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DEMS > Stomach Diseases > Flashcards

Stomach Diseases Flashcards

1
Q

What slows down gastric emptying?

A

• 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

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2
Q

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

A
  • 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
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3
Q

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

A
  • Oxyntic

* pyloric

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4
Q

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

A 
• 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
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5
Q

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

A 
• Hyperplastic
		○ Increase in organ cell number
		○ Menetrier's disease
		○ Gastrinoma
			§ Producing zollinger-ellison syndrome
	• Non-hyperplastic
		○ Lymphocytic
		○ Neoplastic
		○ H pylori infection
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6
Q

What’s up with menetrier’s disease?

A 
• SUPER RARE
	• Mucous cell hyperplasia
	• Gastric acid secretion low-normal
	• Signs/symptoms
		○ Abdominal pain, weight loss, N/V, hypoalbuminemia
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7
Q

What’s up with Zollinger- Ellison syndrome?

A

• 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

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8
Q

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

A
  • Autoimmune
    • Infectious
    • Lymphocytic
    • Eosinophilic
    • Gastritis associated with systemic disease
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9
Q

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

A

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

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10
Q

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

A
  • Over 50% of the world’s population is infected
    • Most common human bacterial infection
    • Nearly EVERYBODY in developing countries has this infection
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11
Q

What about H pylori in particular is good to know?

A

• 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

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12
Q

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

A 
• 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
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13
Q

Why is H pylori associated with PUD?

A

• 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

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14
Q

When do you test for h pylori infection?

A

• 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

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15
Q

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

A 
• 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
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16
Q

What are the tests done for dx during endoscopic evaluation?

A 
• Histology
		○ Pre-pyloric biopsy
		○ High sens/spec
	• Rapid urease test
		○ CLOTest
		○ 90% sensitive, 95% specific
17
Q

How do you treat H pylori infection?

A 
• 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
Q

What are the NON H pylori causes of gastritis?

A

• 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
Q

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

A 
• The gastropathies
		○ Ethanol
		○ Nsaids (common)
		○ Stress ulceration
		○ Cocaine
		○ Bile reflux
20
Q

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

A 
• Disrupts mucosa
	• Increases acid secretion
	• Peptic ucer disease association
		○ High concentration (over 10%)
		○ High amounts of use
		○ CONCURRENT NSAID use
21
Q

What are the prostaglandin dependent gastric protective mechanisms?

A
  • Mucous layer thickness
    • Cell membrane hydrophobicity
    • Bicarbonate secretion
    • Mucosal blood flow
    • Epithelial cell migration and proliferation
22
Q

Which prostaglandin is important for protection of gastric mucosa?

A

• Prostaglandin E2

23
Q

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

A
  • COPD
    • Cirrhosis
    • Chronic renal failure
    • Post-transplantation
    • smokers
24
Q

Where might you see stress ulcers

A

• 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
Q

What are the complications of peptic ulcer disease?

A

• 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
Q

What is the treatment for PUD?

A 
• PPI therapy
		○ Ulcer healing after 4-8 weeks
	• Test for and treat H pylori
	• Avoid risk factors
		○ NSAID use, smoking
27
Q

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

A
  • Polyps
    • Adenocarcinoma
    • Stromal tumors
    • Neuro-endocrine tumors
    • lymphoma
28
Q

What are the benign type gastric polyps?

A

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

29
Q

What is the 2nd most cancer world-wide?

A
  • Gastric adenocarcinoma
    • 2nd most common cause of death from cancer world wide
    • Incidence decreasing in developed countries
30
Q

What is linitis plastica?

A

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
Q

What is GIST?

A

• 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
Q

What is up with gastric carcinoid?

A 
• 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
Q

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

A

• 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

DEMS (30 decks)

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