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Flashcards in Stomach Diseases Deck (33)
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What slows down gastric emptying?

• Decrease in pH (acid)
○ Does this mean that increased H+ pump activity in H pylori also slows down the movement, pre-disposing to stuff sitting too long on the mucosa causing problems?
• Fatty acids and caloric density
• Increase in osmolality


Where do the gastric progenitor cells sit in the gastric pit?

• Progenitor zone
• Foveolus = gastric pit
• The progenitor zone is pretty high up, above the neck, but below the surface
• The progenitor cells can go "up" and become surface mucous cells OR "down" becoming the specialized cells like G, D, ECL, or EC cells


What are the two different types of normal glands in the stomach?

• Oxyntic
• pyloric


What cellular receptors on the parietal cell will influence acid secretion?

• M3 receptor
○ Ach straight from vagus nerve
• CCK-2 receptor
○ Gastrin from the Gastrin cells
○ Through the blood vessel, more of an endocrine signaling event
• SSTR2 receptor
○ SST from the D cell
• H2 receptor
○ Histmaine from the ECL cell


Large gastric fold syndromes can be split into what two categories?

• Hyperplastic
○ Increase in organ cell number
○ Menetrier's disease
○ Gastrinoma
§ Producing zollinger-ellison syndrome
• Non-hyperplastic
○ Lymphocytic
○ Neoplastic
○ H pylori infection


What's up with menetrier's disease?

• Mucous cell hyperplasia
• Gastric acid secretion low-normal
• Signs/symptoms
○ Abdominal pain, weight loss, N/V, hypoalbuminemia


What's up with Zollinger- Ellison syndrome?

• Caused by gastrinoma
• Neuroendocrine tumor in pancreas or duodenum
• Gastrin secreted leading to hyperplasia of parietal cells
• Signs/symptoms:
○ Chonic diarrhea, abdominal pain and peptic ulcers


What are the different causes of gastritis to be aware of?

• Autoimmune
• Infectious
• Lymphocytic
• Eosinophilic
• Gastritis associated with systemic disease


You are given an endoscopic picture of a stomach that has no ruggae. What are you thinking?

• Autoimmune atrophic gastritis
• Results from an attack on parietal cells
○ Achlorhydria
○ Pernicious anemia
• Can develop intestinal metaplasia
• Carries a higher risk of gastric cancer


How many people in the world are infected with H pylori?

• Over 50% of the world's population is infected
• Most common human bacterial infection
• Nearly EVERYBODY in developing countries has this infection


What about H pylori in particular is good to know?

• Acidophile, likes the acidic environment
• Spiral shape with multiple flagella
○ Move through the gastric mucous layer
○ Colonize surface epithelium (neutral pH)
○ Urea will end up neutralizing H+
○ Alkaline ammonia + CO2 is the breakdown product
○ This reaction forms the basis of routine H pylori testing
*Virulence factors of bacteria:
• Rarely penetrates epithelium but causes robust inflammatory response
• Injects proteins (CagA)
○ Decreased cell adhesion - associated with both gastric and duodenal ulcers
○ Linked to cancer
• VacA
○ Exotoxin - puts bacterial pores in the membrane of T cells
○ Inhibits host response


H pylori infection leads only to gastritis, no other disease states. True or false?

• There is a wide spectrum of disease associated with H pylori infection
○ Due to the bacterial strain and poorly understood host/environment characteristics
• Asymptomatic infection
• Gastritis (common)
• Peptic ulcer disease (common)
• Neoplasia
○ Gastric cancer and lymphoma


Why is H pylori associated with PUD?

• PUD = peptic ulcer disease
• High prevalance of H pylori in patients with PUD
• H pylori infection precedes ulcer
• H pylori proteins cause inflammation, apoptosis, disrupt cell adhesion
○ Essentially breakdown the tissue of the stomach and allow for erosion due to acidic environment and chronic inflammatory cell action
• Cure of infection leads to cure of ulcer


When do you test for h pylori infection?

• Active PUD
• History of PUD without prior treatment
• Gastric neoplasia
• Uninvestigated dyspepsia
• Consider:
○ FDR with gastric cancer
○ Immigrant from region with high prevalance of gastric cancer


What are the non-endoscopic ways to dx h pylori infection?

• Blood antibody test
○ Shows any prior infection
○ 85% sensitivity and 79% sensitivity
• Stool antigen test
○ Identify ACTIVE infection
○ Accuracy decreased by PPI
○ This has high sensitivity and specificity
• Urea breath test
○ ID active infection
○ Accuracy decreased by PPI
○ This has high sensitivity and specificity


What are the tests done for dx during endoscopic evaluation?

• Histology
○ Pre-pyloric biopsy
○ High sens/spec
• Rapid urease test
○ CLOTest
○ 90% sensitive, 95% specific


How do you treat H pylori infection?

• Triple therapy
○ PPI + 2 antibiotics
§ 14 days
○ Clarithromycin and amoxicillin
• Quadruple therapy
○ PPI + bismuth + 2 antibiotics
§ 14 days
○ Metronidazole and tetracycline
• Sequential therapy
○ PPI + amoxicillin (7 days)
○ THEN PPI + clarithromycin + metronidazole (another 7 days)
○ Through stool antigen, which is the test for ACTIVE infection


What are the NON H pylori causes of gastritis?

• The super uncommon ones that appear in immunosuppressed people
○ CMV, candidiasis, aspergillosis, strongyloides
• Eosinophilic causes
○ Can have ulceration
○ Early satiety, nausea and vomiting
○ Increased eos in the blood
○ Rare, and unknown cause


What might cause gastroduodenal injury in the absence of significant inflammation?

• The gastropathies
○ Ethanol
○ Nsaids (common)
○ Stress ulceration
○ Cocaine
○ Bile reflux


What does ethanol do to the stomach to predispose it to disease?

• Disrupts mucosa
• Increases acid secretion
• Peptic ucer disease association
○ High concentration (over 10%)
○ High amounts of use


What are the prostaglandin dependent gastric protective mechanisms?

• Mucous layer thickness
• Cell membrane hydrophobicity
• Bicarbonate secretion
• Mucosal blood flow
• Epithelial cell migration and proliferation


Which prostaglandin is important for protection of gastric mucosa?

• Prostaglandin E2


There is an increase in PUD associated with what other chronic disease states?

• Cirrhosis
• Chronic renal failure
• Post-transplantation
• smokers


Where might you see stress ulcers

• In ICU patients
○ CNS injury (cushings ulcer with is overactive vagal nerve)
○ Burns (curling's ulcer
○ Prolonged mechanical ventilation (over 48 hours)
○ Coagulopathy
• In the fundus and body of the stomach
• In context of impaired mucosal protection
• In context of increased acid secretion


What are the complications of peptic ulcer disease?

• Anemia, either acute or chronic
○ Iron deficiency from chronic blood loss
○ Bleeding looks like hematemesis or melena
• Perforation
○ Acute abdominal pain
○ Peritonitis (super tender, NOT soft abdomen)
• Gastric outlet obstruction
○ Nausea, vomiting, abdominal pain


What is the treatment for PUD?

• PPI therapy
○ Ulcer healing after 4-8 weeks
• Test for and treat H pylori
• Avoid risk factors
○ NSAID use, smoking


What are the types of gastric neoplasms we should know about?

• Polyps
• Adenocarcinoma
• Stromal tumors
• Neuro-endocrine tumors
• lymphoma


What are the benign type gastric polyps?

• Fundic gland polyps
○ Associated with chronic PPI use
• Hyperplastic polyps
○ Rare malignant potential (over 1cm)


What is the 2nd most cancer world-wide?

• Gastric adenocarcinoma
• 2nd most common cause of death from cancer world wide
• Incidence decreasing in developed countries


What is linitis plastica?

Linitis plastica, also known as Brinton's disease or leather bottle stomach, is a morphological variant of diffuse (or infiltrating) stomach cancer.

Causes of linitis plastica could be lye ingestion or metastatic infiltration of the stomach, particularly breast and lung carcinoma.[1] It is not associated with H. pylori infection or chronic gastritis. The risk factors are undefined, except for rare inherited mutations in E-cadherin, which are found in about 50% of diffuse-type gastric carcinomas.[1]


What is GIST?

• GI stromal tumor
• Most common gastric mesenchymal tumor (60%)
• Leiomyomas are NOT GISTs
• Worse prognosis than other GI stromal tumors
Cell of origin
• Interstitial cell of cajal (pacemaker)
• Positive for c-kit (CD117), mutation in transmembrane receptor tyrosine kinase
10%-30% of cases become malignant
• Surgery
• Imatinib (Gleevac)
○ Small molecule RTK inhibitor


What is up with gastric carcinoid?

• Neuroendocrine tumor
• Found in fundus/body
• Predisposing factors
○ Autoimmune atrophic gastritis
§ Hypochlorhydria leads to elevated gastric and stimulation of ECL cells
○ ZE syndrome/gastrinoma
§ MEN1
§ Elevated gastrin which leads to increased ECL histamine release
○ Sporadic
§ The more dangerous kind actually


What is the evidence for H pylori playing a role in MALT lymphoma?

• Low grade B-cell lymphomas arise in gastric MALT
○ Stimulated by H pylori infection
• Eradication of H pylori reservoir can sometimes induce regression of lymphoma