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79 Cards in this Set
- Front
- Back
what is the wall of the esophagous made of (inside out)
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1. non kerat strat squam epithelium
2. lamina propria 3. submucosa 4. muscularis propria 5. adventitia |
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what are the 2 high pressure areas in the esophagous
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1. upper esophageal sphincter
2. lower esophageal sphincter |
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what are the sx that are common to all diseases of esophagous
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1. dysphagia
2. heartburn 3. pain 4. hematemesis |
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what is the most common congenital tracheosophageal fistula?
what are the sx |
esophagous ends in blind end sac, there is a connection btwn distal esophagous and trachea
*immediate regurg after feeding, Aspiration, paroxysmal suffocation, pneumonia |
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atresia
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atresia- a hole that shoule be open but it closed
fistula- a hole that should not be there |
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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 |
its a congenital tracheosephageal fistula (an opening that shoudlnt be there)
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whats a nutcracker esophagous
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esophageal dysmotilty: outer long SM layer contracts BEFORE inner circular layer
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what is the location and name for 3 esophageal diverticulum
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1. zenker- above UES. neck mass, food accumulation, no dysphagia, aspiration pneumonia
2. Traction- midpoint 3. Epiphrenic- above LES **these are obstructions |
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what is zenker diverticulum
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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 |
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mostly we have dysphagia with anything with the esophagous, do we get it with zenker diverticula
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NO, not a problem with esophagous so swallow is OK
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what is enlarged in esophageal stenosis
what does it look like what can it cause |
thickened submucosa, atrophy of muscularis propria
**esophageal injury with inflammation and scarring bc of: GERD, irradiation, caustic injury Causes dysphagia |
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whats a mucosal web, who gets them
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ledgelike semicircumferential
protrusions of mucosa into lumen women over 40. Upper web with iron deficiency anemia, glossitis and chelosis |
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whats a Schazki ring
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like a web but circumferential and thick
A ring at GE junction B ring at squamocolumnar junction |
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what is it called when there is a mass just above the UES
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zenker diverticula
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whats achalasia
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Esophageal dysmotility disorder
1. aperistalisis 2. partial/incomplete relaxation of LES with swallow 3. increased resting tone of LES *caused by who knows what?! |
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what are the 3 major abnormalities associated with achalasia
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Esophageal dysmotility disorder bc there is too high resting tone of LES, the LES wont fully relax and tehre is aperistalis
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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
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Achalasia
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tell me about a hiatal hernia
morph sx complication |
*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: |
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when are the sx (regurg, heartburn, LES incompetence) of hiatal hernia worse
what would really complicate things |
laying on back
bending forward **complications: ulcerate, perforation |
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what is mallory weiss syndrome
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Longitudinal tears in esophagus at esophagogastric junction
caused by: severe vomit, EtOH, also seen in ppl w/o these risk factors |
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what is common in an EtOH who vomits
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mallory weiss tear
Longitudinal tear in esophagous at the esophagealgastraic junction |
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is mallory weiss (long tear in esophagous where it meets stomach) common? how is it treated
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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 |
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whats a varicie
what causes it? what are the clinical features and complications |
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 |
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what disease are varicies associated with
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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 |
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in pts with advanced cirrhosis what causes death in 1/2 the ppl.
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varicies- portal HTN
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___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 |
1. Variceal hemorrhage
2. Nonselective beta blockers |
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what are the final steps in the final common pathway for esophagitis
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esophagitis- inflammation. lots of causes: smoke, EtOH, hit liquids, fungus, etc
Final common path: severe acute inflammation, superficial necrosis and ulceration, granulation tissue, fibrosis |
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describe esophagitis due to...
1. Candida 2. Herpes/CMV 3. Foerign Pill what is the final common path in ALL |
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 |
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in what form of esophagitis does the intima get thick
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irradiation, this makes the lumen seem narrow
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who gets esophagitis usually
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debilitated, immunosuppressed
HIV, preggo, BMT, steroids |
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whats GERD
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reflux can lead to esophagitis
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what things decrease LES tone or increase abd pressure related to GERD
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EtOH
Obesity Tobacco CNS depressants preggo hiatal hernia |
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wwhat are hte 3 morphologoical features of GERD
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1. inflammatory cells- eos, PMN
2. Basal Zone Hyperplasia- 3. Elongation of lamina propria papillae with congestion |
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what are hte sx and complications of GERD
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dysphagia, heart burn, regurg
**bleeding, stricture, barret esophagous **these sx dont always match the morphology of the esophagous |
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what does GERD look like
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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 |
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who gets GERD (reflux esophagitis)
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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 |
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barrett esophagous is a complication of what
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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 |
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what does barrett esophagous look like
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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 |
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what are the clinical features of barrett esophagous
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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 |
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what does barrett esophagous increase the risk of
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esophageal adenocarcinoma
**HAVE to have had GERD in order to have barrets, barretts is the result of prolonged reflux |
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tell me the kinds of benign esophageal tumors
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1. leiomyoma: SM
2. polyps: fibrous, vascular, fat, inflamed granulation tissue- resemble malignant lesion |
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what are the 2 main malignant tumors of the esophagous
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1. squamous
2. adenocarcinoma |
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for both malignant tumors of the esophagous describe the risk factors, age sex and morph/clinical
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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 |
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tell me in general about squamous cell carcinoma of the esophagous and adenocarcinoma
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not common but deadly
*asx, discovered too late for cure *arise from epithelium |
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tell me about squamous cell carcinoma
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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 |
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what type of malignant cancer is assoicated with diet, environment, EtOH and TOB
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squamous cell carcinoma of esophagous
**also have loss of p53 tumor suppressor |
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whats the pathogensis of normal squamous epithelium to squamous cell carcinoma
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male over 45 with chronic exposure to carcinogens. increased epithelial cell turnover in a carcinogenic environment --> dysplasia --> carcinoma
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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
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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 |
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what are the 3 morphologies of the later squamous cell carcinoma lesions
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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 |
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is the onset of squamous cell carcinoma abrupt or insidious
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insidious, dysphagia, obstruction
weight loss, solid to liquid diet |
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tell me about esophageal adenocarcinoma
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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) |
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ok so burkitts has progressed into adenocarcinoma, what does the lesion look like
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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) |
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in adenocarcinoma does dysplasia always mean cancer
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nope, can regress
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what is the clinical picture of a person with esophageal adenocarcinoma
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men over 40, Whites
dysphagia, weight loss, bleeding, chest pain, vomit |
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describe all of the features of congenital hypertrophic pyloric stenosis
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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 |
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what are some things that cause acute gastritis
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NSAIDS
Excess EtOH TOB cancer chemo uremia, infection, stress, ischemia/shock etc |
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acute gastritis
risks: morphoogy: clinical |
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 |
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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
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acute gastritis
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what is chronic gastritis?
what is ti caused by |
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 |
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what is the important etiology of chronic gastritis
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H pylori
**seen w/poverty, croding, limited education, low SES, rural |
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describe H pylori with respect to:
risk factors morphology associated disease |
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 |
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risk for gastric cancer is increased by what
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h pylori infection
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what are the micro about H pylori
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gram -, rod
motile- flagella urease bacterial adhesions, toxins lived in superficial epithelial layer **associated with: chronic gastritis, peptic ulcer disease, gastric carcinoma, |
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whats pan gastritis, what is it associated with
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mucosal atrophy
decreased acid secretion increstinal metaplasia increased risk of gastric cancer **assoicated with H pylori |
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where is h pylori, what is associated with it
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in duperficial mucosa, epiuthelium
PMN, plasma cells are characteristic H pylori is NOT in regions of intestinal metaplasia |
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how is H pylori dx
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serology for AB, bacteria in poo, urea breath test
gastric biopsy |
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infection with H pylori causes chronic gastritis how
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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 |
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what are hte clinical features of autoimmune gastritis
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less common
AB to parietal cells and IF (detected in serum) *decreased pepsinogen I endocrine cell hyperplasia B12 deficit achlorhydria (decrease acid secretion) |
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compare:
autoimmune gastritis and H pylori |
Autoimmune gastritis: AB to parietal cells and IF --> B12 deficit, decreased acid --> gastrin secretion and large G cells
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what things are inhibited bc in autoimmune gastritis there are AB to parietal cells and IF
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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 |
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whats the morph of autoimmune gastritis
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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) |
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a 60 yo male tested + for AB to parietal cells 20 years ago, he now has some mucosal atrophy. is this normal
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yep, autoimmune gastritis
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what are the microscopic features of chronic gastritis
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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 |
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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 |
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 |
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what is eosinophilic gastritis
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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 |
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tell me about lymphocytic gastritis
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women with celiac
aka carioform gastritic thick folds with nodules w/central ulcerations |
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tell me about granulomatous gastritis
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granulomas: chrons, sarcoid, mycobacteria, fungi, CMV, H pylori
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case
esophageal biopsy shows reflus with eosionophiles, squamous and glandular (columnar) epithelium present, will there be dysplasia? what can it develop into |
barretts esophagous
yes dysplasia develop into adenocarcinoma |
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case 2
mass in esophagous, shows Squamous cell carcinoma (SCC) |
weird case presentation
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