Stomach Flashcards
Protective fx for gastritis/duodenitis (7)
mucus, bicarb, mucosal blood flow, prostaglandins, alkaline state, hydrophobic layer, epithelial renewal
Gastritis/duodenitis causes
- Autoimmune (pernicious anemia) or noninfectious –> type A gastritis – body of stomach
- HPylori: g-, spiral shaped bacillus – almost all non-NSAID induced GI mucosal inflamm
- NSAIDs – dec prostaglandin production in stomach/duodenum
- Stress from CNS inj/burns/sepsis/surg –> erosion
- OH use
ASA and PUD MOA
ASA blocks prostaglandins –>PUD (NOT d/t local irritation)
PUD gen/causes
Any ulcer of upper GI system
Cause: any discreet break in mucosa caused by inj, NSAIDs, stress, OH, irritants (MCC: HP)
Lifetime risk: 5-10%
Men = Women
PUD and HP are highly assoc w/ gastric malignancy
PUD clinical
Abd pain/discomfort (burning/gnawing) – radiates to back/R shoulder
Pain improves w/ food in DUODENAL, worsens w/ food in GASTRIC –> anorexia/wt loss
Dyspepsia (belch, bloat, distend, heartburn)
PUD complications
bleeding (melena), perforation, penetration
PUD MCC of nonhemorrhagic GI bleeds
PUD labs
Endoscopy: best for detecting small/healing ulcers
Ba readiography: cheaper/less sensitive, 30% false neg. rate
Urea breath: for HP
PUD tx
avoid smoke, NSAIDs, OH
HP regimen:
–PPI w/ clarithromycin and amox (+/- metro)
–Bismuth subsalicylate + tetracycline, metro, and PPI
Prophylaxis: misoprostol or PPI in pt w/ h/o PUD who require daily NSAID use, h/o complications (bleed), chronic steroids or anticoag, significant other comorbidities
Zollinger Ellison Syndrome general
60% males (MC in relatively young males)
–onset 20-50y
2/3 of tumor are malignant
gastrin-secreting tumor (gastrinoma) –> hypergastrinemia –> refractory PUD
1% of PUDs caused by ZES
Most gastrinomas in pancreas or duodenum
1/3 of gastrinoma are part of mult endocrine neoplasia, type I (MEN1), autosomal dominant condition
ZES clinical
PUD that is more adv. or refractory to tx
–perforation, penetration/bleeding, obstruction
Pain +/- secretory diarrhea that improves w/ H2 blockers or PPI
Occult or frank bleeding –> anemia
ZES lab findings
Mult ulcers in 2nd, 3rd, 4th portion of duodenum/jejunum (NOT 1ST PART) Fasting gastrin > 150pg/mL --PPIs on reg basis can elev gastrin lvl Gastrin>300 per Medina's lec Secretin test REQ to find ZES --pts given 2U/kg IV, then if +ZES, gastrin inc by >200pg/mL Endoscopy, CT, or MRI can localize tumor HyperCa w/ MEN-1
ZES tx
use PPI to ctrl gastrin secretion
Surgical resection of gastrinoma
Gastric adenocarcinoma
Gastric AC, MC type of CA worldwide, not as much so in US
2x more CMN in men than women
Almost NEVER in pt <40y/o
Early dx, 80% cure rate
Involvement of muscularis propria, 50% cure rate
Lymphatic spread, 10% cure rate
STRONG assoc w/ HP
Gastric AC clinical
CMN: dyspepsia, wt loss, anemia, occult GI bleed
Progressive dysphagia – neoplasm impinging of esophagus
Postprandial vomiting– neoplasm near pylorus
Metastatic spread: L supraclav LAD (Virchow’s node), umbilical nodule (Sister Mary Joseph nodule)
Gastric AC labs
MC finding: IDA
Liver enz elev w/ hepatic metastases
Endoscopy w/ cytology: on any pt>40+ w/ dyspepsia who is unresponsive to therapy
After dx, abd CT to determine extent
Gastric AC tx
tx: curative or palliative resection of tumor
Chem or radiation can be palliative
Carcinoid tumors of stomach
rarely occur in response to hypergastrinemia
USU benign and self-limited
Gastric lymphoma
< 2% of gastric malignancies
Stomach is MC extranodal site for non-hodgkin’s
Risk is greater 6x if HP infxn present
SIMILAR TO Gastric AC – only different by pathology
Tx: resect w/ or w/o radiation/chemo
Role of gastrin and pepsin
Gastrin– produced in stomach –> blood to stimulate acid production in stomach
Pepsin– helps protein digestion, an aggressive factor that can lead to ulceration
Acethycholine’s role in PUD
Cephalic phase of digestion: brain stimulates INC ACh –> stimulates parietal cells –>INC in acid production (also stim. prod of proton pump K+, H+, ATPase)
Billroth surgery
Cut out portion of stomach that has parietal cells that produce HCl acid – old way to tx PUD
NSAIDs role in PUD
Prostaglandin blocker in inflammation injury and stomach – bad.
Celecoxib/celebrex block prostaglandins NOT in stomach
Endogenous prostaglandins produce MUCUS and BICARB
Prostaglandin mechanism
membrane phospholipids –>prostaglandins–> araciodonic acid –> COX1 and 2
COX1: GOOD. protects stomach lining (COX non-selective inhibitors –> bleeding risk)
COX2: inflammation
NSAID use –> Renal, GI, platelet issue
H Pylori MOA
INC HCl acid secretion
Causes INC in WBC, all chemical mediators/body’s defenses cause the ulcer
Protects itself from acid by producing ammonium ions which accept the H+ –> neutralizing environment around it w/ enzyme, urase
INC pepsin production
Highest prevalence of HP
10% in Caucasians < 30
Recent immigrants to US
Individuals w/ low socioecon. status – MOST POTENT FX
Pt>60y/o, 50%+
Majority of infxns acquired as kid
Stomach cell locations
Esophageal entrance of stomach: Mucus secreting cells
Body of Stomach: Parietal cells and chief cells –> pepsinogen –>pepsin
End of stomach: G cells –> gastrin, stimulates proton pumps to prod HCl
Histamine and acid production
Histamane stim. acid production in parietal cell
– H2 blockers –> less acid production
PPI
NOT dose dependent, take 30min to work
HP labs
Serum IgG Ab detectable by ELISA
–IgM NOT reliable
–better for pts who have NOT been tx for HP before
C-14 and C-13 urea breath tests
–HP contain a lot of urease which breaks down into CO2 and ammonia
–Drink urea, wait 0.5h, if you have HP, breaks down the urea
Stool and urine Ag test verify eradication
DO STOOL/BREATH 4 wks after complete tx of ABX and PPIs
Duodenal ulcer
Men>women
2-3x more CMN than gastric ulcers
95% occur in duodenal bulb
Mult in different parts of duodenum? –> GASTRINOMA! or due to HP
20-25% have minor obstruction, esp from scarring
PUD timing
45-60min after meal; worse b/w midnight and 2AM
-Wake up w/ pain
Relief by food, milk, alkali, vomiting w/in 5-30min
–MILK has protein which can be acid stimulator
PUD red flags
SEND TO GASTRO AND SCOPE:
early satiety, anorexia, older than 45y/o, rectal bleeding or melena, wt loss>10% of wt, anemia, dysphagia, abd mass, jaundice, FHx of gastric CA, PMH of peptic ulcer
PUD Labs
Hypochromic Anemia if bleeding --adult w/ Fe deficiency anemia: maj source: GI --females could be menstrual Occult blood Amylase in ulcer penetration to pancreas X-ray single contrast upper GI, +50-80%, Double contrast is 90% accurate --not really done, except in dysphagia --endoscopy way better
X-ray findings suggestive of ulceration
- rritability of bulb, difficulty retaining barium
- pylorospasm
- gastric hyperperistalsis
- hypersecretion
Cholelithiasis populations
Native Americans, Latinos
Gastric ulcer gen
HP assoc less in gastric than duodenal ulcer
More CMN in 55-70y/o
DEC tissue resistance more imp than hypersecretion
60% of ulcers occur 6cm from pylorus
if see ulcers in upper GI, MUST bx ulcers to r/o gastric carcinoma
Peritonitis, complication of PUD
Acute epigastric pain, radiate to shoulder
N/V
Rigid abd, fever, absent B/S
XR: free air under diaphragm
MC organs penetrated from PUD
pancreas, liver – elev serum amylase or ALT/AST
pain radiates to back – does NOT improve w/ food
Obstruction, complication of PUD
20-25% of duodenal ulcers
S/sx: epigastric fullness, heaviness, vomit after meals w/ partially digested food
Dx by endoscopy
tx: PPI
PUD Diets
Diet has no therapeutic value – no bland diets
Acid stim w/ both decaf/reg coffee
Restrict coffee, tea, cola, OH
CEASE SMOKING – most imp.
Gastric ulcer s/sx differ from duodenal
Gasric: referred to L subcostal
Duodenal: referred to back/R shoulder
