Gastric Disorders 1 Flashcards
GERD patho
LES barrier is breached and reflux of caustic gastric acid interacted with unprotected esophagus
mechanisms that can cause reflux
- loss of LES tone
- increased frequency of relaxation
- loss of secondary peristalsis after relaxation
- increased stomach volume/pressure
- increased acid production
risk factors for GERD development
impaired LES tone (abnormal location, extrinsic compression)
extrinsic, increased pressure on intra abdominal organs
decreased acid cleaned
delayed gastric emptying/duodenalgastric reflux
hypersecreiton of acid
hiatal hernia and GERD
causes deficient LES bc removes added constriction to diaphragmatic cura
more acid reflux, slow acid clearance, inflammation
typical s/signs of GERD (5)
heartburn (after meals, received with antacid)
bitter regurgitation
increased salivation
chest and epigastric pain
dysphagia
atypical symptoms
chronic cough, asthma, hoarseness, sore throat
what exacerbated GERD symptoms
meals, bending or reclining/lying supine
factors that worsen GERD
increase acid
fatty food
spicy food
acidic food/drink
bananas
factors that worsen GERD
slow gastric emptying
TCA
anticholinergics
opioids
factors that worsen GERD
lower LES pressure
nitroglycerine CCB progesterone benzos alchol opiods chocolate coffee pepperment
diagnostic workup of GERD
presumptive diagnosis on clinical ground
six week trial of PPI or H2
endoscopy
when do we preform endoscopy in GERD
- doubt of diagnosis (alarm symptoms, persistent, erosive espohagitis)
- men > 50 with chronic GERD (increased risk of esophageal cancer)
complications of GERD
- esophageal stricture
- Barrett’s esophagus
- esophageal ulcers
- hemorrhage/perforation
- fistula formation
barrett’s esophagus
replacement of normal squamous epithelium with columnar epithelium
precursor of esophageal adenoma
dyspepsia
EPIGASTRIC pain/burning
early salty
fullness after meal
gastritis
inflammation associated with mucosal injury
gastropathy
non inflammatory mucosal injury
gastritis mc causes
nonspecific inflammation of mucosal surfaces
- H. pylori
- NSAIDs
- stress related changes
can also be alcohol or atrophic
h. pylori
gram negative rod found in gastric epithelium
60% of gastric,80% of duodenal ulcers
fecal orla
MC in low SES
h. pylori pathophys
imbeds into mucosal layer and colonizes causing acute and chronic inflammation of gastric mucosa
produces large amounts of urease to break down acidic environment
increased risk of gastric adenocarcinoma and MALT lymphoma
h. pylori urease
breaks down urea to alkaline ammonia and carbon dioxide
allows the immediate and surrounding areas to have a more neutral pH
h. pylori gastritis
acute gastritis in antrum and then extends to entire mucosa (acute –> chronic)
may cause ulceration
when is h. pylori detection performed
active PUD
early gastric CA/MALT lymphoma
CAN do IgG but unable to distinguish past or present infection
h. pylori detection tests
- urea breath test
- stool antigen test
- stomach biopsy
urea breath test
pt drinks radioactive urea
h. pylori urease will split the urea and detectable CO2 will be exhaled
wat can give false negative on urea breath test?
PPI
Abx
bismouth
UGIB
stool antigen test
examine stool to look for h. pylori
can document successful tx and presence
NOT impacted by UGIB
stomach biopsy
lining of stomach/small intestine taken during EGD and rapid urease test done
false neg: PPI, ABX, bismuth, UGIB
h. pylori triple therapy
10-14 days
- proton pump inhibitor
- Amoxicillin
- Clarithromycin
quadruple therapy h. pylori
10-14 days
- PPI
- Bismuth
- Metronidazole
- Tetracycline
who gets quadruple h. pylori tx
resistance to clarithromycin or metronidazole
previous/recent metronidazole exposure
NSAID gastritis
loss of prostaglandin/COX 1 to stimulate new mucosal formation AND loss of blood supply to mucosal wall (decreased vasodilation)
risk factor of NSAID gastritis
duration of NSAID therapy
increasing age, high NSAID dose, prior NSAID complication, concurrent steroid/anticoagulant/clopidigrel use
how do NSAIDS cause gastritis?
DIRECT toxic effect (topical injury)
INDIRECT effect (hepatic metabolite damage, decreased production of mucosal prostaglandin)
prevention of NSAID gastritis
PPI/misoprostol can prevent BOTH gastric and duodenal ulcers
H2 blockers can prevent duodenal ulcers
alarm dyspepsia features
weight loss without cause, anorexia vomiting dysphagia anemia GI bleed abdominal mass FH of GI CA previous malignancy
PUD
defect in GI mucosa of stomach or duodenum
MC cause h. pylori infection and NSAIDS
PUD s/s
Ulcer or acid dyspepsia (gnawing/burning pain, relieved with food)
food provoked dyspepsia/indigestion (aggravated by food)
reflux dyspepsia
PUD diagnostic studies
empically tx with H2 blockers if mild
> 45, alarm symptoms = EGD + biopsy
complications of PUD
GI bleed
tachycardia/pallor
outlet obstruction
perforation
