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ICOM- GI system > GI- Path- Non-neoplastic diseases of the Stomach > Flashcards

GI- Path- Non-neoplastic diseases of the Stomach Flashcards

1
Q

The stomach is a muscular of the digestive tract where mechanical and chemical digestion occurs.

A

dilation

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2
Q

The stomach is divided into four major anatomic regions:

A

the cardia, fundus, body, and pyloric antrum.

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3
Q

The cardia is lined mainly by mucin-secreting cells that form shallow glands.

A

foveolar

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4
Q

The antral glands are similar cardia but also contain cells, such as cells, that release gastrin to stimulate luminal acid secretion by parietal cells within the gastric and body.

A

endocrine

G

fundus

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5
Q

The well-developed glands of the body and fundus also contain cells that produce and secrete digestive enzymes such as

A

chief

pepsin

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6
Q

Pyloric glands. The pyloric region of the stomach has deep gastric pits (P) leading to short, coiled pyloric glands (G) in the

A

lamina propria (LP)

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7
Q

Parietal cells stain and chief cells stain .

A

pink (eosinophillic)

purple (basophillic)

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8
Q

Surface mucous cells secrete fluid containing mucin (yellow)

Mucous neck cells secrete fluid containing mucin (light pink)

Parietal cells secrete and HCl (dark pink)

Chief cells secreted pepsinogen and gastric (purple)

G cells (enteroendocrine cells) secrete into the blood (green)

A

alkaline

acidic

intrinsic factor

lipase

gastrin

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9
Q

Gastritis results from injury.

  • When are present, the lesion is referred to as acute gastritis.
  • When cell injury and regeneration are present but inflammatory cells are rare or absent, the term is applied.
A

mucosal

neutrophils

gastropathy

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10
Q
  • When cell injury and regeneration are present but inflammatory cells are rare or absent, the term gastropathy is applied.
  • Agents that cause gastropathy include , alcohol, bile, and
A

NSAIDS

stress-induced injury.

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11
Q
  • Both gastropathy and acute gastritis may be asymptomatic or cause variable degrees of epigastric pain, nausea, and vomiting.
  • In more severe cases, there may be mucosal , ulceration, hemorrhage, , melena, or, rarely, massive blood loss.
A

erosion

hematemesis

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12
Q

What is hematemesis and melena?

A

hematemesis = vomiting of blood

melena = dark sticky feces containing partly digested blood

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13
Q
  • The gastric lumen is strongly acidic, with a pH close to , more than 1 million times more acidic than the blood.
  • This harsh environment contributes to digestion but also has the potential to damage the
A

1

mucosa.

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14
Q

What are some normal damaging forces and protective forces in the stomach?

A

Damaging = gastric acidity, peptic enzymes

Defensive= mucus, bicarb, mucosal blood flow, epithelial regeneration, prostaglandins

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15
Q

Ulcers contain layers of necrotic debris, acute ,

granulation tissue, and (fibrosis).

A

inflammatory cells

scarring

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16
Q

Multiple mechanisms have evolved to protect the gastric mucosa.

  • secreted by surface foveolar cells forms a thin layer of mucus that prevents large food particles from directly touching the epithelium.
  • The mucus layer also promotes formation of an “unstirred” layer of fluid over the epithelium that protects the mucosa; it has apH as a result of secretion of ions by surface epithelial cells.
  • The rich of the gastric mucosa efficiently buffers and removes that back-diffuse into the lamina propria.
A

Mucin

neutral

bicarbonate

blood supply

protons

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17
Q

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX)- dependent synthesis of E2 and I2, which stimulate nearly all of the above defense mechanisms including and bicarbonate secretion, mucosal flow, and restoration.*

A

prostaglandins

mucus

blood

epithelial

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18
Q

The gastric injury that occurs in uremic (kidney failure) patients and those infected with urease-secreting H. pylori may be due to inhibition of gastric transporters by ions from the urease.

A

bicarbonate

ammonium

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19
Q

Ingestion of harsh chemicals, particularly acids or bases, either accidentally or in a suicide attempt, leads to severe gastric damage as a result of direct injury to and cells.

A

mucosal

epithelial

stromal (supportive cells)

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20
Q

• Direct cellular damage also contributes to gastritis induced by excessive consumption, use, and therapy.

A

alcohol

NSAID

radiation

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21
Q

Agents that inhibit DNA synthesis or the mitotic apparatus, including those used in , may cause generalized mucosal damage due to insufficient epithelial renewal.

A

cancer chemotherapy

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22
Q

What signifies active gastritis?

A

presence of neutrophils above the basement membrane in contact with epithelial cells

-note: the epithelium is inbetween the squiggly lines and the neutrophils are circled (inside the lines=active gastritis)

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23
Q

inflammation is preferred over acute inflammation throughout the luminal GI tract, since inflammation may be present in both acute and chronic disease states.

A

active

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24
Q

What can happen with more severe mucosal damage?

A

erosions and hemorrhage develop

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25
Q

Concurrent presence of erosion and hemorrhage is termed:

A

acute erosive hemorrhagic gastritis

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26
Q

severe trauma, extensive burns, intracranial disease, major surgery, serious medical disease, and other forms of severe physiologic stress can lead to what type of gastric injury?

A

stress-related gastric injury

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27
Q

Over 75% of critically ill patients develop endoscopically visible gastric during the first 3 days of their illness.

A

lesions

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28
Q

Which type of ulcer is being described?

affecting critically ill patients with shock, sepsis, or severe trauma

A

stress ulcers

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29
Q

Which type of ulcer is being described?

occur in the proximal duodenum and are associated with severe burns or trauma.

A

• Curling ulcers

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30
Q

Which type of ulcer is being described?

  • arise in the stomach, duodenum, or esophagus of those with intracranial disease and have a high incidence of perforation.
A

• Cushing ulcers

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31
Q

The pathogenesis of stress-related gastric mucosal injury is most often due to ischemia

This may be caused by systemic or reduced blood flow resulting from stress-induced splanchnic *

A

local

hypotension

vasoconstriction.

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32
Q

What type of ulcers are thought to be caused by direct stimulation of vagal nuclei resulting in acid hypersecretion?

A

Cushing ulcers

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33
Q

Systemic may also contribute to mucosal injury by lowering the intracellular pH of cells.

A

acidosis

mucosal

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34
Q

-Stress-related gastric mucosal injury ranges from shallow erosions caused by superficial epithelial damage to deeper lesions that penetrate the depth of the

  • Acute ulcers are rounded and typically less than in diameter.
  • The ulcer base frequently is stained brown to black by acid-digested .
A

mucosa.

1 cm

red blood cells.

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35
Q

Unlike ulcers, which arise in the setting of chronic injury, acute stress ulcers are found in the stomach and are often multiple.

  • They are sharply demarcated, with essentially normal adjacent mucosa.
  • Healing with complete re-epithelialization occurs days or after the injurious factors are removed.
A

peptic

anywhere

weeks

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36
Q

Some/Most critically ill patients admitted to hospital intensive care units have histologic evidence of gastric mucosal damage.

Ulcers are associated with nausea, vomiting, melena, and coffee-ground

Prophylaxis with may lessen the impact of stress ulceration, but the most important determinant of outcome is the

of the underlying condition.

A

Most

hematemesis

proton pump inhibitors

severity

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37
Q

The most common cause of chronic gastritis is infection with

  • gastritis represents less then 10% of cases of chronic gastritis but is the most common cause in patients without H. pylori infection.
  • Chronic use is a third important cause of gastritis in some populations.
A

Helicobacter pylori.

Autoimmune

NSAID

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38
Q

Other than H. Pylori, autoimmune issues, and chronic NSAID use, what are 2 other less common causes of chronic gastritis?

A

radiation injury

chronic bile reflux

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39
Q

The signs and symptoms associated with chronic gastritis typically are less/more severe but less/more persistent than those of acute gastritis.

• Nausea and upper-abdominal discomfort may occur, sometimes with vomiting, but is uncommon.

A

less severe

more persistent

hematemesis

40
Q

H. pylori, These spiral-shaped or curved are present in gastric biopsy specimens from almost all patients with duodenal ulcers and a majority of those with gastric ulcers or chronic gastritis.*

A

bacilli

41
Q
  • H. pylori infection most often presents as an gastritis with increased/decreased acid production.
  • The increased acid production may give rise to ulcer disease of the duodenum or stomach.
A

antral

increased acid production

peptic

42
Q
  • While in most cases H. pylori gastritis is limited to the antrum, in some individuals it progresses to involve the gastric and resulting in reduced parietal cell mass and acid secretion.*
  • Extension of the gastritis to the gastric body and fundus results in intestinal and increased risk of gastric cancer.
A

body

fundus

metaplasia

43
Q

What gastro infections in the U.S is associated with poverty, household crowding, limited education, residence in areas with poor sanitation, and birth outside of the U.S.?

A

H. pylori infection

44
Q

H. Pylori infection is typically acquired in and may then persist for life.

• In the United States, the prevalence of H. pylori infection is also higher in Americans and Americans.

A

childhood

African

Mexican

45
Q

What are the 4 virulence factors of H. Pylori?

A

• Flagella, which allow the bacteria to be motile in viscous mucus.

• Urease, which generates ammonia from endogenous urea, thereby elevating local gastric pH around the organisms and protecting the bacteria from the acidic pH of the stomach.

• Adhesins, which enhance bacterial adherence to surface cells.

• Toxins, such as that encoded by cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer development.

46
Q

Flagella, which allow the bacteria to be motile in viscous

  • Urease, which generates from endogenous urea, thereby elevating/decreasing local gastric pH around the organisms and protecting the bacteria from the acidic pH of the stomach.
  • Adhesins, which enhance bacterial adherence to cells.
  • Toxins, such as that encoded by cytotoxin-associated gene A , that may be involved in ulcer or cancer development.
A

mucus

ammonia

elevating

surface

(CagA)

47
Q

What gene is associated with the toxins released by H. Pylori and can be involved in ulcer and cancer development?

A

cytotoxin-associated gene A (CagA)

48
Q

The factors allow H. pylori to create an imbalance between gastroduodenal mucosal defenses and damaging forces that overcome those defenses.

A

virulence

49
Q

Where is H. Pylori concentrated within mucus of epithelial cells?

A

surface and neck regions of the glands

50
Q

The inflammatory reaction includes a variable number of within the lamina propria, including some that cross the basement membrane to assume an location and accumulate in the lumen of gastric pits to create pit abscesses.

A

neutrophils

intraepithelial

note: inflammation in the gastric pit (at the bottom of the pit H and E stain)

51
Q

The superficial lamina propria includes large numbers of plasma cells, often in clusters or sheets, as well as increased numbers of lymphocytes and macrophages.

• Lymphoid aggregates, some with centers, are frequently present and represent an induced form of mucosa-associated lymphoid tissue (MALT) that has the potential to transform into

A

germinal

lymphoma.

52
Q

What condition is characterized by the presence of goblet cells and columnar absorptive cells, also may be present and is associated with increased risk of gastric adenocarcinoma caused by H. pylori?

A

Intestinal metaplasia,

53
Q

• H. pylori shows tropism for gastric epithelium and generally is/is not found in areas of intestinal metaplasia, acid-producing mucosa of the gastric body, or duodenal epithelium.

biopsies are therefore preferred for evaluation of H. pylori gastritis.

A

foveolar

Antral

54
Q

Other than histology to identify H. Pylori, what other diagnostic tests are available?

A

serologic test for anti-H. pylori antibodies,

a stool test for the organism,

and the urea breath test (ammonia produced)

55
Q

Gastric biopsy specimens also can be analyzed by the urease test, bacterial , or polymerase chain reaction (PCR) assay for bacterial DNA

A

rapid

culture

56
Q

What type of stain?

A

silver stain

57
Q

What are the effective treatments for H. pylori infection?

A

antibiotics

proton pump inhibitors

58
Q

What can happen if incomplete eradication of H. pylori infection?

A

relapse or reinfection

59
Q

The second most common cause of gastritis is gastritis and how does it differ from H.Pylori gastritis?

A

autoimmune

spares the antrum and induces marked hypergastrinemia.

60
Q

What 5 things characterizes autoimmune gastritis?

A
  • Antibodies to parietal cells and intrinsic factor that can be detected in serum and gastric secretions.
  • Reduced serum pepsinogen I levels (damaged chief cells).
  • Impaired gastric acid secretion (achlorhydria).
  • Antral endocrine (G) cell hyperplasia.
  • Vitamin B12 deficiency leading to pernicious anemia and neurologic changes.
61
Q

At the esophagogastric junction, stratified squamous epithelium (SSE) lining the esophagus is abruptly replaced by epithelium (SCE) of the stomach.

A

simple columnar

62
Q

Autoimmune gastritis is associated with immune-mediated loss of cells and subsequent reductions in acid and intrinsic factor secretion.

A

parietal

63
Q

Deficient acid secretion stimulates release, resulting in hypergastrinemia and hyperplasia of antral gastrin-producing G cells.

A

gastrin

64
Q

Lack of intrinsic factor disables ileal vitamin B12 absorption, leading to B12 deficiency and a particular form of megaloblastic anemia called

A

pernicious anemia.

65
Q

Autoimmune gastritis is characterized by diffuse damage of the (acid-producing) mucosa within the body and fundus.*

• With diffuse atrophy, the mucosa of the body and fundus appears markedly thinned, and folds are lost.

A

oxyntic

oxyntic

rugal

66
Q

Concerning autoimmune gastritis:

Neutrophils may be present, but the inflammatory infiltrate more commonly is composed of , macrophages, and cells

In contrast with H. pylori gastritis, the inflammatory reaction most often is deep and centered on the

• Parietal and chief cell loss can be extensive, and intestinal may develop.

A

lymphocytes

plasma

gastric glands

metaplasia (change in cells)

67
Q

Identify the deeper inflammatory cell infiltrate of the autoimmune gastritis

A
68
Q

Antibodies to parietal cells and intrinsic factor are present early/late in the disease, and B12 deficiency and pernicious anemia develop a minority/majority of patients.

A

early

only a minority of patients

69
Q

The median age at diagnosis is years, and there is a slight predominance.

• Autoimmune gastritis often is associated with other autoimmune diseases but is/is not linked to specific human leukocyte antigen (HLA) alleles.

A

60

female

is not linked

70
Q

H. Pylori associated gastritis:

located:

inflam infiltrate:

acid production:

gastrin:

other lesions:

serology:

sequelae:

associations:

A
71
Q

Autoimmune associated gastritis:

located:

inflam infiltrate:

acid production:

gastrin:

other lesions:

serology:

sequelae:

associations:

A
72
Q

What are the 3 important complications of chronic gastritis?

A
  1. Peptic ulcer disease
  2. Mucosal atrophy and intestinal metaplasia
  3. Dysplasia
73
Q

Peptic ulcer disease (PUD) most often is associated with infection or use

A

H. pylori

NSAID

74
Q

• PUD may occur in any portion of the GI tract exposed to acidic gastric juices but is most common in the gastric and first portion of the .*

A

antrum

duodenum

75
Q

The lifetime risk for developing an ulcer is ~ for males and for females

A

10%

4%

76
Q

More than 70% of PUD cases are associated with infection and in these individuals peptic ulcer disease generally develops on a background of gastritis.

• Because only % of H. pylori-infected individuals develop ulcers, it is probable that host factors, as well as variation among H. pylori strains also contribute to the pathogenesis.

A

H. pylori

chronic

5%-10%

77
Q

is fundamental to the pathogenesis of peptic ulcer disease.

A

Gastric acid

78
Q

As concerning Peptic Ulcer disease

• Hyperacidity may be caused by what 3 things?

A

H. pylori infection,

parietal cell hyperplasia, and

excessive secretory responses.

79
Q

What disease is characterized by multiple peptic ulcerations in the stomach, duodenum, and even jejunum, is caused by uncontrolled release of gastrin by a tumor and the resulting massive acid production.?

A

Zollinger-Ellison syndrome

80
Q

Cofactors in peptic ulcerogenesis include chronic use; cigarette smoking, which impairs mucosal flow and healing; and high-dose corticosteroids, which suppress synthesis and impair healing.

A

NSAID

blood

prostaglandin

81
Q

What 4 conditions are peptic ulcers more frequent?

A

alcoholic cirrhosis,

COPD,

chronic renal failure, and

hyperparathyroidism.

82
Q

Of those conditions where peptic ulcers are more frequent, what conditions can lead to hypercalcemia which stimulates gastrin production and thereby increases acid secretion?

A

chronic renal failure

hyperparathyroidism

83
Q

Where are peptic ulcers four times more common than in the stomach?

A

proximal duodenum

84
Q

Duodenal ulcers usually occur within a few centimeters of the valve and involve the anterior/posterior duodenal wall.

• Gastric peptic ulcers are predominantly located near the of the body and antrum.

A

pyloric

anterior

interface

85
Q
  • Peptic ulcers are in more than 80% of patients.*
  • The classic peptic ulcer is a round to oval, sharply punched-out defect.
  • The base of peptic ulcers is smooth and clean as a result of peptic digestion of exudate, and histologically is composed of richly granulation tissue.
A

solitary

vascular

86
Q

Perforation is a complication that demands emergent intervention.

A

surgical

87
Q

Peptic ulcers are acute/chronic, recurring lesions that occur most often in younger/middle-aged to older adults with/without obvious precipitating conditions, other than chronic gastritis.

A

chronic

middle-aged

without

88
Q

What are the 4 main reasons people come for clinical attention for peptic ulcer disease?

A

epigastric burning or aching pain

iron deficiency anemia

frank hemorrhage

perforation

89
Q

When does the pain occur and when is it at its worst from PUD?

A

1 to 3 hours after meals during the day, is worse at night, and is relieved by alkali or food.

90
Q

What is the treatment for PUD?

A

aimed at H. pylori infection

antibiotics

PPIs

91
Q

Long-standing chronic gastritis may be associated with intestinal

, recognized by the presence of cells.

A

metaplasia

goblet

92
Q

Intestinal metaplasia (from long standing gastritis) is associated with what type of cancer?

A

gastric adenocarcinoma.

93
Q

Concerning gastric andenocarcinoma from intestinal metaplasia ( from chronic gastritis)

The achlorhydria of gastric mucosal atrophy, which is commonly associated with intestinal metaplasia, permits overgrowth of bacteria that produce carcinogenic

A

nitrosamines.

94
Q

How does chronic gastritis lead to carcinoma?

A

Chronic gastritis exposes the epithelium to inflammation-related free radical damage and proliferative stimuli, which can lead to the accumulation of genetic alterations that result in carcinoma.

95
Q

Preinvasive in situ lesions can be recognized histologically as , marked by variations in epithelial size, shape, and orientation along with coarse chromatin texture, hyperchromasia, and nuclear enlargement.*

A

dysplasia

96
Q

H. pylori induces MALT that can give rise to B-cell

A

lymphomas (MALTomas)

97
Q
A

ICOM- GI system (12 decks)

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