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Nichols + ??? Flashcards

1
Q

Cells in Gastric Glands

A
  1. Parietal Cells - make HCL
  2. Chief Cells - secrete pepsinogen
  3. Mucus Cells - bicarbonate rich mucus
  4. G Cells - only in antrum, secrete gastrin
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2
Q

Cephalic Phase of Acid Secretion

A

-taste, smell, chewing food stimulates acetylcholine release via the vagal nerve

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3
Q

Gastric Phase of Acid Secretion

A

-chemical effects of food and distention of stomach causes release of gastrin by the G cells

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4
Q

Intestinal Phase of Acid Secretion

A

-food & acid in small bowel cause release of CCK and secretin which inhibit acid production

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5
Q

What does the Mucous-bicarbonate Layer in the Stomach do?

A

-causes a pH gradient, secreted by mucus cells, prevent autodigestion

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6
Q

Peptic Ulcer Disease (PUD)

A
  • defect in GI mucosa extending though muscularis mucosae
  • costs $5.65 billion
  • annual incidence is 0.1-0.3% in US
  • decrease over decades
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7
Q

Symptoms of Peptic Ulcer

A
  • Abdominal Pain (80%), epigastric burning, nocturnal or relieved by food
  • nausea, anorexia
  • asymptomatic & present with complication (more common in elderly or patients taking NSAIDs)
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8
Q

Risk factors for PUD

A
  • Helicobacter pylori gastritis
  • Meds: ASA, NSAIDs, clopidogrel
  • Smoking
  • Genetic factors
  • Acid must be present for PUD to occur
  • additive risk factors*
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9
Q

PUD associated with Chronic Disease

A
  • stress ulcers in ICU patients on vents
  • Cirrhosis
  • Organ transplantation
  • COPD
  • normally get prophylactic PPI while in ICU to prevent ulcers
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10
Q

Helicobacter pylori and PUD

A
  • present in 70% of patients with PUD
  • only 10-15% of patients with H.pylori get PUD
  • associated with both duodenal and gastric ulcers
  • produces urease-makes organism resistant to gastric acid
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11
Q

Morphology of Helicobacter pylori?

A
  • spiral-shaped, gram -, 4-6 unipolar shethed flagella
  • stomach and duodenum
  • infections seen in healthy patients and patients with GI disease
  • can move through mucus layer
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12
Q

H. Pylori & mucosal inflammation?

A
  • resides in mucus layer overlying gastric epithelium
  • in lamina propria-always associated inflammatory infiltrate
  • epithelial layer is intact: evoke mucosal inflammatory cells
  • secretes peptide and LPS (chemotactic for neutrophils & monocytes)
  • peptide is heat, acid, alkali stable (MW 3000)
  • inflammatory cells: oxygen radicals, prostaglandins, IL-1, TNF
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13
Q

High risk factors for NSAID GI toxicity?

A
  • history of previous complicated ulcer

- multiple >2 risk factors

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14
Q

Moderate risk factors for NSAID GI toxicity?

A
  • age > 65
  • high-dose NSAID
  • previous history of uncomplicated ulcer
  • concurrent use of aspirin, glucocorticoids, or anticoagulants
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15
Q

Diagnosis of PUD

A
  • UGI-barium X-ray of stomach

- Upper endoscopy (allows biopsy for H. pylori)

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16
Q

Complications of PUD

A

-bleeding-hematemesis, melena, anemia
-perforation (surgery)
-penetration-may penetrate into adjacent organs-pancreas, colon, liver
-gastric outlet obstruction (blocks pylorus or duodenum, may be caused by active ulcer or healing of prior ulcer)
Poorer outcomes in older patients or co-morbid illness with complicated PUD

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17
Q

Treatment of PUD

A
  • anti-secretory agents-H2 blockers or PPI (treat 6-8 weeks)
  • Treat H. pylori if present (abx), eradication decreases recurrent PUD
  • avoid smoking, NSAIDS, ASA if possible
  • select patients may use maintenance medicine
  • surgery (complications)
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18
Q

Tests for H. Pylori treatment

A
  1. urea breath test (no bismuth, PPI, abx)
  2. Fecal antigen test using monoclonal ab
  3. Serological test, not good for evaluating successful treatment
  4. Biopsy of antrum- urease based tests, no bismuth, PPI or antibioticts, histological evaluation
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19
Q

Gastritis

A
  • pathological diagnosis of gastric inflammation of mucosa (not submucosa)
  • may be acute or chornic
  • may be caused by NSAIDS, H. pylori, alcohol, ischemia or extreme stress
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20
Q

Acute Hemorrhagic Gastritis

A
  • associated with alcohol, NSAID, bile reflux, trauma, burns, sepsis, shock
  • present with abdominal discomfort or pain, heartburn, nausea, vomiting, hematemesis (massive)
  • typically have numerous petechiae, erosions, +/- ulcers, +/- bigger hemorrhages
  • heals rapidly
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21
Q

Chronic Gastritis leads to??

A

-atrophy, intestinal metaplasia, dysplasia, or neoplasia or combo
Causes: H. pylori, autoimmune, bile reflux

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22
Q

Helicobacter Pylori Gastritis

A

-common (inc. with age)
-chronic active gastritis, more sever in antrum, lymphocytic inflammation, germinal centers and neutrophils (active), spiral bacteria in superficial mucus layer
Diagnosis: gastric biopsy or serology & other non-invasive
-leads to gastric adenocarcinoma (1-3%) or low grade lymphoma (0.1%)

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23
Q

Helicobacter Pylori Gastritis: Pathology

A
  • neutrophils infiltration gland in center
  • favors neck of gastric glands (lined by mucous cells)
  • Giemsa stain: easier to see H. pylori, also immuno stain
  • lymphoid follicles (germinal centers) common
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24
Q

Helicobacter Pylori toxins

A
  • Cytotoxin-associated gene A (CagA) protein
  • causes degradation of p53
  • activates pathways to cell proliferation (via RAS, MEK, ERK, NF-kappaB, beta-catenin)
  • messes up cell polarization

-injected into cells by syringe-like type IV secretion systems (T4SS) pilus structrue

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25
Q

Autoimmune Atrophic Gastritis

A

<10% of chronic gastritis with Ab to parietal cells (achlorhydria) and intrinsic factor (pernicious anemia)

  • can have intestinal metaplasia like w/H. pylori
  • can get G-cell hyperplasia
26
Q

Gross Pathology: PUD

A
  • ulcers are small, round, deep and “punched out”
  • duodenum, stomach, GE junction (GERD), margins of gastrojejunostomy
  • ZE patients: near Meckel diverticulum containing epigastric mucosa
27
Q

Layers of Chronic Peptic Ulcer

A
  • necrosis
  • inflammation
  • granulation tissue
  • scar
28
Q

Gastric Benign Ulcer

A
  • round-oval
  • flat or overhanging margins
  • deeper, punched out
  • perpendicular walls or flask shaped
  • smooth clean base
  • smaller (<2cm)
  • radiating rugal folds
29
Q

Gastric Malignant Ulcer

A
  • irregular shape
  • heaped-up or nodular margins
  • shallower, sloping
  • ulcerated mass or bowl shape
  • necrotic shaggy base
  • bigger (ofter >3cm)
30
Q

Stress Ulcers

A
  • occur with brain injury (Cushing ulcer) or burns (Curling ulcer)
  • typically 3 to 7 days after the stressful event
  • deep, single, hemorrhagic and small (<1cm) but associated with numerous petechiae or larger hemorrhages
31
Q

Factors Associated with Squamous Cell Carcinoma

A
  • alcohol, smoking, urban & lower SEC populations
  • dietary & environmental factors that cause chronic esophageal irritation-lye ingestion, achalasia, high red meat consumption, vit or trace mineral deficiency, head and neck cancer
  • rare: Tylosis, Plummer-Vinson syndrome, HPV infection
32
Q

Adeoncarcinoma of Esophagus: Risk Factors

A
  • Barrett’s Esophagus (intestinal metaplasia)
  • GERD
  • Truncal Obesity
    rare: scleroderma, ZE syndrome
33
Q

Symptoms of Esophageal Carcinoma

A
  • result from narrowing or ulceration of esophagus
    1. dysphagia
    2. weight loss
    3. odynophagia
    4. aspiration
    5. anemia
34
Q

Esophageal Carcinoma Epidemiology (SSC)

A 
male (4:1)
black (6:1)
mid-esophagus
age: 60-70
risk factors: smoking, ETOH
35
Q

Esophageal Carcinoma Epidemiology (adeno)

A 
male (7:1)
white (4:1)
distal esophagus 
age: 50
risk: barrett's esophagus
36
Q

Is adeno or SCC of Esophagus more common?

A

equal (50/50)

37
Q

Diagnosis of Esophageal Cancer

A
  • barium x-rays will show asymmetrical narrowing or mass

- endoscopic: shows mass or stricture for advanced lesions, early lesion: ulcer, nodule, plaque, allows biopsy

38
Q

Staging of Esophageal Cancer

A
  1. CT of chest (look for spread)
  2. EUS helps determine depth of penetration into wall of esophagus & presence of lymph mets
  3. decreases survival if lymph node metastases is present
39
Q

Treatment of Esophageal Cancer

A
  • curative: surgery with or w/o radiation
  • 50-60% present incurable locally advanced/mets
  • surgery & XRT for palliation
  • endoscopic prosthesis may help for dysphagia
  • 5 year survival is 5%
40
Q

Hyperplastic Gastric Polyps

A

-seen with chronic inflammation, H. pylori, and atrophic gastritis
-usually asx; may cause microscopic blood loss or intermittent prolapse if large
-rarely become malignant-ususally if >2cm
-treatment: remove endoscopically if >1cm
75% of gastric polyps

41
Q

Fundic Gland Gastric Polyps

A
  • occur in gastric corpus

- usually 1cm

42
Q

Adenomatous Gastric Polyps

A
  • 10% of gastric polyps
  • most are in antrum and associated with atrophic gastritis
  • sessile or pedunculated, precursor of some gastric lesions
  • treatment: endoscopic removal or surgery
  • risk of malignancy increases with size, villous lesions, or high grade dysplasia
43
Q

Gastric Cancer

A
  • more common in lower SEC and dev. countries
  • male (2:1)
  • peaks in 7th decade
  • declining in US (of distal gastric cancers)
44
Q

Risk Factors for Distal Gastric Cancer

A
  • chronic atrophic gastritis
  • pernicious anemia
  • prior gastric surgery
  • high dietary nitrates
  • adenomatous gastric polyps
  • H. pylori infection(3-6X inc)
45
Q

Types of Gastric Neoplasia

A

75% adenocarcinoma

25% lymphoma - better prognosis

46
Q

Symptoms of Gastric Cancer

A
  • diaphragmatic invasion: hiccupps
  • weightloss, early satiety
  • bleeding, ulceration
  • pain, nausea, melena
47
Q

Clinical course of gastric cancer?

A
  • may metastasize to liver, peritoneum, or distal lymph nodes
  • Virchow’s node - left supraclavicular node
  • Sister Mary Joseph node - periumbilical nodule
48
Q

Linitis Plastic

A
  • aggressive diffuse gastric cancer
  • 5% of gastric cancers
  • gastric wall is infiltrated by malignancy
49
Q

Treatment of Gastric Cancer

A
  • CT used for staging before surgery
  • Surgery is only change for cure (rarely curative)
  • May also be used for palliation for obstruction of bleeding
  • chemo may improve survival in patients who have surgery
50
Q

Chronic Inflammation & Neoplasia in Esophagus & Stomach

A
  1. Chronic Inflammation
  2. Cell Death
  3. Accelerated Regeneration
  4. Mistake in Replication
    (normal to metaplasia/dysplasia to neoplasia)
51
Q

What makes malignant tumor malignant?

A
  1. Invasion

2. Metastasis

52
Q

Squamous Cell Carcinoma of the Esophagus

A
  • p53 point mutation are common early in pathogenesis
  • K-RAS and APC gene mutations are not present in squamous cell carcinoma of esophagus
  • HPV DNA is sometimes present in tumors from high incidence areas q
53
Q

SSC of Esophagus: location

A
  • 20% upper 1/3
  • 30% mid 1/3
  • 30% lower 1/3
54
Q

SSC of Esophagus: gross pathology

A

early: small grey-white plaque-like thickening
late: months to years after early: 60% protruding
15% flat, 25% excavated

55
Q

Molecular Pathogenesis of Adenocarcinoma of Esophagus

A
  • early: p53 mutation or overexpression in metaplastic intestinal type Barrett’s epithelium
  • allelic loss of epigenetic silencing by hypermethylation of p16/INK4a cyclin-dependent kinase inhibitor
  • mutation in retinoblastoma (RB) tumor suppressor
  • amplification of cERB-B2, cyclin D1 or cyclin E
56
Q

Hyperplastic Gastric Polyp: Pathology

A
  • hyperplastic mucosal epithelium

- inflamed edematous stroma

57
Q

Fundic Gland Polyp: Pathology

A

-dilated corpus (body) oxyntic type glands

58
Q

Adenomatous Polyp: Pathology

A

closely packed, disturbed glandular architecture

-stratified columnar epithelium

59
Q

Intestinal Type: Gastric Carcinoma

A
  • typically masses

- intestinal metaplasia = precursor

60
Q

Diffuse Type: Gastric Carcinoma

A

-nasty
-typically linitis plastica
-infiltration by single cells resembling signet rings
(individual cells)

GI (19 decks)

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