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GI II Exam 1 > Chapter 17. Congenital Disorders of the Stomach > Flashcards

Chapter 17. Congenital Disorders of the Stomach Flashcards

1
Q

Disorders of the stomach are a frequent cause of clinical disease, with _______________ lesions being common.

A

inflammatory and neoplastic lesions

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2
Q

Diseases of the stomach account for nearly _____ of all heath care spending on GI diseases.

A

1/3

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3
Q

What are the 4 anatomic regions of the stomach?

A
  1. Cardia
  2. Fundus
  3. Body
  4. Antrum
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4
Q

RECAP:

  • ACh and Histamine => parietal cell => _____________
  • Prostaglandins => parietal cells => ________________
  • Parietal cells are mostly found in ______ and ____ of stomach, not the _____.
A
  • ACh and Histamine: ↑ acid production
  • Prostaglandins: ↓ acid production
  • Parietal cells are found in fundus and body, not antrum
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5
Q

What is gastrin?

Released by what?

A
  • Gastrin is a hormone that stimulates secretion of gastric acid (HCl) by the parietal cells of the stomach
    • Released by G cells in the pyloric antrum of the stomach, duodenum, and the pancreas.
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6
Q

The ______ and _____ are lined by mucin-secreting foveolar cells that form small glands.

A
  1. Cardia
  2. Antrum
    1. ​However, also contains endocrine cells, like G-cells, => release gastrin that stimulate parietal cells in fundus and body to secrete acid.
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7
Q

Glands in the ______ and ________ have chief cells, which produce and secrete digestive enzymes like pepsin.

A

body

fundus

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8
Q

What is the difference between erosion and an ulcer?

A
  • Erosion: loss of epithelial layer that extends into the muscularis mucosa.
  • Ulcer: Loss of the mucosal layer that can extend into [submucosa and muscular layer], are usually focal and mostly occur in the stomach and duodenum.
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9
Q

What is gastritis?

A

Inflammation of the mucosa that is often generalized

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10
Q

What differentiates Acute Gastritis from Gastropathy?

Causes of each?

A
  • Acute gastritis: neutrophils are present
  • Causes: Autoimmune or H.pylori
  • Gastropathy: gastric mucosal disorder with minimal to no inflammation (no inflammatory cells are present)
  • Causes: NSAIDs, EtOH, Bile, Stress
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11
Q

Can gastropathy and acute gastritis be distinguished clinically?

A

No

Both cause epigastric pain, N/V. If severe, mucosal erosion, ulceration, hemtaemesis, melena.

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12
Q

What mechanisms protect the gastric mucosa?

A
  1. Surface mucus secretion
  2. HCO3- secretion into mucus
  3. Mucosal blood flow
  4. Epithelial barrier
  5. Epithelial regeneration
  6. Prostaglandins
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13
Q

What NL mechanisms damage the gastric mucosa?

A
  1. Gastric acidity
  2. Peptic enzymes
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14
Q

What causes injury to the gastric mucosa?

A
  1. H. pylori
  2. NSAIDS
  3. Tobacco and alochol
  4. Gastric hyperacidity
  5. Duodenal-gastric reflux
  6. Ischemia and shock
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15
Q

Ulcers associated with acute and chronic gastritis may include layers of what type of injury? (hint: mnemonic to remember layers)

A
  • Necrotic debris
  • Inflammation
  • Granulation tissue
  • Scar (fibrosis)

*NIGS

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16
Q

What are causes of acute gastritis?

A
  1. NSAIDS
  2. alcohol
  3. chemo
  4. H. Pylori
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17
Q

NSAIDs contribute to gastritis how?

A

Inhibit synthesis of prostaglandin E2 and I2 by COX => inhibit mucus/bicarb/phospholipid secretion/ mucosal BF, epithelial restitution, => increase acid production.

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18
Q

Why are older adults more prone to gastritis?

A

↓ mucin and bicarb

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19
Q

What is the morphology seen in acute gastritis?

A
  1. Surface epithelium is intact
  2. Foveolar cell hyperplasia that look like corkscrews
  3. Epithelial proliferation
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20
Q

Presence of _________ above the BM in direct contact w/ epithelial cells is abnormal in all parts of the GI tract and signifies active inflammation (acute/chronic gastritis)

A

Neutrophils

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21
Q

Concurrent erosion and hemorrhage is called ________.

A

acute erosive hemorrhagic gastritis

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22
Q

How is the response to PPI’s different if the patient is suffering from NSAID-induced gastropathy vs. pain associated w/ bile reflux?

A
  • NSAID-induced: asymptomatic or have persistent epigastric pain that responds to antacids or PPI’s
  • Bile reflux is typically unresponsive and may have occasional bilious vomiting
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23
Q

Severe acute gastritis can result in _______.

A

Acute gastric ulcerations

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24
Q

Stress-related mucosal diseases occur in patients with severe trauma, burn, incranial diseases, surgery, etc.

Stress ulcers are most common in individuals with what 3 things?

How are they caused?

Common in ______ patients.

A

1) Shock
2) Sepsis
3) Severe trauma

  • => decreased mucosal perfusion, causing loss of protective barrier of mucus and bicarb.
  • Common among critically ill patients.
  • Like Curlings ulcers => all ICU pts are given prophylactic therapy includes PPIs (pantaprazole, omeprazole, etc)
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25
Q

Stress-related mucosal diseases occur in patients with severe trauma, burn, incranial diseases, surgery, etc.

Ulcers in the prox. duodenum and occur in patients with burns or trauma are called?

A
  • Curling ulcers (Think curling irons will burn you!)
    • ​Loss of skin => decrease plasma volume => dehydration => hypotension to stomach/ mucosa => damage mucosa). Result: acute gastritis and ulcers
  • Give PPIs to any pt that comes in w burns
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26
Q

Stress-related mucosal diseases occur in patients with severe trauma, burn, incranial diseases, surgery, etc.

Gastric, duodenal, and esophageal ulcers that occur in persons w/ ↑ intracranial pressure (tumor or hemorrhage) are termed?

What causes them?

Increase risk of?

A
  1. Cushing ulcers
  2. Increased intracranial pressure => Direct stimulation of vagal nuclei => increase ACh to stomach => hypersecretion of gastric acid => gastritis and ulcers
  3. *Perforation
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27
Q

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

A

Hypotension, hypoxia or stressed-induced splanchnic vasoconstriction that cause [local ischemia].

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28
Q

What determines acute vs chronic gastritis?

A

Types of infiltrates that are seen.

  • Acute gastritis = neutrophil infiltration
    • Often due to mucosal damage from acids
  • Chronic gastritis = lymphocytes, plasma cells and MO
    • 2 common causes: AI or H.pylori
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29
Q

Symptoms of gastritis

A
  • Dyspepsia (N, V, loss of appetite, abdominal or epigastric pain)
    • Worse w/ food because they cause more acid (H+) secretion.
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30
Q

What are the causes of ischemia seen in stress-related gastric mucosal injury?

A
  1. Systemic hypotension
  2. Stress-induced splanchnic vasoconstriction => ⬇︎ blood flow
  3. ↑ of inducible NOS
  4. ↑ release of vasoconstictor endothelin-1
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31
Q

What is the morphology of the acute ulcers seen in stress-related mucosal diseases?

A
  • Sharply demarcated, multiple ulcers less than 1 cm in diamater, found anywhere in the stomach.
  • Base of the ulcer is brown (blood) and the adjacent mucosa is NL.
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32
Q

How are acute ulcers in stress-related gastric mucosal injury different from chronic peptic ulcers?

A
  1. Multiple and located anywhere in the stomach
  2. Scaring and thickining of BV is NOT present
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33
Q

Most critically ill patients admitted to ICU have evidence of what damage?

A

Damage to the gastric mucosa

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34
Q

In critcally ill patients admitted to the ICU, what is the most important determinant of clinical outcome?

A

- Ability to correct the underlying condition-

Removal of the injurous factor normally causes healing with complete re-repithlialization.

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35
Q

What are the 2 non-stress related causes of gastric bleeding?

A
    1. Dielafoy lesions
    1. GAVE (gastric antral vascular ectasia)
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36
Q

What is a Dieylafoy lesion?

A

Non-stress related cause of gastric bleeding where there is erosion over a submucosal artery has improper branching of w/i wall of stomach, forming a LARGE mucosal artery.

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37
Q

Where does a Dieufaloy lesion most commonly occur and what causes it?

A
  • Along the lesser curvature, near the GE junction.
  • Erosion due to NSAIDS
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38
Q

What is responsible for 4% of non-variceal upper GI bleeding?

A

GAVE (gastric antral vascular ectasia)

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39
Q

Gastric antral vascular ectasia (GAVE) can be recognized endoscopically how?

A

Alternating longitudinal stripes of edematous red mucosa w/ pale mucosa that is less injured (“watermelon stomach”)

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40
Q

While often idiopathic, gastric antral vascular ectasia (GAVE) can be associated with what underlying pathologies?

Patients may present how?

A
  • Cirrhosis and Systemic Sclerosis
  • Occult fecal blood and iron-deficiency anemia
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41
Q

What are the 2 common causes of chronic gastritis (inflammation + mucosal atrophy, providing a template for dysplasia and cancer to arise)?

A
  • 1. H. Pylori (90%)
    1. AI gastritis (10%)
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42
Q

How are the symptoms in chronic gastritis different than acute gastritis?

A

Less severe, more persistant.

N, V, upper abdominal pain, but hematemesis is NOT common.

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43
Q

What type of bacteria is H. Pylori?

A

Gram (-) rod (baccillus); spiral-shaped

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44
Q

What part of the stomach does H. Pylori and AI gastritis cause chronic gastritis?

A
  • H. Pylori: antrum
  • AI gastritis: body and fundus
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45
Q

How does chronic gastritis due to H. pylori progress?

A
  • [Initial antral gastritis] can progress to involve body or fundus
    • Multifocal atrophic gastritis, which is patchy mucosal atrophy and ⬇︎ acid production due to ⬇︎ parietal cells,
    • Intestinal metaplasia (increase risk of gastric adenocarcinoma)
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46
Q

How does atrophic gastritis caused by H. pylori differ from chronic gastritis?

A

Atrophic gastritis has a MULTI-FOCAL pattern, not diffuse.

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47
Q

Who is H. pylori most common in?

A
  1. Poverty
  2. Household crowing
  3. Decreased education
  4. AA/Mexicans
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48
Q

How does H.pylori cause chronic gastritis?

A

H.Pylori does not invade mucosa. It sits on top of epithelial cells and secretes a protective barrier to survive in the acidic stomach via urease

  • (makes ammonia => protect the bacteria from stomach acid and forms ammonium chloride => damages stomach; ↑ pH => ↑ gastrin release and ↑ acid production)
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49
Q

What are other H. Pyrlori VF?

A
    1. Flagella
    1. Adhesins
    1. Toxins (CagA) that are involved in disease progression
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50
Q

Who is the primary carrier of H. pylori and how is it transmitted?

A

- Humans

- Fecal-oral

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51
Q

What 2 malignancies are associated with H.pylori?

A
    1. Gastric adenocarcinoma
    1. MALT lymphoma (B-cell cancer that occurs in stomach and HIGHLY assx with H.pylori infection)
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52
Q

When inflammation caused by H. pylori is limited to the antrum there is an increased risk of?

A

Duodenal peptic ulcer

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53
Q

Which virulence factor of H. pylori is associated w/ elevated gastric cancer risk and allows for colonization of gastric body causing multifocal atrophic gastritis?

A

CagA gene

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54
Q

Polymorphisms of which immunologic mediators are associated w/ development of pangastritis, atrophy, and gastric cancer associated w/ H. pylori?

A
  • Increased: TNF and IL-1β
  • Decreased: IL-10 (anti-inflammatory)
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55
Q

Which vitamin deficiency is a risk factor for H.pylori-associated gastric cancer?

A

Iron

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56
Q

What inflammatory infiltrate are characteristic of H. pylori chronic gastritis?

  • Gastrin?
  • Acid production?
  • Other lesions?
A
  • Intraepithelial neutrophils and subepithelial plasma cells
  • Gastrin: NL to ↓
  • Acid production: ↑ or slightly ↓
  • Other lesions: Hyperplastic/inflammatory polyps
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57
Q

Build-up of neutrophils in lumen of gastric pits often seen with H. pylori gastritis can form what?

A

Pit abcesses

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58
Q

What serology are characteristic of H. pylori chronic gastritis?

  • Sequelae?
  • MC in?
A
  • AB to H. Pylori
  • Peptic ulcer, adenocarcinoma, MALToma
  • Low SES, poverty, rural areas
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59
Q

H. pylori displays trophism for which cells and part of stomach?

A

Gastric epithelia –> antrum

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60
Q

Intense H. pylori infection can lead to inflammatory infiltrates producing what finding that mimics appearance of early cancer?

A

Thickened rugal folds

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61
Q

Lymphoid aggregates, some with germinal centers are frequently present in H. pylori gastritis and represent an induced form of?

Potential to transform into?

A
  • Induced form of MALT
  • Lymphoma
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62
Q

H. pylori can be stained with?

A

Warthin-Starry silver stain

63
Q

Which tests can be used in the diagnosis of H. pylori infection?

A
  1. anti-H.pylori Abs test
  2. Fecal bacterial detection
  3. Urease breath test
64
Q

Effective treatment for H. pylori infection includes combinations of?

A

Triple therapy for 7-10 days

  • 1. PPI
  • 2. Clarithromycin
  • 3. Amoxicillin/metroniazide
65
Q

Autoimmune gastritis can cause chronic gastritis.

    • Location
    • Inflammatory infiltrate
    • Gastrin
A
  • Body of the stomach
  • Lymphocytes (CD4+ T cells) and MO
  • ↑ gastrin (hypergastrinemia)
66
Q

How does AI gastritis cause chronic gastritis?

A

AI gastritis (pernicious anemia);

  1. CD4+ T cells destroy parietal cells
  2. Cytoxicity of parietal cells and atrophy of gastric body onxytic glands =>
    1. ↓ gastric acid secretion (achlorhydia) => hypergastrinemia and antral G-cell hyperplasia
    2. ↓ of secretion of intrinsic factor, which is needed for B12 absorption in the terminal ileum.
      1. => B12 deficiency => pernicious anemia.
  3. Lead to chronic inflammation in the body
67
Q

Autoimmune gastritis is characterized by 5 findings (i.e., Abs and deficiencies)?

A
  1. Abs to parietal cells and IF
  2. ↓ serum pepsinogen I
  3. Endocrine cell hyperplasia
  4. Vit B12 def
  5. Defective gastric acid secretion (achlorydia) => hypergastrinemia
68
Q

AI gastritis - associated chronic gastritis;

  • Acid production
  • Other lesions
  • Serology
  • Sequelae
A

Acid production: decreased

Other lesions: Neuroendocrine hyperplasia

Serology: AB to parietal cells (H, K, ATPase, IF)

Sequelae: atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor

69
Q

What autoimmune disorders cause AI gastritis?

A
  1. AI disease
  2. Thyroiditis
  3. DM
  4. Graves
70
Q

How is the atrophy of autoimmune gastritis different from that of H. pylori-mediated?

A

DIFFUSE atrophy = achlorhydria

  • H. pylori causes mulitfocal (patchy) = NO achlorhy
71
Q

Autoantibodies to which parietal cell components are most prominently seen in autoimmune gastritis?

Do they cause damage?

A
  1. H+, K+-ATPase
  2. Proton pumps
  3. IF

*Not pathogenic, because neither secreted IF or proton pumps are accessible to circulating antibodies

72
Q

AI gastritis is characterized by WHAT?

A

Diffuse mucosal damage of the oxyntic (acid-producing) mucosa within the body and fundus of the stomach

73
Q

What are some of the characteristic findings morphologically in autoimmune gastritis?

i.e., mucosa, inflammatory rxn, suface changes, and presence of which cells?

A
  1. Oxyntic mucosa of the body is thin and loss of rugal folds
  2. Deeper inflammatory rxn and centered on the gastric glands
  3. No superficial lamina propria cells seen in H. pylori.
  4. no parietal and chief cells
  5. intestinal metaplasia ( goblet cells and columnar absorptive cells)
74
Q

Which stain can allow for visualization of endocrine hyperplasia associated w/ autoimmune gastritis?

A

Immunostains for chromogrannin A

75
Q

What is the progression of autoimmune gastritis like and what is the median age of diagnosis?

Which sex is more affected?

A
  • Progression to gastric atrophy occurs over 20-30 years
  • Median age = 60 yo
  • Slightly more women affected (as w/ most autoimmune dz)
76
Q

What is the clinical presentation of AI gastritis?

A

Linked to sxs of anemia

  1. Atrophic glossitis (smooth and beefy red tongue)
  2. Megaloblastosis of RBC and epithelial cells
  3. Malabsorptive diarrhea
  4. Peripheral neuropathy: paresthesias + bilateral symmetrical numbness in LE => can progress to spastic tingling => complete paraplegia
  5. Spinal cord lesions –> Subacute combined degeneration of SC (loss of dorsal/lateral spinal tracts)
77
Q

What can be corrected in regards to B12 deficiency thru B12 replacement therapy?

A

ONLY anemia sx, however once complete paraplegia has developed, recovery is poor.

78
Q

Why can both forms of chronic gastritis lead to gastric adenocarcinoma?

A
  • Chronic inflammation can lead to metaplastic atrophic gastritis => intestinal metaplasia (stomach tissue changes to intestinal tissue)
    • HY: key path finding is goblet cells in the stomach and inflammatory cells in the lamina propria
79
Q

Eosinophilic gastritis most commonly affects what part of stomach?

Increased serum levels of?

Associated w/ allergic rxns in children to what?

A
  • Antral or pylorus
  • IgE
  • Cows milk, soy protein, immune disorders, parasites, H. pylori.
80
Q

Lymphocytic gastritis (Varioliform Gastritis) is sometimes associated w/ what underlying disease?

Most often in which gender presenting with what sx’s?

A
  • Celiacs disease
  • F, with non-specific abdominal sx
81
Q

What is the most common specific cause of Granulomatous Gastritis in Western populations?

Other causes?

A
  • Crohns disease
  • Sarcoidosis, infection
82
Q

Usually, patients with peptic ulcer disease (PUD) develop in _____ ulcer. 90% occur in________ and 10% occur in the _____.

A
  • Solitary
  • 90% = proximal duodenum
  • 10%= antrum
83
Q

What are the risk factors for PUD (10 of them from table)?

A
  1. H.pylori
  2. Cigarette use (synergizes w/ H.pylori )
  3. NSAIDS (potentiated by steroids
  4. Illicit drugs
    • Alcoholic cirrhosis
    • Psychological stress
    • Endocrine cell hyperplasia
    • ZE syndrome
    • Viral infection (CMV, herpes simplex)
84
Q

Nearly all peptic ulcers are associated w/ what 3 risk factors?

A
  1. H. pylori
  2. Smoking
  3. NSAIDS
85
Q

Most common form of peptic ulcer disease occurs where and is associated with what?

Levels of what will be ↑ and ↓?

A

Antrum or duodenum as result of chronic H. pylori-induced antral gastritis & resulting hyperchlorhydria.

  • ↑ gastric acid secretion
  • ↓ duodenal HCO3- secretion
86
Q

A new group of duodenal PUD patients >60 yo have emerged recently as a result of what?

Presence of what can increase risk?

A
  • ↑ NSAID use
  • Especially when combined w low-dose aspirin (for CV benefit)
  • Facilitated if concurrent H. pylori infection is also present
87
Q

How can cigarette use and CV disease contribute to PUD?

A

↓ mucosal BF, oxygenation and healing

88
Q

Where are most duodonal ulcers located?

A

Anterior part of the proximal duodenum (near pyloric valve)

89
Q

What are complications of duodenal ulcers?

A
  • Upper GI bleeding, more likely when located posteriorly because can erode gastroduodenal artery.
  • Pancreatitis
  • Perforation
90
Q

Grossly how does the classic peptic ulcer appear?

A

Sharply punched-out w/ hemorrhage and fibrosis

*Is virtually diagnostic

91
Q

Perforation of a peptic ulcer into the ___________ is considered a surgical emergency.

How may this be detected clinically?

A

- peritoneal cavity

  • Free air under the diaphragm on upright XR of abomen
92
Q

What is the most frequent complication associated with PUD?

A

Bleeding

*May be first indication of an ulcer

93
Q

Which complication of PUD is most often associated w/ chronic ulcers and more often assoicated w/ pyloric channel ulcers?

Causes what symptoms?

A
  • Obstruction due to edema or scarring
  • Incapacitating, crampy abdominal pain
94
Q

Which complication associated w/ PUD accounts for 2/3 of ulcer deaths?

A

Perforations

95
Q

What are the major clinical signs and symptoms of PUD?

A
  • Epigastric burning or pain
  • Worse at night
  • Relieved by alkali foods
96
Q

How does a meal affect the experience of pain in someone with a gastric ulcer vs. duodenal ulcer?

A
  • Gastric –> pain is worse 1-3 hrs after meal bc stimulates acid release.
  • Duodenal –> pain improves w/ meal bc stim bicarb secretion
97
Q

Penetrating ulcers in PUD may cause pain to be referred where and can be misinterpreted as?

A

Back, LUQ or chest

Can be misinterpreted as cardiac in origin

98
Q

What are the current mainstays of treatment for PUD?

A
  1. Treat H. pylori
  2. PPI’s to neutralize gastric acid
  3. *Important to withdraw agents such as NSAIDs and selective COX-2 inhibitors
99
Q

Which glands are affected in autoimmune gastritis?

A

Gastric body oxyntic glands

100
Q

Oxyntic atrophy may be associated with intestinal metaplasia, recognized by the presence of _____________.

A

Goblet cells

101
Q

_________ of peptic ulcers RARELY occur.

A

Malignant transformation

102
Q

Peptic ulcer are sharply punched out. What is more characteristic of cancers?

A

Heaped up margins

103
Q

Some patients with PUD may present with what complications others than epigastric burning or aching pain (i.e., more serious complications)?

A
    • Iron deficiency anemia
    • Hemorrhage
    • Perforation
104
Q

Where are gastric ulcers most commonly located?

Rupture will cause what?

A
  • Lesser curvature of the stomach.
  • Rupture => bleeding due to L. gastric artery
105
Q

What are causes of gastric ulcers?

A
    1. 70% are due to H. pylori
    1. Adenocarcinoma, thus, they MUST be biopsied,
106
Q

Long-standing chronic gastritis can lead to what?

A
  1. Loss of parietal cells
  2. Intestinal metaplasia
  3. Increased risk for adenocarcinoma
107
Q

The risk for gastric adenocarcinoma is greatest with:

H. Pylori or AI gastritis?

A

AI gastritis

108
Q

__________ due to parietal cell deficiency can predispose to cancer by allowing bacterial overgrowth and producing carcinogens nitrosamines.

A

Achlorhydria (no HCl in gastric secretions)

109
Q

What happens to intestinal metaplasia in H. pylori gastritis when the organism is cleared?

A

It can regress

110
Q

What is hypertrophic gastropathy and what are the 2 most common?

A

Rare diseases that cause by large rugal folds due to epithelial hyperplasia (not inflammation) due to too much GF release.

    1. Menetrier Disease
    1. Zollinger- Ellison syndrome
111
Q

Menetrier disease is associated with excess?

Characterized by?

Anatomicaly where is it seen?

Sx?

A
  • Excess secretion of TGF-α
  • Diffuse hyperplasia of the foveolar mucus cells of the BODY and FUNDUS
  • ↑ mucus secretion => achlorhydria (loss of acid)
  • Protein loss
  • Hypoproteinemia, WL and diarrhea
112
Q

When does Menetrier Disease occur?

A
  • 30-60s (Men)
    • If in kids, sxs and pathology are similar, but self limited and often follows respiratory infection.
113
Q

Zollinger-Ellison disease is caused by?

Characterized by?

Anatomicaly where is it seen?

Sx?

A
  • Gastrin-secreting tumors (gastrinomas) in SI or pancreas
  • Increase in number of parietal cells => double the onxytic mucosal thickness (lesser extent, mucus and endocrine cells)
  • Fundus

- Duodenal ulcers or chronic diarrhea

114
Q

High levels of gastrin associated w/ ZE syndrome induces what changes?

A
  1. Hyperplasia of mucous neck cells
  2. Mucin hyperproduction
  3. Proliferation of endocrine cells
115
Q

ZE is most common in what ages?

A

50s

116
Q

What inflammatory infiltrate is seen in the hypertrophic gastropathies?

A
  • Menetrier Disease: limited (lymphocytes)
  • ZE: Neutrophils
117
Q

What risk factors are seen in the hypertrophic gastropathies?

A
  • Menetrier disease: N/A
  • ZE: MEN (multiple endocrine neoplasia)
118
Q

Are Zollinger-Ellison syndrome and Menentrier Disease associated w/ increased risk for adenocarcinoma?

A

ONLY Menetrier Disease

119
Q

How fast do gastrinomas grow and are they typically benign or malignant?

A
  • Slow growing
  • 60-90% are malignant
120
Q

MEN-1 is associated with what tumor of the GI?

A

Gastrinomas —> Zollinger-Ellison syndrome

121
Q

__________ that project above the level of the mucosa are ID’d in up to 5% of UGI endoscopy.

A

Polyps, nodules or masses

122
Q

What are the 3 types of gastric polyps (benign tumors) and which are the most common?

A
  1. Inflammatory or hyperplastic polyps*** (75%)
  2. Fundic gland polyp
  3. Gastric adenoma
123
Q

Where do the 3 types of polyps occur and what cells are involved?

A
  1. Inflammatory and hyperplasia polyps
    • Antrum > body
    • mucus cells
  2. Fundic gland polyps
    • Body and fundus
    • parietal and chief cells
  3. Gastric adenocarciomas
    • Antrum > body
    • dysplastic intestinal
124
Q

Inflammatory/hyperplastic polyps are most common in what age group?

Develop in association with what underlying disorder?

A

50-60s

Chronic gastritis due to H. pylori

125
Q

The risk of dysplasia associated with inflammatory or hyperplastic polyps is correlates with what?

Which polyps should be resected for further examination?

A

Size, polyps larger than 1.5 cm should be resected

126
Q

What are the symptoms of inflammatory or hyperplastic polyps?

A

Similar to chronic gastritis.

127
Q

Fundic Gland Polyps occur in what 2 ways?

Which is associated with a risk of cancer?

A
  1. Sporadic
    1. most often due to PPIs
  2. Syndromic: pts with FAP (familial adenomatis polyposis) => dysplasia => adenocarcinomo
128
Q

Why has the prevalence of Fundic Gland Polyps increased markedly in recent years?

A

PPIs => increase gastrin => onxytic gland growth

129
Q

What are the symptoms of fundic gland polyps?

A

None, besides nasaeu

130
Q

Gastric adenomas is most common in ____ YO and risk factors include ___________ (3)

A
  • Males 50-60YO
  • RF:
    • Chronic gastritis
    • Atrophy
    • Intestinal metaplasia
    • FAP
131
Q

Are gastric adenomas associated with adenocarcinoma?

A

YES! Frequently, especially if >2cm

132
Q

Gastric adenomas are ____________ neoplastic lesions

A

PRE-MALIGNANT

133
Q

________ develop in a background of chronic gastritis and are associated with intestinal metaplasia and mucosal (glandular atrophy).

A

Gastric adenomas

134
Q

What are the morphological characteristics of Gastric Adenomas?

A

Intestinal-type columnar epithelium w/ varying degrees of dysplasia

135
Q

Which 2 gastric polyp types are associated with familial adenomatous polyposis (FAP)?

A
  1. Fundic polyps
  2. Gastric adenomas
136
Q

What are the malignant tumors of the stomach? (4)

A
  1. Gastric adenocarcinomas
  2. Lymphoma
  3. Carcinoid
  4. GIST (gastrointestinal stromal tumor)
137
Q

What is the most common malignancy of the stomach?

A

Gastric Adenocarcinoma (95%)

138
Q

What are the types of gastric adenocarcinoma?

A
    1. Intestinal type: bulky mass that occurs due to intestinal metaplasia caused by H.pylori and AI gastritis
    1. Diffuse type: stomach diffusely thickens and infilrates the wall, due to thickening of gastric mucosa cells (not intestinal metaplasia)
139
Q

Early symptoms of gastric adenocarcinoma?

Late?

A

Early

  • Resemble those of chronic gastritis and PUD (dyspepsia, dysphagia, N)

Late

  • Weight loss (anorexia)
  • Early satiety (mainly in DIFFUSE cancers)
  • Anemia
  • Hemorrhage
140
Q

Because early symptoms of gastric adenocarcinoma resemble chronic gastritis and PUD, what does this mean?

A

Gastric adenocarcinoma is often found LATE in the disease stage

141
Q

Which countries have a 20-fold higher incidence of gastric adenocarcinomas?

A
  • Japan
  • Chile
  • Costa Rica
  • Eastern Europe

*More common in low SES groups

142
Q

Gastric adenocarcinoma has often spread when found.

Where are the most common sites of metastasis for Gastric Adenocarcinoma?

A
  1. Supraclavicular LN (Virchow node)
  2. Periumbilical LNs (Sister Mary Joseph nodule)
  3. Left axillary LN (Irish node)
  4. Ovary (Krukenberg tumor)
  5. Recto-uterine pouch (of Douglas)
143
Q

What are recognizable precursor lesions seen with gastric adenocarcinoma?

A

1. Gastric dysplasia

2. Gastric adenomas

144
Q

The cause of overall reduction in gastric cancer is most closely linked to what?

Other factors?

A

Decreases in H. pylori prevalence

145
Q

Majority of gastric cancers are ___________ heriditary

A

not

146
Q

Familial gastric cancer is strongly associated with what genetic mutation?

This gene encodes what?

A

LOF of CDH1, which encodes E-cadherin

147
Q

What germline mutations are associated with the development of diffuse gastric adenocarcinoma?

A

Loss of E-cadherin

148
Q

What germline mutations are associated with the development of sporadic/FAP intestinal gastric adenocarcinoma?

A
  • Mutations that cause increased signaling in Wnt pathway
    • LOF in APC
      • ​TGFβ​, BAX, or CDKN2A
    • GOF B-catenin
149
Q

Persons with FAP and what mutations have an increased risk for the intestinal-type gastric cancer, especially in high-risk areas such as Japan?

A

APC

150
Q

What are precursor lesions to intestinal type gastric adenocarcinoma?

A
  1. Metaplasia
  2. Atropgy
  3. Dysplasia
  4. Adenoma
  5. Menetrier
151
Q

Intestinal type of Gastric adenocarcinoma is most common where?

Risk factors?

A

Lesser curvature of the stomach, where ulcers form.

RF: older men, smoking, EToH, nitrosamines/NMDA, Type A blood

152
Q

What is the characteristic gross finding of diffuse gastric adenocarcinoma?

On biopsy?

A
  • Linitis plastica (stomach looks like thick leather)
  • Signet ring cells: mucin forms inside the cell and pushes the nucleus to the periphery.
153
Q
A

GI II Exam 1 (19 decks)

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