PUD and Gastric CA Flashcards
PUD definition
defect in gastric or duodenal mucosa that extends through the muscularis mucosa into deeper layers of the wall
Layers of stomach wall
mucosa, submucosa, muscularis
Etiology of PUD
- H. pylori *
- NSAIDs *
- Other
Most common cause of PUD
H. pylori; incidence increases w/ age
may predispose to gastric CA
Inhibit gastrin release
low pH
prostaglandins
SS
Increase gastrin release
stomach distention
presence of peptides/AA
Gastrin role
increase gastric motility
stimulate parietal cells to secrete HCl and pepsinogen
Secretin role
inhibit stomach motility
decrease bile secretion
increase bicarb secretion from pancrea
1 cause of GI bleed
PUD
H. pylori description
gram (-) rod
Motile flagella (attaches to gastric mucosa)
oral-oral or fecal-oral route
disrupts protective properties by decreasing gastric mucus and mucosal bicarb secretion
raises pH
Increase risk of PUD w/ NSAIDs
- prior hx of PUD/ulcer complications
- H. pylori infection
- > 75 YO
- increased dose, time, duration of use
- concomitant use of steroid, other NSAID, anticoag, low dose ASA, SSRI, alendronate
H. pylori virulence factors
- flagella- attach, move
- urease - hydrolyze gastric urea to form ammonia, that helps neutralize gastric acid, enabling it to penetrate gastric mucosa
- Adhesins: adhere to epithelial cells
- Cause inflammation: causes G cells in antrum to secrete gastrin and therefore HCl increases
(ulcers are immediately friable)
Concomitant drugs that worsen PUD from NSAID
steroid other NSAID anticoagulants ASA SSRI alendronate
NSAIDs
ibuprofen
ASA
naproxen
toradol
MOA of PUD w/ NSAIDs
NSAIDs block COX, therefore preventing prostaglandin synthesis (PGE2) – prostaglandins inhibit gastrin secretion and increase mucous secretion, and promote epithelial cell proliferation
Prostaglandin role in stomach health
- inhibit gastrin secretion
- increase mucous secretion
- promote epithelial cell proliferation
Presentation of PUD
asymptomatic (70%)
Abdominal pain/discomfort
dyspepsia (belching, bloating, distention)
Nausea, early satiety, comiting
Complications: hematemesis, melena, fatigue, dyspnea
Gastric vs. duodenal ulcers
gastric: worse after meal (30min-1hr), vomiting, more likely to hemorrhage/hematemesis; weight loss/anorexia
duodenal: relieved by meals! (worse 2-3 hrs post meal), vomiting uncommon), less likely to hemorrhage (melena), weight gain
Melena
duodenal ulcer
hematemesis
gastric ulcer
Worse w/ meals
Gastric ulcer
vomiting uncommon
duodenal ulcer
weight gain
duodenal ulcer
PUD alarm sx
bleeding unexplained IDA early satiety unintentional weight loss progressive dysphagia/odynophagia acute onset of upper ab pain persistent vomiting family hx of UGI CA
Complications of PUD
bleeding (most common)
perforation
penetration
gastric outlet obstruction (rare)
Hemorrhage in PUD
hematemesis, melena or hematochezia
Dx/Tx of hemorrhage in PUD
stabilize with IV fluids or PRBCs
start IV PPI
perform EGD!!
Dark tarry store (melena)
UGI
Hematemesis
UGI (gastric)
Hematochezia
bad sign! hemorrhaging fast and can’t digest the blood
Tx of bleeding
thermal coagulation
hemoclip placement
injection tx
Perforation presentation
severe, diffuse, abdominal pain tachycardia weak pulse N/V may progress to "board-like abdominal rigidity"
Dx of perforation
hx/PE
UPRIGHT CHEST AND ABDOMINAL X-RAY
possible CT to localize
Tx of perforation
IV fluid NG tube NG suction for gastric decompression IV PPI broad spectrum abx SURGERY!!!
Contraindicated with perforation
UGI with barium (use gastrografin)
Dx of hemorrhage
EGD
Dx of perforation
Upright chest/ab X-ray
Penetration definition
penetration of ulcer through bowel wall w/o free perforation and leakage of luminal contents into peritoneal cavity;
goes into some other structure – pancreas!
Presentation of penetration
sx due to affected structure
sx like pancreatitis
pain w/o meal association, more intense pain, pain referral to back
Gastric outlet obstruction cause
scarring/fibrosis or inflammation/edema in pyloric channel; blockage of contents leaving stomach into duodenum
Presentation of gastric outlet obstruction
vomiting early satiety bloating epigastric pain weight loss anorexia
Dx of gastric obstruction
imaging- dilated stomach
Tx of gastric obstruction
IV fluid
NG tube- gastric decompression
IV PPI
EGD w/ endoscopic balloon dilation or surger – if fail w/ medical tx
PE for PUD
ab exam: epigastric tender, RUQ tender, peritoneal signs (perforation), succussion splash
Vitals: hypotension, tachy (complications)
Rectal exam: melena, hemoccult positive, bright red blood
Succussion splash
place stethoscope over upper abdomen and rock the pt back and forth at hips; retained gastric material >3 hours after meal will generate splash sound and indicate presence of hollow viscus filled w/ both fluid a gas
Succussion splash suggests
gastric outlet obstruction
Dx of PUD
EGD - gold standard
UGI
H. pylori:
- urea breath test
- fecal antigen test
- serology
- bx during EGD (most specific and sensitive!!!)
Urea breath test
identifies active H. pylori infection
- discontinue PPI 2 weeks prior and bsimuth/abx 4 weeks prior
- drink urea, urease converts to CO2 and NH3, test measures radioactive CO2
Fecal antigen test
antigen in feces
discontinue PPI 2 weeks prior
discontinue bismuth/abx 4 weeks prior
Serology
identifies IgG antibody to H. pylori
HIGH FALSE POSITIVE; AND FALSE NEGATIVE
* not recommended *
Tx of PUD
- eradicate H. pylori and confirm eradication in 4 weeks after treatment
- PPI if h. pylori absent or sx after eradication
- if sx persist, treat 8-12 weeks with TCA!
- if sx persist, treat 4 weeks w/ PROKINETIC
- if sx persist, perform EGD
(discontinue NSAID, ASA, alcohol, tobacco)
H. pylori treatment
Bismuth quadruple therapy x 14 days:
- PPI BID
- Bismuth 524 mg QID
- Tetracycline 500 mg QID
- metronidazole 250 mg QID
Zollinger-Ellison Syndrome (ZES): what is if?
gastrinoma (dudoenum or pancreas) hypersecretes gastrin
- increased HCl
- increased gastric motility (absorption issues)
more common in men
Etiology of ZES
sporadic (80%)
MEN1 (20%) - also in pituitary tumors, pancreas, parathyroid
Presentation of ZES
recurrent PUD - often distal to duodenal bulb* (multiple on EGD***)
abdominal pain
diarrhea (steatorrhea)
Dx of ZES
fasting serum gastrin >1000 pg/mL (10x)
gastric pH <2
Secretin stimulation test (gastrin should dec but it doesn’t)
CT abdomen to localize tumor
Tx of ZES
PPI*
or H2 blocker
Gastric CA risk factors
gastric ulcers*** adenomatous polyps intestinal metaplasia dietary (nitroso compounds, high-salt diet w/ few veggies) ETOH/tobacco use Chronic H.pylori infection
Sx of gastric CA
early: asymptomatic weight loss persistent ab pain early satiety nausea, anorexia, dysphagia Gastric ulcer hx (25%) Occult GI bleed Late: palpable stomach mass, succussion splash, paraneoplastic syndromes
Dx of gastric CA
EGD* - gastric vs esophageal CA
UGI- 2nd line
Staging (TNM)
determine nodal involvement, distant lesions, invasion of vasculature, depth of tumor
Most common type of gastric CA
adenocarcinomas (95%)
Gastric CA on EGD
subtle polypoid protrusion, superficial plaque, mucosal discoloration, depression or ulcer
Signs of metastatic disease
Virchow’s node (most specific)
sister Mary Joseph’s node/nodule
Left axillary node (irish node)
Virchow’s node
left supraclavicular lymph node (most common); most specific for gastric cancer
Sister Mary Josephs nodule
periumbilical nodule
irish node
left axillary node (nonspecific)
Tx of Gastric CA
early (rare)- endoscopic mucosal resection
advanced- total or partial gastrectomy if resection possible
unresectable - chemo vs chemoradiotherapy
Workup for dyspepsia
> 60 YO: EGD!!!
- PUD- treat
- no organic cause, either function of H. pylori
<60 YO: EGD if any of the following:
- weight loss
- overt GI bleed (visible)
- > 1 alarm feature
- Rapidly progressive alarm features
if no EGD- test for H. pylori
Alarm features
unintentional weight loss progressive dysphagia odynophagia unexplaind IDA persistent vomiting palpable mass or LAD family hx of UGI CA
