Pathophysiology of Stomach

Question 1

Pathophysiology/sx of gastroparesis

Answer 1

• delayed gastric emptying ==>
• early satiety
• epigastric fullness
• pain
• bloating
• nauseau
• vomiting

Question 2

Causes of gastroparesis

Answer 2

• post-surgical states
• endocrine disorders (diabetes, hypothyroidism)
• muscular disorders
• systemic sclerosis
• drugs**
  
  • narcotics
  • TCADs
  • clonidine
• vagal n. dysfxn**
  
  • most common: secondary to autonomic damage from diabetes
• post-viral**
  
  • norwalk
  • rotavirus

Question 3

Epidemiology of Helicobacter pylori gastritis

Answer 3

• @ developed countries: age-related prevalence
• correlated w/socioeconomic status and crowded living conditions
• many people are infected by H. pylori, but not everyone develps peptic ulcer disease

Question 4

Pathophsyiology of H. pylori

Answer 4

• H. pylori = gram-neg. rod that produces abundant urease ==> ammonia ==> higher local pH
• escapes gastric juice by colonizing surface epithelium
• virulence factors:
  
  • adhesins
  • phospholipase
  • cytotoxins
  • cytokines
  • urease
  • CagA
• elicits robuts inflammatory response ==> damage to epithelium/mucosal layer

Question 5

Testing for H. pylori infection

Answer 5

• mucosal biopsy
  
  • histological demonstration
  • CLO test = detects presence of urease
    
    • blood in stomach, PPI use, or H2 antagonists ==> often false negative rapid urease
• blood antibody tests
  
  • IgG ELISA ab test
  • ==> false positives due to low prevalence
  • cannot be used to corfirm infection eradication
• urea breath test (UBT)
• stool antigen test
  
  • **most commonly used to determine eradication

Question 6

Phenotypic forms of H. pylori gastritis

Answer 6

1. mild, diffuse chronic active superficial gastris ==> no sx/disease
2. antral predominant gastritis + spared gastric body ==> high levels of acid secretion ==> duodenal ulcer
3. mutifocal atrophic gastritis ==> low acid secretion ==> gastric ulceration OR gastric metaplasia/dysplasia ==> gastric adenocarcinoma

Question 7

H. pylori treatment

Answer 7

• First line:
  
  • proton pump inhibitor (antibiotics work better at a more neutral pH)
  • amoxicillin 1 gm
  • clarithromycin 500 mg
  • all 2x/day for 7-14 days
• after failure of first line = “classical quadruple therapy”
  
  • PPI
  • bismuth
  • tetracycline
  • metronidazole

Question 8

Ulceration definition

Answer 8

• lesion greater than 5mm in diameter w/depth that breaches muscularis mucosa

Question 9

Pathophysiology of NSAID-induced injury

Answer 9

• NSAIDs ==> prostoglandin depletion
• pts w/prior ulcer disease and elderly @ increased risk
• gastric or duodenal (less common) ulcers

Question 10

COX-2 selective antagonists relation to ulcers

Answer 10

• developed to decrease gastro-duodenal damage b/c do not inhibit PG formation @ GI tract
• ==> fewer ulcers and complications
• **removed from market b/c increased risk of myocardial infarction

Question 11

Pathophsyiology of Peptic Ucler Disease

Answer 11

• occur when gastroduodenal mucosal defenses are unable to protect epithlium from acid and proteases
• predisposing factors: H. pylori infection, NSAID use.

Question 12

Clinic manifestations of peptic ulcer disease

Answer 12

• burning epigastric pain
  
  • may awaken patient from sleep
  • relieved by antacids
  • intermittent pain

Question 13

Common complications of ulcers

Answer 13

• bleeding (30% of PUD pts)
• anemia
• perforations/penetration
  
  • penetration ==> another structure (liver, pancreas)
  • perforation ==> peritoneum
• obstruction <== edema surrounding ulcer or scar tissue
  
  • nausea, vomiting, early satiety

Question 14

Most common gastric neoplasms

Answer 14

• adenocarcinoma
• gastric polyps
• stromal tumors/GIST
• neuro-endocrine tumors
• lymphoma

Question 15

Characteristics of gastric adenocarcinomas

Answer 15

• histologic = diffuse vs. intestinal
  
  • diffuse = less common
    
    • signet-ring cells
    • excess mucin production
  • intestinal = glandular
    
    • assoc. w/atrophic gastritis & intestinal metaplasia
• prevalence: becoming less common in US
• closse association w/chronic H. pylori gastritis
• overall 5-year survival = 10%

Question 16

Characteristics of gastric polyps

Answer 16

• 3 types: adenoma, hyperplastic, and fundic gland
• hyperplastic = most common
  
  • assoc. w/hypergastrinemia
  • autoimmune body gastritis
  • no risk of transformation to adenocarcinoma
• adenoma = poses cancer risk
• fundic glad = most likely benign

Question 17

Stromal tumors

Answer 17

• benign = leiomyomas & lipomas
• malignant = leimyosarcoma & lipsarcoma
• location: submucosal, subserosal or both=”dumbbell” configuration
• larger tumors assoc. w/abdominal pain or GI bleeding
• GIST (GI stromal tumors)
  
  • express c-KIT = transmembrane tyrosine kinase
  • good response to imatinib (tyr. kinase inhibitor)
  • arise from interstitial cells of Cajal (GI pacemakers)

Question 18

Characteristics of neuro-endocrine tumors

Answer 18

• carcinoid tumors arise from enterochromafin or enterochromaffin-like cells
• carcinoid tumors of stomach = relatively rare
  
  • usually fundus or body
  • sporadic
  • carcinoid tumor in pts w/achlorhydria secondary to atrophic gastritis
    
    • high levels of gastrin
• second-most common cause of duodenal tumor after adenocarcinoma

Question 19

Characteristics of lymphoma

Answer 19

• strong assoc. w/ H. pylori infection and primary gastric B-cell lymphoma