up and how high |
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Surgical GERD therapy
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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 |
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GERD outcomes
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-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 |