Pathophysiology of Stomach Flashcards

1
Q

Pathophysiology/sx of gastroparesis

A
  • delayed gastric emptying ==>
  • early satiety
  • epigastric fullness
  • pain
  • bloating
  • nauseau
  • vomiting
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2
Q

Causes of gastroparesis

A
  • 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
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3
Q

Epidemiology of Helicobacter pylori gastritis

A
  • @ 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
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4
Q

Pathophsyiology of H. pylori

A
  • 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
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5
Q

Testing for H. pylori infection

A
  • 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
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6
Q

Phenotypic forms of H. pylori gastritis

A
  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
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7
Q

H. pylori treatment

A
  • 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
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8
Q

Ulceration definition

A
  • lesion greater than 5mm in diameter w/depth that breaches muscularis mucosa
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9
Q

Pathophysiology of NSAID-induced injury

A
  • NSAIDs ==> prostoglandin depletion
  • pts w/prior ulcer disease and elderly @ increased risk
  • gastric or duodenal (less common) ulcers
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10
Q

COX-2 selective antagonists relation to ulcers

A
  • 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
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11
Q

Pathophsyiology of Peptic Ucler Disease

A
  • occur when gastroduodenal mucosal defenses are unable to protect epithlium from acid and proteases
  • predisposing factors: H. pylori infection, NSAID use.
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12
Q

Clinic manifestations of peptic ulcer disease

A
  • burning epigastric pain
    • may awaken patient from sleep
    • relieved by antacids
    • intermittent pain
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13
Q

Common complications of ulcers

A
  • 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
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14
Q

Most common gastric neoplasms

A
  • adenocarcinoma
  • gastric polyps
  • stromal tumors/GIST
  • neuro-endocrine tumors
  • lymphoma
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15
Q

Characteristics of gastric adenocarcinomas

A
  • 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%
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16
Q

Characteristics of gastric polyps

A
  • 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
17
Q

Stromal tumors

A
  • 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)
18
Q

Characteristics of neuro-endocrine tumors

A
  • 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
19
Q

Characteristics of lymphoma

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