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GI 2 Pathology--Chapt 16 and 17 > Chapter 17 part 4--stomach part 2 > Flashcards

Chapter 17 part 4--stomach part 2 Flashcards

1
Q

Complications of chronic gastritis–list

A
  • Peptic ulcer disease
  • Mucosal atrophy and Intestinal metaplasia
  • Dysplasia
  • Gastric Cystica
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2
Q

Peptic Ulcer Disease (PUD)

A
  • chronic mucosal ulceration affecting duodenum or stomach

- most common form occurs in gastric antrum or duodenum associated with H. pylori infection

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3
Q

PUD in the gastric fundus or body is accompanied by what?

A

-MUCOSAL ATROPHY (due to H. pylori or autoimmune gastritis)

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4
Q

Epidemiology of Peptic Ulcer Disease–associated with what??

A
  • All peptic ulcers are associated with H. pylori infection, NSAIDs (including low-dose aspirin for cardiovascular benefits) or cigarette smoke
  • NSAID risk is increased by concurrent H. pylori infection
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5
Q

Other risk factors for PUD include

A
  • COPD
  • illicit drugs (that reduce mucosal blood flow)
  • alcoholic cirrhosis
  • psychological stress
  • Zollinger-Ellison syndrome
  • certain viral infections–CMV an HSV!!
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6
Q

Pathogenesis of PUD

A
  • imbalances in mucosal damage and defenses
  • Hyperacididty due infection, parietal cell hyperplasia, excessive secretory response, or increased gastrin production (secondary to hypercalcemia or produced by a tumor)
  • NSAIDS and steroids–block normal prostaglandin cytoprotective effects
  • cigarette smoking (and CV disease) impairs mucosal blood flow and healing
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7
Q

Gross Morphology of PUD

A
  • Most ulcers are solitary

- gross: sharply punched out defect with overcharging mucosal borders and smooth, clean ulcer bases

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8
Q

Microscopic morphology of UPD

A
  • thin layers of fibrinoid debris with underlying inflammation merging into granulation tissue and deep scarring
  • surrounding mucosa exhibits chronic gastritis
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9
Q

Clinical features of PUD

A
  • S/S: epigastric gnawing, burning, or aching pain, worse at night and 1-3 hours after meals
  • nausea, vomiting, bloating, belching and weight loss can also occur
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10
Q

Complications of PUD

A
  • anemia
  • hemorrhage
  • perforation
  • obstruction
  • Malignant transformation is rare and is related to underlying gastritis
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11
Q

Treatment of PUD

A

-focused on H. Pylori eradication, removal of offending agents (NSAIDS) and neutralization or reduced production of gastric acid

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12
Q

Mucosal atrophy and intestinal metaplasia

A

–Long standing chronic gastritis leads to parietal cell loss, associated with intestinal metaplasia and an increased risk of gastric adenocarcinoma

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13
Q

Mucosal atrophy and intestinal metaplasia–risk of malignancy is greatest in what kind of gastritis?

A

-autoimmune gastritis

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14
Q

Mucosal atrophy and intestinal metaplasia–Achlorydia

A

-Achlorydia due to parietal cell deficiency may predispose to cancer by allowing bacterial overgrowth with production of carcinogenic nitrosamines

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15
Q

Dysplasia

A
  • Long standing chronic gastritis exposes epithelium to inflammation-related free radical damage and proliferative stimuli
  • overtime, combo can lead to accumulation of genetic alterations resulting in carcinoma; pre invasive, in situ lesions can be recognized histologically as dysplasia
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16
Q

Gastritic cystica

A
  • Exuberant reactive epithelial proliferation with entrapped epithelium-lined cysts that can exhibit changes that mimic invasive adenocarcinoma
  • associated with chronic gastritis and partial gastrectomy
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17
Q

Hypertrophic Gastropathies–what are they?

A
  • uncommon
  • features giant enlargement of gastric rural folds due to epithelial hyperplasia; linked to excessive growth factor production
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18
Q

Hypertrophic Gastropathies–includes what diseases?

A
  • Menetrier Disease

- Zollinger Ellison syndrome

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19
Q

Zollinger-Ellison Syndrome–cause

A

-caused by gastrin-secreting tumors (gastrinomas) typically in the small bowel or pancreas

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20
Q

Zollinger-Ellison Syndrome–presentation

A

-multiple duodenal ulcers and/or chronic diarrhea

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21
Q

Zollinger-Ellison Syndrome–pathogenesis

A

-Elevated gastrin levels induce a marked (unto 5x) increase in gastric parietal cells and more modest increases in mucous neck cells and gastric endocrine cells

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22
Q

Zollinger-Ellison Syndrome–how do they arise and what are they associated with?

A
  • gastronomes are sporadic in 75% of pts
  • in remainder, they are associated with multiple endocrine neoplasia, type I (MEN-I)
  • 60-90% of gastronomes are malignant!!
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23
Q

Gastric polyp

A
  • nodules or masses that project above level of surrounding mucosa
  • can result from epithelial or stromal hyperplasia, inflammation, ectopic or neoplasia
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24
Q

Inflammatory and Hyperplastic polyps

A
  • constitute 75% of gastric polyps
  • incidence depends on local prevalence of H. Pylori infections
  • most common bw age 50 and 60 and arise in association with chronic gastritis
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25
Q

Inflammatory and Hyperplastic polyps morphology

A
  • majority <1 cm and frequently multiple
  • typically have smooth surface, occasionally with superficial erosions
  • histo: show irregular, mystically dilated and elongated glands with variable amounts of acute and chronic inflammation
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26
Q

Inflammatory and Hyperplastic polyps–risk of dysplasia–when?

A

-risk of dysplasia increases with size; polyps>1.5 cm should be resected!

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27
Q

Fundic gland polyps

A
  • occur sporadically
  • women over 50 or in setting of familial adenomatous polyposis (FAP)
  • incidence also increased by proton pump inhibitors and consequent gastrin secretion
  • single or multiple, smooth, well-circumscribed lesions composed of irregular, mystically dilated glands with minimal inflammation
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28
Q

Gastric adenoma

A
  • comprise 10% of gastric polyps
  • almost always occur with FAP or chronic gastritis with atrophy and intestinal metaplasia
  • male:female=3:1 and incidence increases with age
  • usually solitary and <2cm but all exhibit some dysplasia
  • 30% harbor carcinoma and lesions >2cm are concerning
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29
Q

Gastric adenocarcinoma–2 types

A
  • More than 90% of gastric malignancies are adenocarcinomas
  • divided into intestinal and diffuse–have different risk factors, genetic perturbations and clinical and pathologic presentations
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30
Q

Epidemiology of gastric adenocarcinoma–incidence

A
  • distribution widely variable
  • Japan, Chile, Costa Rica, and Eastern Europe=20x more than North America and N. Europe
  • The U.S. incidence decreased 85% in the 20th century bc of decreases in the intestinal form that is associated with atrophic gastritis
  • responsible for <2.5% of all cancer deaths in US
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31
Q

Environmental factors that play a role in gastric adenocarcinoma

A
  • H. pylori infections
  • Diet also influences risk
  • dereased consumption of carcinogens (N-nitroso compounds and bento [a] pyrene, associated with some forms of food preservation and increased intake of antioxidants in green leafy vegetables and fruits reduce gastric cancer incidence
32
Q

role of partial gastrectomy (e.g. for PUD) in gastric adenocarcinoma

A

-increases risk for adenocarcinoma by permitting bile reflux and the development of chronic gastritis

33
Q

Pathogenesis of gastric adenocarcinoma

A
  • Loss of intercellular adhesion is a key step in oncogenesis, particularly of DIFFUSE gastric cancer
  • germline mutations in the CDH1 gene encoding E-cadherin are associated with familial gastric carcinomas and also occur in 50% of sporadic lesions
34
Q

INTESTINAL-TYPE gastric cancers pathogenesis

A

-associated with FAP, mutations in proteins that associate with E-cadherin (e.g., B-catenin), TGFBRII, BAX, IGFRII, and p16/INK4a

35
Q

In both types of gastric cancer associated with H. pylori infections (diffuse and intestinal-type), what influences risk for development of cancer?

A
  • immune response gene polymorphisms

- p53 mutations are also present in the majority of sporadic cancers of both types

36
Q

What part of the digestive tract/stomach is more commonly involved in gastric cancers? order of involvement?

A

-Antrum>lesser curvature>greater curvature

37
Q

Tumors with INTESTINAL morphology

A

-form bulky exophytic tumors composed of glandular structures; these develop from precursor lesions, including flat dysplasia and adenomas

38
Q

Tumors with DIFFUSE INFILTRATIVE pattern of growth tend to be

A

-composed of SIGNET-RING CELLS (intracellular mucin vacuoles push the nucleus to the periphery) that are discohesive and do not form glands–also tend to induce a fibrous desmoplastic response

39
Q

precursor lesions for gastric adenocarcinomas

A
  • no identified precursor lesions

- gros correlate to these tumors is a rigid thickened gastric wall termed linitus plastica (“leather bottle”)

40
Q

Clinical features of gastric carcinoma

A
  • insidious disease
  • early symptoms: resemble those for chronic gastritis—dysphagia, dyspepsia, and nausea
  • Advanced stages=weight loss, anorexia, altered bowel habits, anemia, and hemorrhage
41
Q

Prognosis of gastric carcinoma

A
  • depends on DEPTH OF INVASION and the EXTENT OF NODAL OR DISTANT METASTASES
  • 5yr survival of early gastric cancer after resection is >90% even with nodal spread
  • advanced gastric cancer 5yr survival <20%
  • overall 5 yr survival in US is 30%
42
Q

Lymphoma–extranodal lymphomas arise where?

A

-can arise in any tissue but do so most commonly in GI tract and especially in stomach

43
Q

Lymphoma presentations

A

-dsypepsia and epigastric pain; hematemesis, melon or weight loss can also occur

44
Q

GI lymphomas

A
  • aka mucosa-associated lymphoid tissue or MALTOMAS
  • make up 5% of gastric malignancies
  • most are marginal zone B-cell lymphomas
  • smaller fraction of primary GI lymphomas are large B-cell lymphomas
45
Q

Pathogenesis of Extranodal marginal B-cell lymphomas

A
  • arise at sites of chronic inflammation
  • in stomach, associated with chronic H. pylori infection
  • antibiotic treatment and H. pylori eradication can induce durable tumor regression
46
Q

Antibiotic resistant tumors harbor what kind of genetics??

A
  • t (11;18) translocation!!!

- t (1;14) and t(14;18) translocations are less common but are predictive for response failure!

47
Q

t(11;18) translocation–what does it do?

A

-links the apoptosis inhibitor 2 gene (API2 on chromosome 11) with the “mutated in MALT lymphoma gene” (MLT on chromosome 18)

48
Q

What does the t(14;18) translocation do?

A

-increases MLT!!

49
Q

What does the t(1:14) translocation do?

A

-increases BCL-10 expression!

50
Q

Each of the translocations (11;18), (1:14); (14:18) leads to what?

A

-constitutive NF-kB transcription factor activation, promoting B-cell growth and survival

51
Q

With time, these MALTomas can transform into

A

-the more aggressive diffuse large B cell lymphomas, often associated with inactivation of p53 and/or p16 tumor suppressor gene

52
Q

Morphology of B-cell lymphomas (MALTomas)–microscopic

A
  • dense infiltrate of atypical lymphocytes in the lamina propria
  • focal invasion of the mucosal epithelium forms diagnostic lymphoepithelial lesions
  • Markers are the same as for other mature B-cell tumors
53
Q

Carcinoid tumor

A
  • carcinoma like
  • arises from diffusely distributed endocrine cells
  • referred to as well-differentiated neuroendocrine tumors
  • Most arise in the gut (lungs are second in frequency)
  • 40% occur in small intestine
  • cells of origin in the GI tract are responsible for hormone secretion that coordinate gut function
54
Q

Gastric carcinoid tumors are associated with

A

-endocrine cell hyperplasia, autoimmune chronic atrophic gastritis, MEN-I, and Zollinger-Ellison synrome

55
Q

Endocrine cell hyperplasia is linked to?

A

-proton pump inhibitor therapy

56
Q

Carcinoid tumor vs. carcinoma course

A

-carcinoid tumors follow a more indolent course than most carcinomas

57
Q

Gross morphology of carcinoid tumors

A
  • yellow-tan intramural or submucosal masses forming small polypoid lesions
  • An intense desmoplastic response makes them firm and can cause bowel obstruction
58
Q

Microscopic morphology of carcinoid tumos

A
  • tumors range from islands to sheets of uniform cohesive cells with scant granular cytoplasm and oval, stippled nuclei
  • cells are typically positive for neuroendocrine markers like chromogranin A and synaptophysin
59
Q

Clinical features of Carcinoid tumors

A
  • peak incidence=6th decade
  • usually indolent, slow growing malignancies
  • symptoms are a fnx of hormones produced
60
Q

Ileal carcinoid tumors secrete

A

-vasoactive products that manifest with cutaneous flushing, bronchospasm, increased bowel motility, and right sided cardiac valve thickening—carcinoid syndrome!!

61
Q

Incidence of carcinoid syndrome

A
  • occurs in less than 10% of patients with GI carcinoid due to hepatic metabolism of secreted products
  • presence of syndrome is usually associated with bulky hepatic metastatic disease
62
Q

The most important prognostic factor for GI carcinoid tumors is what??

A

-the primary site of the tumor!

63
Q

Prognosis of FOREGUT carcinoid tumors

A
  • esophagus, stomach and duodenum

- RARELY metastasize and are are cured by resection

64
Q

Midgut carcinoids

A
  • jejunum and ileum

- usually multiple and aggressive!!

65
Q

Hindgut tumors

A
  • only found incidentally

- includes appendiceal carcinoids, colonic carcinoids and rectal carcinoids

66
Q

Appendiceal carcinoid tumor

A
  • usually found at the tip

- less than 2 cm and usually benign

67
Q

Colonic carcinoids

A

-can be large and metastasize

68
Q

Recta carcinoids

A

-can secrete polypeptide hormones and/or cause pain but usually do NOT metastasize!!

69
Q

Gastrointestinal stromal tumor

A
  • aka GIST
  • most common GI mesenchymal tumor
  • more than half are in the stomach
70
Q

Epidemiology of GIST

A
  • peak age of Dx=6th decade

- incidence is increased in patients with NF type 1 and in children (usually females) with Carney triad!!!

71
Q

Carney triad

A

-non hereditary syndrome with GIST, paragangliomas and pulmonary chondromas

72
Q

Pathogenesis of GIST

A
  • arises from interstitial cells of Cajal (pacemakers for gut peristalsis) in muscular propria
  • 75-80% of all GISTs contain oncogenic GoF mutations in the gene coding for tyrosine kinase c-KIT (stem cell factor receptor)
  • 8% have activating platelet-derived growth factor receptor-a (PDGFRA) mutations
  • Constitutive tyrosine kinase activity leads to downstream activation of RAS and PI3K/AKT pathways promoting tumor cell proliferation and survival
73
Q

GIST WITHOUT mutated mutated c-KIT or PDGFRA

A
  • can have mutations in other genes that function in these pathways (NF1, BRAF, HRAS, or NRAS)
  • more common =mutations in genes encoding mitochondrial succinate dehydrogenase (SDH) complex proteins–may cause accumulation of succinate that dysregulates hypoxia inducible factor 1a (HIF-1a), increasing the transcription of vascular endothelial growth factor VEGF and insulin-like growth factor-1 (IGF1R) genes
74
Q

Gross morphology of GIST

A
  • usually solitary
  • well-circumscribed fleshy masses
  • can grow as large as 30cm
75
Q

Microscopic morphology of GIST

A
  • classified as either epithelioid (plump and cohesive cells) or spindle cell type
  • c-KIT expression is the most useful diagnostic marker
76
Q

Clinical features of GIST

A
  • symptoms are related to mass effects or blood loss
  • surgical resection is primary Tx for localized gastric GIST
  • Metastases are rare when tumors are <5cm but common when >10cm–usually take the form of peritoneal serial nodules or liver implants
  • spread outside abdomen is uncommon
77
Q

GIST tumors not amenable to resection can be treated with?

A

-imantinib–a tyrosine kinase inhibitor that inhibits c-KIT and PDGFRA

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

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