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6. HDS GI Repro > Stomach Disorders > Flashcards

Stomach Disorders Flashcards

1
Q

Stomach Anatomy

A

Divided into four regions:

  1. Cardia
  2. Fundus
  3. Corpus (Body)
  4. Antrum
    • Pylorus
    • Pyloric sphincter
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2
Q

Stomach Epithelium

A
  • Foveolar cell: tall columnar cell w/ apical mucus
    • Lines surface and gastric pits
  • Mucus cell: columnar or cuboidal cell w/ clear cytoplasm
    • Lines isthmus and neck
    • Lines glands of the cardia and antrum
    • Contains mucin
  • Parietal cell: polygonal cell w/ eosinophilic cytoplasm
    • Present in the fundus and body glands (oxyntic area)
    • Produces HCl, intrinsic factor, TGFα, cathepsins B and H
  • Chief cell: cuboidal cell w/ basophilic cytoplasm
    • Present in fundus and body glands (oxyntic area)
    • Produces pepsinogen
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3
Q

Diaphragmatic Hernia

A
  • Incomplete formation of the diaphragm
  • Allows the abdominal viscera to herniate into the thoracic cavity
  • Can cause pulmonary hypoplasia ⇒ lungs don’t have space to develop
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4
Q

Omphalocele

A
  • Abdominal musculature doesn’t close completely
  • Abdominal viscera herniate into a ventral membranous sac
  • Can fix w/ surgery
  • Need to look for other anomalies including diaphragmatic hernia and cardiac malformations
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5
Q

Gastroschisis

A

Ventral abdominal wall defect of all layers

Viscera protrude through opening, not in a sac

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6
Q

Infantile Hypertrophic Pyloric Stenosis

A
  • Clinical features
    • Postprandial projectile vomiting onset week 2-3 of life
    • 0.3-0.4% livebirths, more common in males
    • ± palpable abdominal mass
  • Etiology
    • Muscular hypertrophy of circular muscle of pylorus
    • Possible causes: excess gastrin, nerve fiber abnormalities, lack of nitric oxide synthetase
  • Pathology
    • Hypertrophic, hyperplastic circular muscle w/ pyloric channel narrowing and lengthening
    • Ex. of polygenic inheritance
  • Treatment
    • Surgical muscle splitting
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7
Q

Heterotopic Pancreas

A
  • Most common gastric heterotopia
  • Typically incidental finding
  • 0.4-4cm hemispheric, umbilicated mass
    • Antrum > pylorus > greater curvature
  • Variable mix of pancreatic tissue
    • Exocrine and endocrine elements
    • Exocrine alone
    • Only smooth muscle and/or pancreatic ducts
  • Secondary changes
    • Pancreatitis, cysts, neoplasia
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8
Q

Gastritis

Terminology

A
  • Gastritis: injury to the stomach dominated by an inflammatory infiltrate
  • Gastropathy: injury to the stomach dominated by epithelial injury and loss
  • Activity: presence of a neutrophilic infiltrate
  • Acute: a process believed to be of recent onset and transient
  • Chronic: chronic inflammatory process that may go on to metaplasia and atrophy
  • Atrophy: loss or replacement of native gastric glands
  • Metaplasia: conversion of the epithelium lining the surface, pits and glands from a native gastric cell type to another cell type, (e.g. intestinal)
  • Erosion: tissue loss confined to the mucosa
  • Ulcer: tissue loss extending below the mucosa
  • Hyperplasia: ↑# of cells
  • Dysplasia: neoplastic alteration of the epithelium
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9
Q

Acute Gastritis

Pathogenesis

A
  • Protective mechanisms
    • Mucin from foveolar cells protects
    • Excellent vascular supply
    • Delivers oxygen, bicarb, nutrients
    • Washes away acid that has back-diffused into the lamina propria
  • Overcome by:
    • NSAIDS counter protection from prostaglandins and bicarb, makes mucosa more vulnerable
      • Also inhibit bicarb via uremia, H. pylori (which secretes urease)
    • Ingest harsh acid or base directly injures mucosal cells
      • Also injure via NSAIDS, alcohol, radiation, chemotherapy
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10
Q

Mild Acute Gastritis

A
  • Surface epithelium intact
  • May see a few neutrophils, edema and vascular congestion of lamina propria
  • PMNs in direct contact w/ epithelial cells ⇒ active inflammation
  • Applies all through the GI tract
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11
Q

Acute Erosive Hemorrhagic Gastritis

A
  • Erosion: loss of superficial epithelium, defect limited by lamina propria
  • See PMNs in mucosa and fibrinopurulent exudate in lumen
  • Can see hemorrhage w/ dark spots in the mucosa
  • Next erosions can progress to ulcers
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12
Q

Acute Gastric Ulceration

Types

A
  • NSAID ulcers
    • ↓ Prostaglandins ⇒ ↓ bicarbonate secretion, ↑ acid secretion, ↓ mucin synthesis, ↓ vascular perfusion
  • Stress ulcer
    • Seen in shock, sepsis, severe trauma
    • Systemic acidosis ⇒ ↓ pH of mucosal cells
    • Splanchnic vasoconstriction ⇒ ↓ blood flow
  • Curling ulcer
    • Ass. w/ severe burns or trauma
  • Cushing ulcer
    • Seen in pts w/ brain conditions (e.g. tumors)
    • Intracranial injury ⇒ direct stimulation of vagal nuclei ⇒ hypersecretion of gastric acid
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13
Q

Acute Gastric Ulcer

Morphology

A
  • Anywhere in stomach, single or multiple
  • Round and > 1 cm
  • Can extend completely through mucosa
    • Risks: bleeding, perforation
  • Base often stains black d/t acid digesting the extravasated blood
  • Not indurated d/t acute nature, sharply demarcated
  • No scarring or thickened vessels as in chronic peptic ulcers
  • Can heal completely in days-weeks once stimulus is removed
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14
Q

Chronic Gastritis

A
  • Symptoms are less severe, but more persistent
    • Can see nausea, epigastric pain, vomiting
  • Most common cause is infection w/ H. pylori
  • In those w/o H. pylori, most common form is atrophic gastritis (autoimmune)
  • Less common are radiation injury or systemic disease like Crohns
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15
Q

Helicobacter pylori

Overview

A
  • Acute infection doesn’t usually cause sx
  • Chronic infection: ↑ acid production despite low gastrin levels, disrupt protective mechanisms
  • Associated w/ poverty, crowding
  • Often acquired in childhood, w/ up to 70% colonization
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16
Q

H. pylori Infection

Associated Diseases

A
  • (Antral) Chronic gastritis
    • Can progress to multifocal atrophic gastritis
  • Peptic ulcer disease: duodenal ulcers, gastric ulcers
  • Gastric carcinoma
    • Diffuse type
    • Intestinal type
  • Gastric lymphoma
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17
Q

H. pylori Gastritis

Morphology

A
  • EGD: erythema and coarse/nodular appearance
  • Antral biopsy:
    • Organisms in the mucus coating epithelial cells
    • Highlighted by special stains (ex. Warthin-Starry stain)
    • PMNs in lamina propria and epithelium, can accumulate in gastric pit lumen (pit abscess)
    • Plasma cells and lymphocytes that can thicken rugal folds
    • Lymphoid aggregates are MALT and may transform into lymphoma
    • Eventually, mucosa can become atrophic
  • Can also test w/ serology for Ab, urea breath test, fecal bacterial detection
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18
Q

Autoimmune Gastritis

Overview

A
  • Chronic gastritis predominantly affecting body and fundus
    • < 10% of Chronic Gastritis
  • Due to autoantibody attack on gastric cells and proteins
    • Auto-Ab present in >70% of those w/ disease early in the course
    • Include Ab vs parietal cells and intrinsic factor
  • Over 2-3 decades, progress to gastric atrophy
  • Some w/ pernicious anemia (10%)
  • Usually not dx until later adulthood, F>M, some w/ other autoimmune disorders
  • ~20% of relatives of pts w/ pernicious anemia have autoimmune gastritis
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19
Q

Autoimmune Gastritis

Pathogenesis

A
  • Loss of parietal cells ⇒ ↓ acid and intrinsic factor
    • Low acid levels ⇒ hyperplasia of G cells in antrum and gastrin secretion
    • Lack of intrinsic factor ⇒ ⊗ B12 absorption ⇒ pernicious anemia
  • Chief cell destruction ⇒ ↓ pepsinogen
  • CD4+ T cells directed against parietal cell components (H+, K+-ATPase) causes injury
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20
Q

Autoimmune Gastritis

Morphology

A
  • Damage to oxyntic (acid-producing) mucosa in body and fundus
    • Thinning of mucosa
    • Extensive loss of parietal and chief cells
  • Infiltrate of lymphs, MΦ, plasma cells
  • ± Intestinal metaplasia w/ goblet cells
  • ± Antral endocrine cell hyperplasia ⇒↑cancer risk
21
Q

Reactive Gastropathy

A
  • See foveolar hyperplasia, glandular regenerative changes, and mucosal edema
  • Due to chemical injury, NSAIDs, bile reflux
  • Can see after gastric surgery that bypass pylorus
22
Q

Eosinophilic Gastritis

A
  • See infiltrates of eosinophils in mucosa and muscularis in antrum and pylorus
  • Can see peripheral eosinophilia and ↑ serum IgE levels
  • May be caused by allergic reactions to foods or drugs, parasitic infection
  • Also seen in pts w/ collagen-vascular disease
23
Q

Lymphocytic Gastritis

A
  • Nonspecific symptoms
  • Seen more in women
  • 40% of pts have celiac disease, so may be immune mediated
  • Causes varioliform gastritis
    • Thickened folds covered by small nodules w/ aphthous ulceration in center
  • See increase in intraepithelial T lymphs, mostly CD8+
24
Q

Granulomatous Gastritis

A

Can be part of Crohn disease, sarcoid or some infections

25
Q

Peptic Ulcer Disease (PUD)

Overview

A
  • PUD due to hyperacidity
    • Helicobacter infection
      • Duodenal ulcers (85-100%)
      • Gastric ulcers (65%)
      • 20% of pts w/ HP infection get PUD
    • Chronic NSAID use
    • Smoking, high dose steroids, cirrhosis, COPD, renal failure, stress
  • Complication of chronic gastritis
    • Imbalance of mucosal defenses and assaults ⇒ chronic gastritis
  • Most often in gastric antrum and 1st part of the duodenum
26
Q

Peptic Ulcer Disease (PUD)

Morphology

A
  • Solitary in 80% of pts
  • Sharply punched-out defect coated by fibrinopurulent exudate
  • Granulation tissue underneath and scar
  • Do not see ‘heaped-up’ margins
  • Size doesn’t separate benign vs. malignant
    • PUDs rarely become malignant
  • Complications include perforation, bleeding
27
Q

Peptic Ulcers

Clinical Manifestations

A
  • Chronic and recurring
  • Most often in adults, present w/ epigastric burning or aching pain
  • Pain tends to occur 1-3 hours after meals
  • Relieved by alkali or food
  • Many therapies available
28
Q

Chronic Gastritis

Consequences

A
  • Atrophy and intestinal metaplasia ⇒ ↑ risk of gastric adenocarcinoma
    • Greatest risk from autoimmune gastritis
      • ↓ acid ⇒ ↑ bacteria ⇒ ↑ nitrosamines
  • Dysplasia can be the next step
    • Epithelium exposed to inflammation, free radicals, etc.
    • See change in nuclei
    • Cells are cytologically immature
29
Q

Hypertrophic Gastropathies

A
  • See giant ‘cerebriform’ enlargement of rugal folds
  • Due to epithelial hyperplasia w/o inflammation
  • Linked to excessive growth factor
    • Ex. Menetrier Disease and Zollinger-Ellison Syndrome
30
Q

Menetrier Disease

A
  • Excess secretion of TGF-α
  • Diffuse hyperplasia of body and fundus foveolar epithelium ⇒ enlarged rugae ⇒ protein loss from GI tract
    • ↑ Risk of gastric adenocarcinoma
    • Slight ↑ risk of gastric carcinoma
  • M:F 3:1, 30-50s peak age
  • Clinical: diarrhea, discomfort, weight loss vs. asymptomatic
31
Q

Zollinger Ellison Syndrome

A
  • Caused by gastrinoma of sm. intestine or pancreas
    • ↑ Gastrin secretion ⇒ gastric gland hyperplasia
      • ↑ Parietal cells ⇒ ↑ acid secretion
      • ↑ Mucous neck cells ⇒ ↑ mucus hyperproduction
      • Proliferation of endocrine cells
  • Pts present w/ duodenal ulcers or chronic diarrhea
  • Treat by blocking acid hypersecretion
  • Need to remove tumor
    • Most are malignant
    • Can be part of MEN I
32
Q

Menetier vs Zollinger Ellison

A
33
Q

Hyperplastic/Inflammatory

Gastric Polyps

A
  • Non-neoplastic
  • 75% gastric polyps
  • Seen in adults w/ chronic gastritis
  • Should resect if > 1.5 cm to check for dysplasia
34
Q

Fundic Gland Polyp

A
  • Non-neoplastic
  • Can be sporadic or in people w/ Familial Adenomatous Polyposis
  • Associated w/ PPIs ⇒ ↑ incidence
  • W > M
  • Cause sx like nausea, vomiting or pain or can be asymptomatic
  • Have cystically dilated irregular glands
35
Q

Gastric Adenoma

A

Neoplastic polyp

  • 5-10% of gastric polyps
  • ↑ Incidence:
    • Age
    • Pops. w/ ↑ risk for adenocarcinoma (M>F)
    • Familial Adenomatous Polyposis
  • Background of chronic gastritis w/ atrophy and intestinal metaplasia
  • Dysplastic intestinal-type epithelium w/ nuclear enlargement, elongation, and hyperchromasia
    • If high-grade dysplasia ⇒ irregular architecture
  • ↑ Risk of adenocarcinoma if > 2 cm in diameter
36
Q

Inflammatory/Hyperplastic Polyps

vs

Gastritis Cystica

vs

Gastric Adenomas

A
37
Q

Gastric Adenocarcinoma

Epidemiology

A
  • 90% of Gastric CA
  • Incidence in Japan, Chile, Costa Rica, Eastern Europe is 20x that in US
  • US gastric CA rate ↓ by 85% during 20th century
    • Can detect early cancer w/ screening
    • Due to environmental and dietary factors: more fresh food, less salting and smoking of foods
    • Seen most often in lower socioeconomic groups and pts w/ mucosal atrophy and intestinal metaplasia
  • Incidence of adenocarcinoma of gastric cardia ↑ d/t Barrett esophagus
38
Q

Gastric Carcinoma

Risk Factors

A
  • Environmental
    • Diet
    • Nitrites derived from nitrates smoked and salted food, pickled foods
    • Lack of fresh fruit and vegetable
    • Low socioeconomic status
    • Cigarette smoking
  • Host factors
    • Chronic gastritis
    • H. pylori
    • Autoimmune
    • Partial gastrectomy
    • Menetrier disease
    • Gastric adenomas
    • Barrett’s esophagus (GEJ tumors)
  • Genetic
    • Blood group A
    • Fhx of gastric CA
    • Hereditary nonpolyposis colon cancer syndrome
39
Q

Gastric Adenocarcinoma

Pathogenesis

A
  • Loss of E-cadherin function
    • Key step in developing diffuse-type gastric cancer
  • Familial Adenomatous Polyposis
    • ↑ Risk of intestinal-type gastric cancer
    • Esp. high-incidence in Japan
  • Chronic inflammation promotes neoplastic progression
40
Q

Gastric Adenocarcinoma

Morphologic Classification

A
  • Based on location in stomach
    • Most involve the antrum, lesser curvature > greater
  • By gross and histologic appearance:
    • Intestinal pattern
      • Micro: gland formation
      • Gross: large, bulky tumor
    • Diffuse pattern
      • Micro: infiltration by tumor cells containing mucin (signet ring cells)
      • Gross: thickening of the gastric wall (linitis plastica)
        • Due to a desmoplastic reaction to tumor cells
41
Q

Gastric Adenocarcinoma

Clinical Characteristics

A
  • Intestinal type
    • Predominates in high-risk areas
    • Develops from precursor flat dysplasia or adenoma
    • Mean age at dx is 55 y/o
    • M:F 2:1
    • Dramatic ↓ linked to ↓ atrophic gastritis and intestinal metaplasia
  • Diffuse type
    • Uniform incidence across countries
    • No precursor lesion
    • M = F
  • Incidence of intestinal and diffuse are now equal
  • Presentation
    • Usu. similar to chronic gastritis
    • Later get weight loss, early satiety, anemia, etc
    • Periumbilical subcutaneous nodule ⇒ Sister Mary Joseph nodule
  • Prognostic Indicators
    • Depth of invasion, ± nodes, ± distant metz
  • Treatment
    • If limited to mucosa and submucosa ⇒ resection can yield 90% 5-year survival
    • If advanced ⇒ 5-year survival < 20%
    • In US, overall 5-year survival < 30%
42
Q

Gastric Lymphoma

Overview

A
  • Indolent extra-nodal marginal zone lymphomas of MALT
  • 5% of all gastric malignancies
  • 3 associated translocations:
    • Most common is t(11;18)(q21;q21) ⇒ ⊕ transcription factor promoting B-cell growth and survival
  • Arise at sites of inflammation
  • Many H. pylori ⊕
    • Low-grade MALT lymphoma regresses if HP is eradicated w/ abx w/ loss of detectable mAb pop.
    • Tumor may recur w/ re-infection by HP
43
Q

Gastric Lymphoma

Morphology

A
  • Dense lymphocytic infiltrate in lamina propria, often infiltrate gastric glands
  • Results in lymphoepithelial lesions
  • Express B cell markers
  • Can show monoclonality
  • Present w/ pain, later weight loss, etc
44
Q

Carcinoid Tumor

A
  • Arise from endocrine cells
    • GI tract (small intestine) > lung
  • Can be associated w/:
    • Endocrine cell hyperplasia
    • Chronic atrophic gastritis
    • Zollinger Ellison Syndrome
  • Gross:
    • Intramural or submucosal lesion w/ ulceration
    • Tumors are yellow or tan, and firm
  • Micro:
    • Islands or strands of tumor cells w/ ‘salt and pepper’ chromatin
    • Stain for NE markers (chromogranin, synaptophysin)
    • NE granules on EM
45
Q

GI Stromal Tumor (GIST)

Overview

A
  • Most common abdominal mesenchymal tumor
  • 60 y/o, slight M>F
  • If seen in a child:
    • Carney triad ⇒ young female w/ gastric GIST, paraganglioma and pulmonary chondroma
    • Neurofibromatosis type I
  • Clinical manifestations:
    • Sx related to mass effects
    • ± Blood loss due to mucosal ulceration
  • Treatment:
    • Complete resection if localized
      • Gastric GISTS usually less aggressive than intestinal GISTS
    • Can treat w/ imantinib
      • Tyrosine kinase inhibitor of c-KIT
      • Also used in CML
46
Q

GI Stromal Tumor (GIST)

Origin & Genetics

A
  • Arise from interstitial cells of Cajal
    • Located in the muscularis propria
    • Pacemaker cells for gut peristalsis
    • Express c-KIT (CD117) and CD34
  • Oncogenic GOF mutations of tyrosine kinase c-KIT ⇒ receptor for stem cell factor
    • Early event in sporadic GIST
    • Promotes tumor cell proliferation and survival
    • Target of therapy
47
Q

GI Stromal Tumor (GIST)

Morphology

A
  • Single, well-circumscribed, fleshy mass
  • Covered by either ulcerated or intact mucosa,
  • Up to 30 cm diameter
  • Metastasizes as nodules in peritoneal cavity or as liver nodules
  • Micro: spindle cells, sometimes see rounder epithelial-type cells
  • Immunohistochemistry cells mark w/ c-KIT in 95% of GISTs
48
Q

Other GI Tumors

A
  • Lipoma
  • Metastatic tumors
    • Breast Carcinoma
    • Melanoma
    • Others

6. HDS GI Repro (30 decks)

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