GI Stomach & Duodenum

What are the 4 lays of the GI wall?

What are the 4 lays of the GI wall?

mucosa, submucosa, muscular (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 produces 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 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 are symptoms of erosive & hemorrhagic lesions?

• anorexia, N, V

• epigastric pain

• UGI bleeding → Hematemesis; insignificant, “coffee ground emesis”, bloody aspirate w/ NG suction, possible melena

How are erosive & hemorrhagic lesions diagnosed?

upper endoscopy → sub epithelial hemorrhages, petechiae, erosions

Stress gastropathy - How fast to mucosal erosions & sub epithelial hemorrhages develop in majority of critically ill patients?

w/in 72 hrs

(bleeding assoc w/ high mortality, but rarely cause of death)

What should begin upon a patient’s admission to the ICU for stress gastropathy?

pharmacologic prophylaxis for erosive & hemorrhagic lesions to decrease incidence of bleeding

ex: IV H2RA, IV PPI, sucralfate suspension, omeprazole + bicarb (zegerid) rapid release suspension

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 sx from NSAID induced injury does not correlate w/ disease severity, mucosal abnormalities, or development of adverse events. 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

vascular 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 treatment for H. pylori?

• first line: triple therapy x 10-14 days

  • prevpac → 1 tab lansoprazole, clarithromycin, 2 tabs amoxicillin

  • helidac → 2 tabs bismuth subsalicylate, 1 tab metronidazole, tetracycline HCl, H2RA (ranitidine)

What condition?

• autoimmune disorder of 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 (can be life threatening)

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

AIDs pts, 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 → can invade all 3 layers of stomach

• peripheral eosinophilia

• rare

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

• rx: 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

• rx: cetuximab, gastric resection

menetrier disease / hypertrophic gastropathy

what condition?

• loss of gastric or small intestine 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 are the most common risk factors for PUD?

H. pylori infection + NSAID / ASA use

what are symptoms of PUD?

• recur over wks-mos

• epigastric pain- dull, gnawing, aching, “empty, hunger like” sensation (classic sx)

• gastric ulcer → pain w/ eating, N; relieved w/ fasting- pt avoid food → wt loss, anorexia

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

• acute / worsening pain may indicate ulcer penetration or perforation

How is PUD diagnosed?

• endoscopy- procedure of choice; rapid urease test

  • all gastric ulcers need to be bx

• BA UGI- alternative; limited accuracy & not capable of bx

• asses for h. pylori

what kind of ulcer?

• antrum & lesser curvature

• later in life - 55-70

• normal or increased acid secretion

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

duodenal

What is the treatment for H. pylori PUD?

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

PPI

H2RA

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

What patients are at an increased risk of GI bleeding, especially in combo with ASA use?

pts requiring chronic antiplatelet therapy

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

• restarting ASA before ulcer heals inc risk of recurrent bleeding

• delayed restarting of ASA may lead to CV or ischemic events in high risk pts

• 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 → asx, occult blood in stool or melena, hematemesis or coffee ground emesis, anemia

What is a peptic ulcer perforation?

erodes into adjacent organ; infrequent comp of PUD

sx → severe abd pain, peritonitis (rigid abdomen w/ rebound tenderness), leukocytosis

what should be avoided with peptic ulcer perforations?

endoscopy

How do you diagnose PUD?

xray → free air under diaphragm

if suspect perf & 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

What is the dx for gastric outlet obstruction?

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 would a decubitus abdominal xray of a gastric outlet obstruction show?

prominent gastric air bubble, gastric air fluid level, dilated stomach w/ particulate matter within

What condition?

• constellation of sx - gastric acid hyper secretion, severe PUD, gastrin secreting tumors

• caused by gastronomas

• sx: unresolved reflux sx, diarrhea, wt loss

zollinger-ellison (ZE) syndrome

What is the pathophysiology of ZE syndrome?

low pH inactivates pancreatic digestive enzymes & damages intestinal epithelial cells → both maldigestion & malabsorption

high serum gastrin concentrations may inhibit absorption of sodium & water by small intestine

Where do most gastronomas arise?

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

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

• measurement of gastric pH important to exclude secondary hypergastrinemia due to achlorhydria

• secretin stimulation test- can differentiate gastrinomas from other causes

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?

• h. pylori

• older age; male

• diets high in salt, preserved food (nitrates)

• tobacco smoking

• pernicious anemia

• hx stomach surgery

• FHX (first degree relative 2-3 fold risk

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

what are sx of gastric cancer?

• often asx until advanced

• palpable epigastric mass/tenderness

• dyspepsia, abd fullness

• vague abd pain

• early satiety / anorexia / wt loss

• signs of metastatic dz - virchow’s node (supraclavicular), sister mary joseph nodule (umbilical), blumer shelf (rigid rectal shelf), krukenberg tumor (ovarian mets)

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

mets of gastric carcinoma

What are endoscopy indications for gastric cancer?

• any pt > 60 w/ new onset dyspepsia

• dyspepsia resistant to tx or persistent

• screening in high areas of occurrence

what is the treatment for gastric cancer?

surgery, staging by TNM, chemo & radiation

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

what is the second most common gastric tumor?

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 tumors

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 o 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 99 labeled food, performed 1-4 hrs after food ingestion

what is the treatment for gastroparesis?

pro kinetics → erythromycin IV or PO; metoclopramide (reglan) 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)