GiniClust: detecting rare cell types from single-cell gene ...
STOMACH Cell types:
description
Transcript of STOMACH Cell types:
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STOMACH Cell types:
Mucosal surface & foveolae: Surface foveolar cells - secrete mucous
Mucous neck cells - progenitor cells Glands:
Mucous cells - secrete mucous & pepsinogen II
Parietal cells - secrete HCl & IFChief cells - secrete pepsinogen I & IIEndocrine cells - secrete peptide & amine
hormones
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• Congenital Anomalies
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CONGENITAL ANOMALIES
Diaphragmatic Hernia:
Defect in diaphragm, away from esophageal hiatus
Portions of stomach & SI herniate pulmonary hypoplasia & respiratory impairment
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CONGENITAL ANOMALIES
Heterotopic rests:
Location: Anywhere in the GITMC: Pancreatic & gastricS/S: Usually asymptomatic but may cause
ulceration
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CONGENITAL ANOMALIES
Congenital Hypertrophic Pyloric Stenosis:CHiPs
M > F (3:1), 1 in 200 infant males, multifactorial inheritance
Cause: Hypertrophy & hyperplasia of circular muscle of pylorus
regurgitation, projectile non- bilious vomiting commences at 2 - 6 wks of age
May be due to defective autonomic regulation Dx: Visible peristalsis & palpable mass in RUQ Tx: Pyloromyotomy is curative
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ACUTE GASTRITIS
Other Causes:
Ingestion of strong acids or alkaliCa chemotxRadiationIschemia & shockNGTs
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- Reduced mucosal blood flow - Direct damage to mucosal epithelium
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ACUTE GASTRITIS
Clinically:
Asymptomatic to epigastric pain of varying severity, up to acute abdomen w/ hematemesis & shock
major cause of massive hematemesis (esp. alcoholics)
Common in those who take daily aspirin for RA
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ACUTE GASTRITIS
Morphology:
Mucosal edema & congestion, PMN infiltration (milder cases)
Erosions (not deeper than muscularis mucosa) & hges (acute erosive gastritis)
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/ dysplasia
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CHRONIC GASTRITIS
Pathogenesis:
Autoimmune: Abs to parietal cells parietal cell destruction ( HCl & IF)
Environmental: Chronic infection by H. pylori Alcohol, tobacco, radiation, bile reflux, Crohn’s
disease, uremia, gastric atony
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CHRONIC GASTRITIS
Gross:Red mucosa (thickened or flattened)
Autoimmune fundus & body H pylori antrum & bodyBile reflux antrum
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CHRONIC GASTRITIS
Histology:
Lympho & plasma cell infiltrates in LP (superficial or involving entire mucosal thickness)
Others:
Regenerative atypia Intestinal metaplasia Atrophy Dysplasia
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CHRONIC GASTRITIS
Clinical: Mild abdominal discomfort, nausea,
vomiting, hypochlorhydria
Autoimmune gastritis: Hypo- / a- chlorhydria, hypergastrinemia, ~
10% overt PA, long-term risk of Ca is 2-4%
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Helicobacter pylori
~ 50% of asymptomatic American adults > 50 yrs are infected
Dx: CLO test
Diseases Association:
Chronic gastritis PUD Gastric ca/ lymphoma
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PEPTIC ULCERS
Usually solitary ~ 0.6 - 4 cm MC: duodenum & antrum Ratio of duodenal: gastric PU is ~ 4 : 1~ 4 M Americans have PU Life-time incidence in USA is 10% for men
& 4% for women
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PEPTIC ULCERS
Clinical:
Epigastric pain 1-3 hrs PC & worse at night; nausea; vomiting; belching, weight loss
Complications:
Hemorrhage - 25% of ulcer deaths
Perforation - ~ 2/3 of ulcer deaths
Obstruction - causes severe crampy abdominal pain
Malignant transformation extremely rare
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HYPERTROPHIC GASTROPATHTY
Zollinger-Ellison Syndrome:
Hypertrophic rugal folds Parietal cell hyperplasia Peptic ulcers Markedly elevated serum gastrin levels Caused by a gastrin secreting tumor
(gastrinoma) Pancreas is the usual primary site
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HYPERTROPHIC GASTROPATHY
Menetrier’s disease:
Affects men in 4th to 6th decades Epigastric pain, anorexia, vomitting, wt. loss &
peripheral edema Diffuse rugal hypertrophy Marked foveolar hyperplasia, smooth muscle
proliferation in LP, glandular atrophy Hypochlorhydria Protein-losing enteropathy
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GASTRIC POLYPS
Mucosal masses projecting above level of surrounding mucosa
> 90% non-neoplastic polyps - no malignant potential
Hyperplastic polyps: MC type of gastric polyp Small sessile polyps May be multiple No dysplasia no malignant potential
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GASTRIC POLYPS (CONT.)
Adenomatous polyps (Adenomas): May be sessile or pedunculated Usually solitary May reach 3-4 cm in dia Contain proliferating dysplastic epithelium Are true neoplasms Up to 40% contain a focus of ca at time of biopsy Patients with autoimmune gastritis or colonic polyposis Syndromes have an increased incidence Gastric polyps need to be biopsied
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GASTRIC CARCINOMA
Worldwide distribution variableUS 2.5% of all Ca deaths5-6 fold decline in incidence over last 70
yrs (for unknown reasons)
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GASTRIC CARCINOMA Classification:
According to Depth of invasion: Early Gastric Ca:
Confined to mucosa & submucosa Very good prognosis - ~ 90% 5-year survival, even w/
limited LN spread Advanced Gastric Ca:
Extended beyond submucosa Spread by local invasion, lymphatics, blood (to liver,
lungs & bone) Virchow node Bilateral ovarian metastases - Krukenberg Poor prognosis (<15% 5-year survival)
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GASTRIC CARCINOMA Classification:
According to Gross Pattern: Exophytic Flat/depressed Excavated (ulcerative)
According to Histologic Pattern:Intestinal type, glandular, expansile Diffuse type, “signet ring cell”, infiltrating
(linitis plastica)
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GASTRIC CARCINOMA Classification: Pathologic stage is the most important
prognostic indicator
Less Common Gastric Tumors:Lymphomas (~ 5%) Stromal tumors (~ 2%) Carcinoid tumors (rare)
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GASTRIC CARCINOMA
Risk Factors: Diet: Nitrites (food preservatives), smoked &
salted foods, deficiency of fresh fruits & vegetables
Host Factors: chronic gastritis (autoimmune & H. pylori), adenomatous polyps, partial gastrectomy
Genetic Factors: only ~ 4% of patient’s w/ gastric CA have a family Hx
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