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39 Cards in this Set
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Epigastric pain, nausea and vomiting
Overt hematemesis, melena and significant blood loss may occur especially in alcoholics |
Acute gastritis an Acute mucosal inflammatory process usually of a transient nature, often associated with hemorrhage or erosion of superficial mucosa
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What are the risk factors for acute gastritis?
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-Severe burn (Curling ulcer)-hypovolemia leads to decreased blood supply
-NSAIDs (Decreased PGE) -Heavy drinking. -Chemo -Cushing ulcer: Increased intracranial pressure |
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Although the pathogenesis of acute gastritis is not fully known some of the things that occur are
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Increased acid production with back diffusion
Decreased production of bicarbonate buffer Reduced blood flow Disruption of mucus layer Direct damage to epithelium Regurgitation of detergent bile acids and lysolecithins from duodenum Decreased production of prostaglandins |
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An ulcer than can develop as a complication of acute gastritis is
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• Acute Gastric Ulcerations,Also called stress ulceration. Common in hospitalized patients
1 to 4 % of these may lead to significant hemorrhage requiring transfusions There is a tendency to heal after the underlying condition causing hospitalization is cured |
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What is the morphology of acute gastric ulcers?
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Multiple, small usually <1cm, sharp punched out ulcers occurring anywhere in the stomach
Adjacent mucosa and rugal folds normal Base is dark brown due to digestion of extruded blood |
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acute gastric ulcers morphology presents as
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Abrupt lesions in the mucosa, may extend up to muscularis mucose (erosions) or deeper (ulcerations)
Absence of thrombosed vessels in the base |
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Chronic gastritis is divided into 2 types
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Chronic autoimmune gastritis and chronic H pylori gastritis.
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Patient presents with megaloblastic anemia due to lack of instrinsic factor. Examination reveals atrophy of the mucosa with epithelial metaplasia. Achlorhydria with increased gastrin levels and antral G cell hyperplasia is observed
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Chronic autoimmune gastritis due to autoimmune destruction of parieral cells in the body and funds of stomach
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Chronic H Pylori gastritis can present in 2 ways
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1. Antral – type with high acid production (despite low serum gastrin), risk of duodenal ulcer (low production of IL-1β as part of organism-host interaction) –Most common
2. Multifocal diffuse type leading to multifocal atrophic gastritis – low production of acid, increased risk of gastric carcinoma (increased production of IL-1β) – Less common |
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How does chronic H pylori gastritis present?
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Present in 90% of patients presenting with antral chronic gastritis. Epigastric ab pain, with nausea, vomiting, abdominal pain, bloating, anemia, weight loss and/or hypochlorhydria
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What are the diagnostic tests to find H pylori chronic gastritis?
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1. Noninvasive – serologic test for antibodies, fecal bacteria detection and urea breath test
2. Invasive – Biopsy with visualization of the organism on histology, bacterial culture, rapid urease test (usually Clo-test), and polymerase chain reaction (PCR) |
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what are the complications of chronic gastritis H pylori?
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include peptic ulcer disease, gastric carcinomas and lymphomas
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Autoimmune gastritis is associated to
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diseases like Hashimoto thyroiditis, Addison disease and type I diabetes. In contrast to other autoimmune diseases there is no known linkage to specific HLA alleles.
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Peptic ulcer disease is a
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Solitary lesions usually < 4 cm, located in GI tract exposed to action of gastric acid / pepsin secretions
Location in decreasing order of frequency: Duodenum first portion Stomach, usually antrum GE junction Margins of gastrojejunostomy |
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What type of ulcers are caused by H pylori?
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Duodenal ulcers
Gastric ulcer |
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Duodenal ulcer presents with
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epigastric pain that improves with meals. Endoscopy shows ulcer with hypertrophy of brunner glands.
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What is the complication of duodenal ulcers?
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Rupture leading to bleeding from the gastroduodenal artery or acute pancreatitis.
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Gastric ulcer presents with
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epigastric pain that worsen with meals. Ulcers is located on the lesser curvature of the antrum
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Gastric ulcer complication
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rupture carries risk of bleeding from the left gastric artery.
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Which ulcers are associated to cancer?
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Duodenal ulcers are almost never malignant. However gastric ulcers can be caused by gastric carcinomas.
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What is the apperance of benign peptic ulcers?
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small, sharply demarcated (punched out) surrounded by radiating folds of mucosa
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How do malignant ulcers look like?
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large, irregular with heaped up margins.
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Gastric carcinoma is a malignant proliferation of surface epithelial cells (adenocarcinoma) which is classified into
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intestinal and diffuse types
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Gastric carcinoma type most common
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intestinal type. Age – 55 yrs, M:F = 2:1Presents as large, irregular ulcer with heaped up margins and involves the lesser curvature of the antrum like gastric ulcers.
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Intestinal type gastric carcinoma risk factors include
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intestinal metaplasia (due to H pylori and autoimmune gastritis), nitrosamines in smoked foods and blood type A
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Diffuse type gastric carcinoma is characterized by
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Age – 48 yrs, M:F = 1:1. signet ring cells that diffusely infiltrate the gastric wall-thickening of the stomach walls due to desmoplasia. Diffuse type not associated to intestinal type risks.
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How does gastric carcinoma present?
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Late with weight loss, ab pain. anemia, and early satiety. Rarely but may present with acanthosis nigricans or Leser trelat sign
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Gastric carcinoma metastasis
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commonly the liver. Intestinal type goes to periumbilical region.
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Extranodal marginal zone lymphoma also know as MALT lymphoma is associated with
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chronic gastritis and H. pylori infection and many cases can be effectively treated with antibiotics.
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MALT lymphoma translocations converge on an oncogenic pathway that involves
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the nuclear factor k-light-chain-enhancer of activated B cells (NF-kB), a transcription factor that promotes B cell growth and survival. The type of translocation affects the ability of antibiotics to effectively treat MALT lymphoma.
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With more genetic alterations, MALT lymphoma may evolve into
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more aggressive diffuse large B cell lymphoma
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Morphologically MALT lymphoma looks like
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Diffuse infiltration of the mucosa and submucosa with atypical lymphoid cells
Lymphoepithelial lesion – lymphocytes infiltrating the epithelium and causing its destruction MALT type is usually CD5, CD10, and CD23 negative Diffuse large B cell lymphoma |
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Slight male predominance, peak age 60 years
Arise from the interstitial cells of Cajal The majority have c-kit mutations |
Gastrointestinal stromal tumors (GIST)(mesenchymal tumors compose ~2% of gastric malignancies),
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Grossly Gastrointestinal stromal tumors (GIST) look like
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Solitary or multiple
Protrude in the lumen with an overlying attenuated mucosa or extrude out on the serosal aspect Cut surface is tan, soft to firm, hemorrhage and necrosis are seen in large tumors |
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Microscopic Gastrointestinal stromal tumors (GIST)
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spindle or epithelioid or a mixture of both
Immunostains for CD117 and CD34 |
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Malignant GISTS are
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larger, have mitotic activity, and usually have necrosis.
In GISTs with tumor syndromes may see hyperplasia of Cajal cells. |
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Gastrointestinal stromal tumors (GIST) have modifications on c-KIT and PDGFRA (receptor for platelet derived growth factor alpha) mutation which lead to
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uncontrolled activation of tyrosine kinase with downstream signaling leading to uncontrolled proliferation and inhibition of apoptosis
Imatinib mesylate - a tyrosine kinase inhibitor is effective treatment for most GISTs. Other tyrosine kinase inhibitors are also available to treat GISTs. |
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Gastrointestinal stromal tumors (GIST) lacking c-KIT mutation are less likely to
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to be immunoreactive to CD117).
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Gastrointestinal stromal tumors (GIST) May be part of tumor syndromes, such as
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Carney's triad (gastric GIST, paraganglioma and pulmonary chondroma), or neurofibromatosis type 1, especially in women with Carney’s triad, cases in tumor syndromes may occur in younger age groups.
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