Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hypertrophic gastropathy

A

-describes Menetrier disease or Zollinger-Ellison syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathogenesis of gastropathy/gastritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

-ammonium ion inhibition of gastric bicarbonate transporters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mechanisms of gastric injury and protection–normal damaging forces

A
  • gastric acidity

- Peptic enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Things that cause injury to stomach layers

A
  • H. pylori infection
  • NSAID
  • Aspirin
  • Cigarettes
  • Alcohol
  • Gastric hyperacidity
  • Duodenal-gastric reflux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Gross morphology of gastropathy/acute gastritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Microscopic morphology of gastropathy/acute gastritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Stress ulcers

A

-occurs after shock, sepsis or severe trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Curling ulcers

A

-occurs in proximal duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cushing ulcers

A
  • gastric, duodenal and esophageal ulcers arising in patients with intracranial disease
  • have high risk of perforation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

-may lower intracellular pH of mucosal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Diulafoy lesions

A
  • 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
Q

Gastric antral vascular ectasia (GAVE)

A
  • 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
Q

Chronic gastritis

A
  • ongoing mucosal inflammation with mucosal atrophy

- provides substrate in which dysplasia and carcinoma can arise

28
Q

Acute vs. chronic gastritis

A

-compared to acute gastritis, chronic gastritis symptoms are less severe but more persistent

29
Q

Causes of chronic gastritis

A
  • 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
Q

Epidemiology of Helicobacter pylori Gastritis

A
  • 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
Q

How H. pylori is spread

A
  • Humans are only host
  • spread via fecal-oral, oral-oral or environmental routes
  • lower socioeconomic status and crowding lead to higher colonization routes
32
Q

Pathogenesis of H. pylori gastritis

A

-induces mostly an antral gastritis with increased acid production and disruption of normal mucosal protection mechanism

33
Q

Virulence factors in H. pylori infections include

A
  • Motility via flagella
  • Urease production
  • Bacterial adhesins
  • Toxins (cagA and vacA cytotoxins)
34
Q

Virulence factors in H. pylori infections–motility

A

-via flagella

35
Q

Virulence factors in H. pylori infections–urease production

A

-generates ammonia that raises local pH, enhances bacterial survival, and inhibits gastric bicarbonate transport

36
Q

Virulence factors in H. pylori infections–bacterial adhesins

A

binds surface epithelial cells

37
Q

Virulence factors in H. pylori infection–toxins

A

(cagA and vacA cytotoxins)

38
Q

Pathogenesis of H. pylori infections–initial antral gastritis progresses to?

A
  • multifocal atrophic gastritis: mucosal atrophy with reduced acid production
  • and intestinal metaplasia
39
Q

What determines whether gastritis results from initial infection?

A

-Host-pathogen interactions like polymorphisms in IL-1b and TNF genes correlate with development of chronic disease

40
Q

Gross morphology of H. pylori gastritis

A

-infected mucosa is erythematous and coarse to nodular

41
Q

Microscopic morphology of H. pylori gastritis

A
  • 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
Q

Long standing gastritis is associated with?

A

-DIFFUSE MUCOSAL ATROPHY with intestinal metaplasia and prominent lymphoid aggregates occasionally with germinal centers

43
Q

Clinical features of H. pylori gastritis–how to diagnose??

A
  • Dx with Ab serologic test
  • urea breath test
  • bacterial culture
  • direct bacterial visualization in gastric biopsy or
  • DNA based tests
44
Q

Clinical features of H. pylori gastritis–H. pylori is risk factor for

A

-peptic ulcer disease (PUD), gastric adenocarcinoma, and gastric lymphoma

45
Q

Autoimmune gastritis

A
  • SPARES THE ANTRUM!

- associated with hypergastrinemia!!

46
Q

Pathogenesis of autoimmune gastritis

A
  • 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
Q

Pathogenesis of autoimmune gastritis–achlorhydria

A
  • 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
Q

Morphology of autoimmune gastritis

A
  • 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
Q

Clinical features of autoimmune gastritis

A
  • 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
Q

Autoimmune gastritis–genetics

A
  • 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
Q

Uncommon forms of gastritis

A
  • Eiosinophilic gastritis
  • Lymphocytic gastritis
  • Granulomatous gastritis
52
Q

Eiosinophilic gastritis

A
  • 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
Q

Lymphocytic gastritis

A
  • idiopathic
  • women
  • 40% associated with celiac disease
  • marked accumulation of intraepithelial CD8+ T cells
54
Q

Granulomatous gastritis

A
  • diverse group of diseases sharing presence of granulomas

- sarcoid, CD and infections are causes

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions