GI E1- Stomach & Duodenum

What are the 4 layers of the GI wall?

mucosa, submucosa, muscularis (outer longitudinal & inner circular, oblique in stomach), serosa

What are the 4 main zones of the stomach?

cardia, fundus (above GEJ), body (corpus), antrum

Combined secretions of mucous cells, parietal cells (HCl + intrinsic factor), and chief cells (pepsinogen I&II) are known as _______

gastric juices

_________ is secreted by G cells in response to food entry to increase stomach motility, mediate gastric acid secretion, and promote constriction of LES.

Gastrin

________ is secreted by I cells of the jejunum in response to fatty substances to increase gallbladder contractility for bile, stimulate pancreatic secretion, regulate gastric emptying & bowel motility, and induce satiety.

cholecystokinin

________ is produced by duodenal mucosa w/ entry of gastric juice from the stomach to stimulate pancreatic fluid/bicarb secretion & neutralize the acidity of stomach contents.

secretin

_____ is a peptide that increases appetite, stimulated GH secretion, and produces weight gain.

ghrelin

What is epithelial damage in the mucosa without accompanying inflammation?

gastropathy

What do hemorrhagic and erosive lesions develop from?

exposure of gastric mucosa to injurious substances OR lack of blood flow to mucosa (ischemic)

ex: meds, alc, medical/surgical stress, portal HTN

What condition?

• upper endo findings: sub epithelial hemorrhages, petechiae, erosions

• sx: anorexia, epigastric pain, N, V

• UGI bleeding- hematemesis: “coffee ground” emesis, bloody aspirate w/ NG suction, usually insignificant amounts, possibly melena

erosive & hemorrhagic lesions

What condition?

• mucosal erosions & subepithelial hemorrhages that develop w/in 72 hours in majority of critically ill pts

• bleeding assoc w/ high mortality, but is rarely cause of death

• begin prophylaxis upon admission to ICU

• rx: IV H2RA, IV PPI, sucralfate susp, omeprazole + sodium bicarbonate (zegerid) rapid release susp

stress gastropathy

What factors significantly increase bleeding in stress gastropathy?

coagulopathy: plt < 50,000/MCL; INR > 1.5

mechanical vent > 48 hrs

other: sepsis, vasopressor, steroids, burns, TBI, PUD, GI bleed

NSAIDs selective for which enzyme are associated with a decrease in ulcers/injury, but a twofold increase in CV complications?

COX-2

All NSAIDS except which ones should be used with caution in those w/ CV risks factors?

ASA and naproxen

What is the pathogenesis of NSAID induced gastric injury and bleeding?

inhibition of prostaglandin synthesis, which is needed for mucosal protection and healing; 3 pathways

• inhibit COX-1 activity

• inhibit COX-2 activity

• direct cytotoxic effects on epithelium

Dyspeptic symptoms from NSAID induced injury do not correlate w/ disease severity. When would a diagnostic upper endoscopy be indicated?

alarm sx

What is the treatment for NSAID related injury/dyspepsia?

PPIs > H2RAs; empiric 2-4 wk trial w/ PPIs

refer for EGD if sx persist

misoprostol (cytotec) for prevention of ulcers (avoid in women of childbearing years due to termination of pregnancy)

What is the treatment of alcohol induced gastropathy?

H2RAs, PPIs, or sucralfate initiated empirically for 2-4 wks

What condition?

• portal HTN → gastric mucosal/submucosa capillary/venule congestion

• often asx, possible chronic GI bleeding or hematemesis

• rx: propranolol or naldolol to decrease portal HTN

portal hypertensive gastropathy

Inflammation of the gastric mucosa w/ histologic evidence of inflammation via endoscopic or radiologic evaluation +/- erosions / hemorrhages is known as _______

Gastritis

what bacteria?

• spiral gram negative

• secretes urease → converts urea to ammonia → neutralizes stomach acidity

• spiral shape allows it to bury into mucous layer → CAGA toxin injected into stomach cells → bacteria attach easily → chronic inflammation

• person-person transmission, mode unknown

h. pylori

What is h. pylori associated with?

chronic gastritis / inflammation, PUD, gastric cancer (group 1 carcinogen)

What population is h. pylori increased in?

> 60, non whites, immigrants from developing countries (inversely correlated w/ lower socioeconomic status)

What are the 3 gastritis phenotypes associated with h. pylori?

Mild diffuse w/o disruption of acid secretion & no clinical illness

Inflammation in gastric antrum only, inc risk of duodenal PUD

Inflammation mainly in gastric body, inc risk of gastric ulcers & cancer

When should H. pylori testing be conducted?

pts < 60 w/ uncomplicated dyspepsia,

functional dyspepsia

all immigrants from prevalent regions - Japan, Korea, China

What are noninvasive testing options for H. pylori?

urea breath test & fecal antigen immunoassay

(*** must d/c PPIs 7-14 days prior & abx 28 days prior)

What is the first line treatment for H. pylori?

triple therapy x 10-14 days

Prevpac BID: 1 tab lansoprazole, clarithro, 2 tabs amoxicillin

Helidac QID: 2 tab metro, tetra HCL, 2 tabs bismuth subsalicylate, plus ranitidine (H2RA)

What condition?

• autoimmune; destruction of fundic glands

• anti-intrinsic factor abs, intestinal metaplasia, severe gland atrophy

• loss of acid inhibition of G cells → achlorhydria & hypergastrinemia (> 1000 PG/ml)

• increase risk of gastric cancer (carcinoid tumors)

pernicious anemia gastritis

what is indicated with a new diagnosis of pernicious anemia?

EGD

What is the treatment for acute bacterial infection / phlegmonous / necrotizing gastritis?

broad spectrum abx & possible emergent gastric resection

What kind of patients is viral gastritis due to CMV seen in?

AIDs, bone marrow or solid organ transplant recipients

what kind of patients are fungal gastritis infections seen in?

immunocompromised & diabetics

what condition?

• eosinophils infiltrate antrum and proximal intestine

• +peripheral eosinophilia

• rare

• sx: anemia, abd pain, early satiety, postprandial vomiting

• tx: corticosteroids

eosinophilic gastritis

What condition?

• large thickened gastric folds in body of stomach → chronic protein loss

• unknown eti

• sx: N, epigastric pain, wt loss, diarrhea

• tx: cetuximab, gastric resection

menetrier disease / hypertrophic gastropathy

what condition?

• loss of gastric or SI epithelium that extends to penetrate muscularis mucosa

• erosions- small & superficial; ulcers- 5mm - several cm

• caused when normal mucosal defenses are impaired / overwhelmed by acid or pepsin

peptic ulcer disease (PUD)

What plays an important role in maintaining defenses against ulcers?

prostaglandins

what are the most common risk factors for PUD?

H. pylori infection, NSAID / ASA use

What condition?

• classic sx: epigastric pain → dull, gnawing, aching, “empty, “hunger like” sensation

• recurs over weeks-months

• acute or worsening pain may indicate ulcer penetration/perforation

PUD

What is the workup for PUD?

study of choice: endoscopy (all gastric ulcers need to be bx)

alt: BA UGI

asses for H. pylori

what kind of ulcer?

• antrum & lesser curvature

• later in life - 55-70

• normal or increased acid secretion

• pain & N w/ eating, relieved w/ fasting (look for wt loss, anorexia)

gastric

What kind of ulcer?

• duodenal bulb or pylorus

• younger age - 30-55

• inc acid secretion and dec HCO3 may create small area of gastric metaplasia which becomes colonized by h. pylori

• pain relieved by foot intake, recurs 2-4 hrs later, may awaken pt at HS

duodenal

What is the treatment for H. pylori associated ulcers?

avoid smoking

antibacterial + antiulcer therapy

• PPI + clarithro or metro + amoxi

• PPI + clarithro + metro

• bismuth salicylate + metro + tetra + PPI

How do PPIs treat ulcers?

covalently bind acid secreting enzyme H+/K+ATPase → proton pump must regenerate (18 hrs) → inhibit 90% of acid secretion

(action is > 24 hrs)

What is the treatment for NSAID associated ulcers?

d/c NSAID or use selective COX 2 inhibitors

PPIs, H2RAs,

high risk → test for h. pylori, PPI, misoprostol

What increases the risk of GI bleeding, especially in combo with ASA use?

chronic antiplatelet therapy

What is important to remember about post GI ulcer bleeds in patients on antiplatet therapy?

ASA should be restarted as soon as risk for CV events outweighs risk for recurrent ulcer complications

(PPIs may diminish effects of clopidogrel, but studies show you can use them together; least interactive w/ pantoprazole)

what is the most common complication of PUD?

GI hemorrhage

What condition?

• infrequent complication of PUD → erodes into adjacent organ

• severe abd pain, peritonitis (rigid abd w/ rebound tenderness), leukocytosis

peptic ulcer perforation

what should be avoided with peptic ulcer perforations?

endoscopy

How do you diagnose PUD?

xray → free air under diaphragm

if suspect & no free air → order UGI or CT w/ gastrografin (water soluble contrast)

What is the treatment for peptic ulcer perforation?

NG tube to suction, IV fluids & PPI, consult surgeon for laparotomy or laparoscopy

What condition?

• comp of PUD, occurs in < 2% of ulcer patients

• sx: early satiety, epigastric fullness, vomiting, wt loss, abd distension, vomit previously ingested material

• 2 types:

  • edema/inflammation around acute ulcer

  • chronic permanent scarring/fibrosis w/ outlet narrowing

gastric outlet obstruction

How is gastric outlet obstruction diagnosed?

succussion splash (PE) - audible splash of gastric contents produced by shaking patients torso

barium studies

endoscopy

What is the treatment or gastric outlet obstruction?

NGT aspiration 5-7 days→ large, foul smelling liquid

IV fluids & PPI

may require surgery/endoscopic dilation in 1 yr

What can cause gastric outflow obstruction at the pylorus, producing succussion splash?

antral cancer, bezoar, or PUD

What condition?

• gastric acid hyper secretion, severe PUD, gastrin secreting tumors

• caused by gastronomas

• maldigestion & malabsorption due to low pH

• sx: unresolved reflux sx, diarrhea, wt loss

zollinger-ellison (ZE) syndrome

Where do most gastronomas arise?

gastronoma triangle - junction of cystic duct & common bile duct, head & neck of pancreas, 2nd & 3rd parts of duodenum

90% of ZE patients will develop _____

PUD

What should be obtained with screening for all ZE patients to exclude men 1?

serum PTH, prolactin, LH-FSH, GH

How is ZE syndrome diagnosed?

fasting serum gastrin: > 1000 PG/ml + gastric pH < 4.0

gastric pH: exclude secondary hypergastrinemia due to achlorhydria

secretin stimulation test: differentiate gastrinomas from other causes of hypergastrinemia

What is the best predictor of survival of ZE syndrome?

presence of hepatic mets; tx w/ PPIs & surgical resection

what is the 2nd most common cancer worldwide?

gastric adenocarcinoma

What is a common cause of gastric adenocarcinoma?

chronic h. pylori infection

What are risk factors for gastric cancer?

older age & male, H. pylori, diets high in salt & preserved foods (nitrates), tobacco, pernicious anemia, hx stomach surgery, FHx

Which histologic variant of gastric cancer?

• younger pts

• worse prognosis

• not related to H. pylori

• acquired or inherited mutations

“diffuse” - poorly differentiated

Which histologic variant of gastric cancer?

• forms glandular structures

• more common

• environmental factors

• arises from multi step progression from inflammation (H. pylori) to metaplasia to dysplasia (cancer)

intestinal type

The following symptoms are signs of what?

• virchow’s node (supraclavicular)

• sister Mary Joseph nodule (umbilical)

• blumer shelf (rigid rectal shelf)

• krukenberg tumor (ovarian mets)

metastatic gastric cancer

Virchow’s node (left supraclavicular area) is indicative of _______

mets of gastric carcinoma

What are indications for an endoscopic evaluation for gastric cancer?

any pt > 60 w/ new onset dyspepsia

persistent dyspepsia or resistant to tx

screening in high areas of occurrence

what is the treatment for gastric cancer?

surgery & TNM staging, chemo & radiation

(< 15% long term survival; >45% survive 5 yrs after “curative” resection)

what is the second most common gastric tumor?

gastric lymphoma

What has the same clinical presentation as adenocarcinoma?

Gastric lymphoma

What type of gastric lymphoma?

• most are B cell NHL

• many arise from mucosa assoc lymphoid tissue (MALT)

• infx w/ h. pylori is risk factor

• similar presentation to adenocarcinoma

primary gastric

what type of gastric lymphoma?

• usually present at advanced stage

• seldom curable

nodal lymphoma

what is the treatment for gastric lymphoma?

surgical resection, chemo, +/- radiotherapy

what kind of tumor?

• neuroendocrine

• rare; <1% of gastric tumors

• sporadic or secondary to chronic gastrinemia

• tend to metastasize

carcinoid tumor

what kind of tumor?

• arise from mesenchymal stem cells

• occur throughout GI tract, but 2/3 are in stomach

• types: stromal (MC; GIST); leiomyomas, schwannomas

GI mesenchymal tumor

A symptomatic delay in gastric emptying of solid or liquid meals w/o any obstructing lesion is known as _____

gastroparesis

What are the 3 most common causes of gastroparesis?

idiopathic, diabetic neuropathy, post surgical

What are the sx of gastroparesis?

N/V, early satiety, bloating, wt loss

what is the best test to diagnose gastroparesis?

gastric emptying scintigraphy (uses technetium 99 labeled food, performed 1-4 hrs after food ingestion)

what is the treatment for gastroparesis?

pro kinetics: erythromycin IV or PO, metoclopramide PO (both accelerate gastric emptying & antral contractions)

5HT serotonin agents: granisetron, ondansetron

What drug?

• dopamine agonist w/ pro kinetic & antiemetic properties

• administer w/ meals & at HS

• SE: tremor, dystonic rxns, drowsiness, fatigue tardive dyskinesia (black box warning)

Metoclopramide (Reglan)