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Flashcards in Stomach Diseases Deck (33)
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1

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

2

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

3

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

• Oxyntic
• pyloric

4

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

5

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

6

What's up with menetrier's disease?

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

7

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

8

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

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

9

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

10

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

11

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)
• PRODUCE UREASE
○ 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

12

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

• 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

13

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

14

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

15

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

16

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

17

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)
• CONFIRM ERADICATION
○ Through stool antigen, which is the test for ACTIVE infection

18

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

19

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

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

20

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
○ CONCURRENT NSAID use

21

What are the prostaglandin dependent gastric protective mechanisms?

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

22

Which prostaglandin is important for protection of gastric mucosa?

• Prostaglandin E2

23

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

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

24

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

25

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

26

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

27

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

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

28

What are the benign type gastric polyps?

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

29

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

30

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]

31

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)
Histology
• Positive for c-kit (CD117), mutation in transmembrane receptor tyrosine kinase
10%-30% of cases become malignant
Treatment:
• Surgery
• Imatinib (Gleevac)
○ Small molecule RTK inhibitor

32

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

33

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