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Stomach Flashcards

1
Q

Protective fx for gastritis/duodenitis (7)

A

mucus, bicarb, mucosal blood flow, prostaglandins, alkaline state, hydrophobic layer, epithelial renewal

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2
Q

Gastritis/duodenitis causes

A
  1. Autoimmune (pernicious anemia) or noninfectious –> type A gastritis – body of stomach
  2. HPylori: g-, spiral shaped bacillus – almost all non-NSAID induced GI mucosal inflamm
  3. NSAIDs – dec prostaglandin production in stomach/duodenum
  4. Stress from CNS inj/burns/sepsis/surg –> erosion
  5. OH use
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3
Q

ASA and PUD MOA

A

ASA blocks prostaglandins –>PUD (NOT d/t local irritation)

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4
Q

PUD gen/causes

A

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

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5
Q

PUD clinical

A

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)

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6
Q

PUD complications

A

bleeding (melena), perforation, penetration

PUD MCC of nonhemorrhagic GI bleeds

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7
Q

PUD labs

A

Endoscopy: best for detecting small/healing ulcers
Ba readiography: cheaper/less sensitive, 30% false neg. rate
Urea breath: for HP

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8
Q

PUD tx

A

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

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9
Q

Zollinger Ellison Syndrome general

A

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

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10
Q

ZES clinical

A

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

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11
Q

ZES lab findings

A 
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
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12
Q

ZES tx

A

use PPI to ctrl gastrin secretion

Surgical resection of gastrinoma

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13
Q

Gastric adenocarcinoma

A

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

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14
Q

Gastric AC clinical

A

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)

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15
Q

Gastric AC labs

A

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

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16
Q

Gastric AC tx

A

tx: curative or palliative resection of tumor

Chem or radiation can be palliative

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17
Q

Carcinoid tumors of stomach

A

rarely occur in response to hypergastrinemia

USU benign and self-limited

18
Q

Gastric lymphoma

A

< 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

19
Q

Role of gastrin and pepsin

A

Gastrin– produced in stomach –> blood to stimulate acid production in stomach
Pepsin– helps protein digestion, an aggressive factor that can lead to ulceration

20
Q

Acethycholine’s role in PUD

A

Cephalic phase of digestion: brain stimulates INC ACh –> stimulates parietal cells –>INC in acid production (also stim. prod of proton pump K+, H+, ATPase)

21
Q

Billroth surgery

A

Cut out portion of stomach that has parietal cells that produce HCl acid – old way to tx PUD

22
Q

NSAIDs role in PUD

A

Prostaglandin blocker in inflammation injury and stomach – bad.
Celecoxib/celebrex block prostaglandins NOT in stomach
Endogenous prostaglandins produce MUCUS and BICARB

23
Q

Prostaglandin mechanism

A

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

24
Q

H Pylori MOA

A

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

25
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
26
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
27
Histamine and acid production
Histamane stim. acid production in parietal cell | -- H2 blockers --> less acid production
28
PPI
NOT dose dependent, take 30min to work
29
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
30
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
31
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
32
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
33
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 ```
34
X-ray findings suggestive of ulceration
- rritability of bulb, difficulty retaining barium - pylorospasm - gastric hyperperistalsis - hypersecretion
35
Cholelithiasis populations
Native Americans, Latinos
36
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
37
Peritonitis, complication of PUD
Acute epigastric pain, radiate to shoulder N/V Rigid abd, fever, absent B/S XR: free air under diaphragm
38
MC organs penetrated from PUD
pancreas, liver -- elev serum amylase or ALT/AST | pain radiates to back -- does NOT improve w/ food
39
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
40
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.
41
Gastric ulcer s/sx differ from duodenal
Gasric: referred to L subcostal Duodenal: referred to back/R shoulder

GI (5 decks)

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