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GI 2 Pathology--Chapt 16 and 17 > Chapter 17 part 3--Stomach > Flashcards

Chapter 17 part 3--Stomach Flashcards

1
Q

Acute gastritis vs. gastropathy

A
  • gastritis= transient mucosal inflammatory process
  • gastropathy= when few inflammatory cells are present (with nonsteroidal antiinflammatory agents, alcohol, bile, or stress induced injury)
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2
Q

Hypertrophic gastropathy

A

-describes Menetrier disease or Zollinger-Ellison syndrome

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3
Q

Gastropathy and gastritis symptoms

A
  • can both be asymptomatic or cause varying pain, nausea, and vomiting
  • severe causes=ulceration with hemorrhage presenting as hematemesis or melena
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4
Q

Pathogenesis of gastropathy/gastritis

A

-mechanisms that protect gastric mucosa from acidic environment are overwhelmed or defective

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5
Q

Pathogenesis of gastropathy/gastritis–harmful substances

A
  • Increased acid production with back diffusion, decreased bicarbonate or mucin production or direct mucosal damage can all be pathogenic
  • so chronic use of NSAIDs reduces bicarb production and interferes with the cytoprotective action of prostaglandins (inhibit acid production, promote mucin synthesis, and increase vascular perfusion)
  • excessive alcohol consumption and heavy smoking can be directly toxic
  • hypoxia, ischemia, and shock can secondarily injure mucosa
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6
Q

Gastric injury due to uremia or urease-secreting Helicobacter pylori occurs through

A

-ammonium ion inhibition of gastric bicarbonate transporters

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7
Q

Mechanisms of gastric injury and protection–normal damaging forces

A
  • gastric acidity

- Peptic enzymes

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8
Q

Normal defensive forces against gastric acidity and peptic enzymes

A
  • Surface mucous secretion
  • Bicarb secretion into mucus
  • Mucosal blood flow
  • Apical surface membrane transport
  • Epithelial regenerative capacity
  • Elaboration of prostaglandins
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9
Q

Things that cause injury to stomach layers

A
  • H. pylori infection
  • NSAID
  • Aspirin
  • Cigarettes
  • Alcohol
  • Gastric hyperacidity
  • Duodenal-gastric reflux
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10
Q

Effect of injurious agents to layers of gastric mucosa

A
  • increased damage or impaired defenses:
  • Ischemia
  • shock
  • delayed gastric emptying
  • NSAIDs
  • eventually can lead to ulcers!!
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11
Q

Characteristics of ulcer

A
  • necrotic debris
  • Nonspecific acute inflammation
  • granulation tissue
  • fibrosis

**ulcers include necrosis, inflammation and granulation tissue but a fibrotic scar takes time to develop and is only present in chronic lesions!

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12
Q

Gross morphology of gastropathy/acute gastritis

A

-moderate edema and hyperemia occasionally with hemorrhage (acute hemorrhagic erosive gastritis)

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13
Q

Microscopic morphology of gastropathy/acute gastritis

A

-neutrophils invade the epithelium with superficial epithelial sloughing (erosion) and a fibrinous luminal exudate

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14
Q

Stress related mucosal disease

A
  • focal, acute mucosal defects typically as a complication of NSAID use or as a consequence of severe physiologic stress
  • Stress ulcers, curling ulcers, Cushing ulcers
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15
Q

Stress ulcers

A

-occurs after shock, sepsis or severe trauma

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16
Q

Curling ulcers

A

-occurs in proximal duodenum

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17
Q

Cushing ulcers

A
  • gastric, duodenal and esophageal ulcers arising in patients with intracranial disease
  • have high risk of perforation
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18
Q

Pathogenesis of stress-related mucosal disease (ulcers)—hypotension, hypoxia or stress induced splanchnic vasoconstriction

A

-can cause local ischemia that secondarily leads to gastric mucosal damage

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19
Q

Pathogenesis of stress-related mucosal disease (ulcers)—lesions associated with brain injury

A

-are attributed to direct vagal stimulation causing gastric acid hypersecretion

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20
Q

Pathogenesis of stress-related mucosal disease (ulcers)–systemic acidosis

A

-may lower intracellular pH of mucosal cells

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21
Q

Morphology of stress induced mucosal disease (ulcers)

A
  • usually less than 1cm in diameter
  • multiple and shallow
  • may be found anywhere in stomach
  • ulcer base is brown (blood) whereas adjacent mucosa is normal
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22
Q

Clinical features of ulcers (stress induced mucosal disease)

A
  • Most critically ill patients have some gastric mucosal injury
  • 1-4% will have blood loss sufficient to warrant transfusion
  • after injurious factors are removed, healing occurs with complete reeptithelialization
23
Q

Single most determinant of mucosal disease (ulcer) outcome is

A

-the ability to correct underlying conditions

24
Q

Non-stress related causes of gastric bleeding include

A
  • Dieulafoy lesions

- Gastric antral vascular ectasia (GAVE)

25
Diulafoy lesions
- most common on the lesser curvature near GE junction | - caused by abnormal vascular branching leading to large subepithelial artery that can bleed with minor mucosal erosion
26
Gastric antral vascular ectasia (GAVE)
- idiopathic lesion seen endoscopically as longitudinal stripes of edematous, erythematous mucosa attributed to ectactic mucosal vessels - Histo: antral mucosa shows reactive gastropathy with dilated capillaries containing fibrin thrombi
27
Chronic gastritis
- ongoing mucosal inflammation with mucosal atrophy | - provides substrate in which dysplasia and carcinoma can arise
28
Acute vs. chronic gastritis
-compared to acute gastritis, chronic gastritis symptoms are less severe but more persistent
29
Causes of chronic gastritis
- H. pylori infection--most common! - autoimmune gastritis (10% of cases; second most common!) - radiation - bile reflux - mechanical injury (indwelling nasogastric tube) - involvement by systemic disorders like amyloid or CD
30
Epidemiology of Helicobacter pylori Gastritis
- widely prevalent gastric infection (colonization from 10-80% of population) but only small percentage of those infected develop gastritis - most common cause of chronic gastritis - organisms are present in up to 90% of individuals w/dz
31
How H. pylori is spread
- Humans are only host - spread via fecal-oral, oral-oral or environmental routes - lower socioeconomic status and crowding lead to higher colonization routes
32
Pathogenesis of H. pylori gastritis
-induces mostly an antral gastritis with increased acid production and disruption of normal mucosal protection mechanism
33
Virulence factors in H. pylori infections include
- Motility via flagella - Urease production - Bacterial adhesins - Toxins (cagA and vacA cytotoxins)
34
Virulence factors in H. pylori infections--motility
-via flagella
35
Virulence factors in H. pylori infections--urease production
-generates ammonia that raises local pH, enhances bacterial survival, and inhibits gastric bicarbonate transport
36
Virulence factors in H. pylori infections--bacterial adhesins
binds surface epithelial cells
37
Virulence factors in H. pylori infection--toxins
(cagA and vacA cytotoxins)
38
Pathogenesis of H. pylori infections--initial antral gastritis progresses to?
- multifocal atrophic gastritis: mucosal atrophy with reduced acid production - and intestinal metaplasia
39
What determines whether gastritis results from initial infection?
-Host-pathogen interactions like polymorphisms in IL-1b and TNF genes correlate with development of chronic disease
40
Gross morphology of H. pylori gastritis
-infected mucosa is erythematous and coarse to nodular
41
Microscopic morphology of H. pylori gastritis
- typically found in antrum - gastric biopsy usually shows organisms concentrated in superficial mucous overlying surface and neck epithelium - variable intraepithelial and luminal neutrophils (forms pit abscesses!!) - lamina propria contains abundant plasma cells, macrophages, and lymphocytes
42
Long standing gastritis is associated with?
-DIFFUSE MUCOSAL ATROPHY with intestinal metaplasia and prominent lymphoid aggregates occasionally with germinal centers
43
Clinical features of H. pylori gastritis--how to diagnose??
- Dx with Ab serologic test - urea breath test - bacterial culture - direct bacterial visualization in gastric biopsy or - DNA based tests
44
Clinical features of H. pylori gastritis--H. pylori is risk factor for
-peptic ulcer disease (PUD), gastric adenocarcinoma, and gastric lymphoma
45
Autoimmune gastritis
- SPARES THE ANTRUM! | - associated with hypergastrinemia!!
46
Pathogenesis of autoimmune gastritis
- CD4+ T cell-mediated autoimmune destruction of parietal cells - also circulating and gastric secreted Abs to parietal cells and intrinsic factor--but these are only secondary manifestations of dz, not causal
47
Pathogenesis of autoimmune gastritis--achlorhydria
- Parietal cell cytotoxicity leads in turn to defective acid secretion (achlorhydria) that triggers hypergastrinemia and antral G-cell hyperplasia - Reduced intrinsic factor production impedes vitamin B12 absorption and causes pernicious anemia - secondary bystander damage to chief cells reduces pepsinogen I production
48
Morphology of autoimmune gastritis
- Rugal folds lost - diffuse mucosal damage of acid-producing parietal cells primarily in body and fundus - inflammatory infiltrate is mainly LYMPHOCYTES, MACROPHAGES, and PLASMA CELLS, and lymphoid aggregates can be present
49
Clinical features of autoimmune gastritis
- AutoAbs detected early - progression to gastric atrophy occurs over 20-30 years - Pt. presents with symptoms referable to anemia - VB12 def. can also manifest with atrophic glossitis, malabsorption, peripheral neuropathy, spinal cord lesions, and cerebral dysfunction
50
Autoimmune gastritis--genetics
- strong genetic component bc associated with other autoimmmune diseases like Hashimoto thyroditis, type I DM, and Addison Disease - 20% of relatives of affected patients will also have autoimmune gastritis
51
Uncommon forms of gastritis
- Eiosinophilic gastritis - Lymphocytic gastritis - Granulomatous gastritis
52
Eiosinophilic gastritis
- heavy eosinophilic infiltration of mucosa or submucosa - can be infectious due to allergy to ingested material or part of a systemic collagen-vascular disease (like scleroderma)
53
Lymphocytic gastritis
- idiopathic - women - 40% associated with celiac disease - marked accumulation of intraepithelial CD8+ T cells
54
Granulomatous gastritis
- diverse group of diseases sharing presence of granulomas | - sarcoid, CD and infections are causes

GI 2 Pathology--Chapt 16 and 17 (14 decks)

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