Path 12 Ex 4

Front 1

Epigastric pain, nausea and vomiting
Overt hematemesis, melena and significant blood loss may occur especially in alcoholics

Back 1

Acute gastritis an Acute mucosal inflammatory process usually of a transient nature, often associated with hemorrhage or erosion of superficial mucosa

Front 2

What are the risk factors for acute gastritis?

Back 2

-Severe burn (Curling ulcer)-hypovolemia leads to decreased blood supply
-NSAIDs (Decreased PGE)
-Heavy drinking.
-Chemo
-Cushing ulcer: Increased intracranial pressure

Front 3

Although the pathogenesis of acute gastritis is not fully known some of the things that occur are

Back 3

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

Front 4

An ulcer than can develop as a complication of acute gastritis is

Back 4

• 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

Front 5

What is the morphology of acute gastric ulcers?

Back 5

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

Front 6

acute gastric ulcers morphology presents as

Back 6

Abrupt lesions in the mucosa, may extend up to muscularis mucose (erosions) or deeper (ulcerations)
Absence of thrombosed vessels in the base

Front 7

Chronic gastritis is divided into 2 types

Back 7

Chronic autoimmune gastritis and chronic H pylori gastritis.

Front 8

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

Back 8

Chronic autoimmune gastritis due to autoimmune destruction of parieral cells in the body and funds of stomach

Front 9

Chronic H Pylori gastritis can present in 2 ways

Back 9

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

Front 10

How does chronic H pylori gastritis present?

Back 10

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

Front 11

What are the diagnostic tests to find H pylori chronic gastritis?

Back 11

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)

Front 12

what are the complications of chronic gastritis H pylori?

Back 12

include peptic ulcer disease, gastric carcinomas and lymphomas

Front 13

Autoimmune gastritis is associated to

Back 13

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.

Front 14

Peptic ulcer disease is a

Back 14

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

Front 15

What type of ulcers are caused by H pylori?

Back 15

Duodenal ulcers
Gastric ulcer

Front 16

Duodenal ulcer presents with

Back 16

epigastric pain that improves with meals. Endoscopy shows ulcer with hypertrophy of brunner glands.

Front 17

What is the complication of duodenal ulcers?

Back 17

Rupture leading to bleeding from the gastroduodenal artery or acute pancreatitis.

Front 18

Gastric ulcer presents with

Back 18

epigastric pain that worsen with meals. Ulcers is located on the lesser curvature of the antrum

Front 19

Gastric ulcer complication

Back 19

rupture carries risk of bleeding from the left gastric artery.

Front 20

Which ulcers are associated to cancer?

Back 20

Duodenal ulcers are almost never malignant. However gastric ulcers can be caused by gastric carcinomas.

Front 21

What is the apperance of benign peptic ulcers?

Back 21

small, sharply demarcated (punched out) surrounded by radiating folds of mucosa

Front 22

How do malignant ulcers look like?

Back 22

large, irregular with heaped up margins.

Front 23

Gastric carcinoma is a malignant proliferation of surface epithelial cells (adenocarcinoma) which is classified into

Back 23

intestinal and diffuse types

Front 24

Gastric carcinoma type most common

Back 24

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.

Front 25

Intestinal type gastric carcinoma risk factors include

Back 25

intestinal metaplasia (due to H pylori and autoimmune gastritis), nitrosamines in smoked foods and blood type A

Front 26

Diffuse type gastric carcinoma is characterized by

Back 26

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.

Front 27

How does gastric carcinoma present?

Back 27

Late with weight loss, ab pain. anemia, and early satiety. Rarely but may present with acanthosis nigricans or Leser trelat sign

Front 28

Gastric carcinoma metastasis

Back 28

commonly the liver. Intestinal type goes to periumbilical region.

Front 29

Extranodal marginal zone lymphoma also know as MALT lymphoma is associated with

Back 29

chronic gastritis and H. pylori infection and many cases can be effectively treated with antibiotics.

Front 30

MALT lymphoma translocations converge on an oncogenic pathway that involves

Back 30

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.

Front 31

With more genetic alterations, MALT lymphoma may evolve into

Back 31

more aggressive diffuse large B cell lymphoma

Front 32

Morphologically MALT lymphoma looks like

Back 32

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

Front 33

Slight male predominance, peak age 60 years
Arise from the interstitial cells of Cajal
The majority have c-kit mutations

Back 33

Gastrointestinal stromal tumors (GIST)(mesenchymal tumors compose ~2% of gastric malignancies),

Front 34

Grossly Gastrointestinal stromal tumors (GIST) look like

Back 34

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

Front 35

Microscopic Gastrointestinal stromal tumors (GIST)

Back 35

spindle or epithelioid or a mixture of both
Immunostains for CD117 and CD34

Front 36

Malignant GISTS are

Back 36

larger, have mitotic activity, and usually have necrosis.
In GISTs with tumor syndromes may see hyperplasia of Cajal cells.

Front 37

Gastrointestinal stromal tumors (GIST) have modifications on c-KIT and PDGFRA (receptor for platelet derived growth factor alpha) mutation which lead to

Back 37

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.

Front 38

Gastrointestinal stromal tumors (GIST) lacking c-KIT mutation are less likely to

Back 38

to be immunoreactive to CD117).

Front 39

Gastrointestinal stromal tumors (GIST) May be part of tumor syndromes, such as

Back 39

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.