Gastric Acid Disorders Patho

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Last updated 2:20 AM on 4/7/26
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50 Terms

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gastric pits

there are millions of these in the lining of the GI tract that lead to the gastric glands that produce gastric juice

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g cells

cell type that secretes gastrin

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parietal cells

cell type that secretes gastric acid

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proton pump

hydrogen-potassium pump located on the surface of parietal cells

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hydrogen

the parietal cell proton pump moves one of those ions OUT of the cell into the stomach lumen

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potassium

the parietal cell proton pump moves one of these ions INTO the cell

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concentration gradient

the parietal cell proton pump moves potassium and hydrogen ions against their…

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chloride

this ion enters the parietal cell to form HCl with hydrogen

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gastrin, acetylchloine, histamine

these 3 hormones stimulate acid secretion

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h2

histamine receptor on the surface of parietal cells

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g protein coupled

type of receptor that the h2 receptor is

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h2 receptor

the cellular response of this receptor is translocation of proton pumps to the plasma membrane → dec pH of stomach lumen

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h+ secretion

when the cellular response occurs from h2 receptor, this is the mechanism BY WHICH pH decreases

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acid disorders

these result from an imbalance of aggressive/damaging (or potentially damaging) factors and mucosal defense/protective factors

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mucosal barrier

maintaing the integrity of this in the gastric environment is the key to avoiding damage from acid

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tight junctions

this feature between epithelial cells prevents HCl from leaking into underlying tissue

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HCO3

component of mucosal barrier fluid (mucus) that neutralizes stomach acid

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mucin

protein in mucus that helps it perform its functions

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GERD

symptomatic condition or histologic change associated with retrograde movement of gastric contents to esophagus

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PUD

gastritis, erosions, and ulcers of the GI tract that requires gastric acid for their formation

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duodenum

more common site of peptic ulcers

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lower esophageal sphincter

most commonly, GERD is caused by incompetency of this feature

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pressure

when the LES in incompetent, this is reduced and when stomach pressure exceeds LES pressure the contents will come up

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hiatal hernia

a risk factor for GERD where the stomach bulges up into the chest through the hiatus of the diaphragm

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peppermint

a food that can often trigger GERD in sensitive patients

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barretts esophagus

a sequelae of more severe GERD that involves metaplasia of stratified squamous cells into columnar and goblet cells

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adenocarcinoma

barretts esophagus cellsare more likely to develop into this condition

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PUD

injury to the mucosa of the stomach that can range from slight injury to severe ulceration and bleeding

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helicobacter pylori

bacteria that is the most common cause of PUD

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smoking

increases the risk of developing PUD

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flagella

feature of h. pylori that help it move below the mucosal surface to coloize the gastric epithelium

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mucous layer

h pylori can cause PUD by disrupting this layer, neutralizing pH, and releasing enzymes and toxins

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urease

enzyme that converts urea to CO2 and ammonia, which neutralizes the acid and can injure/irritate the mucosa

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gastric cancer

h pylori is also associated with this condition because it inhibits apoptosis of gastric pit cells and encourages chronic inflammation

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cagA

toxin produced by h pylori that can degrade p53 proteins that normally suppress protein

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de-gelling

this is required before the h pylori can move further and cause damage to gastric epithelium

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endoscopy

gold standard for diagnosing h pylori infection

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breath test

another method of detecting h pylori infection that is less invasive

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co13 and co12 ratio

isotopes used to detect presence of h pylori in breath

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neutrophils

NSAIDS can increase adherence of these to the vascular endothelium, causing more ROS damage

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COX-1 and COX-2

NSAIDs inhibit these, which therefore also inhibit several beneficial prostaglandins

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arachidonic acid cascade

NSAIDs inhibit prostaglandins that are produced in this process

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corticosteroids

combination of this medication class with NSAIDs can make a patient more susceptible to PUD

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stress ulcer prophylaxis

the use of medications to prevent peptic ulcers while a patient is in the hospital

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no

do all patients need stress ulcer prophylaxis

<p>do all patients need stress ulcer prophylaxis</p>
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epigastric pain

main symptom of PUD

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stomach

ulcer type where pain is aggravated by food

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duodenum

ulcer type where pain is relieved by food

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alarm symptoms

present in patients with chronic PUD, can indicate need for emergency care

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alarm symptoms

these include: bleeding (melena or hematemesis), perforation (Radiating pain to back), obstruction (vomiting, abdominal distention)

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