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GI > Benign Gastric Disorders > Flashcards

Benign Gastric Disorders Flashcards

1
Q

Describe morphology of H.pylori; what does it colonize?

A

Spiral shaped, microaerophilic, gram negative
bacteria
• Exclusively colonizes gastric type epithelium

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2
Q

H. pylori is Noninvasive, but

A

stimulates inflammatory and immune responses

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3
Q

What is the hallmark of H.pylori infection?

A

neutrophilic infiltration, along with lymphocytes, plasma cells, macrophages (chronic active gastritis)

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4
Q

Virulence factors of H.pylori

A

cytotoxin associated gene A [CagA]) in some

strains cause more intense inflammation, damage, complications

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5
Q

In EARLY stage H.pylori Gastritis, it is confined to_______ and will ihnibit D cell SST resulting in what?

A

confined to antrum

results in increased gastrin secration thus more acid

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6
Q

Where are ulcers present in early stage H.pylori infection?

A

duodenal ulcers

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7
Q

Chronic H. Pylori Gastritis: Late Stage
Goes to what area of stomach?
Inhibits what cell type to result in increased gastrin secration

A

Colonization and inflammation
expand to corpus/fundus
• Destruction of parietal cells
– Acid decreased → gastrin ↑

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8
Q

Where do we see ulcers in LATE stage H.pylori infection

A

Gastric ulceration

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9
Q

If H.pylori is eradicated, what happens to neutorphilic and lymphocytic infiltration?

A

If H. pylori eradicated:
– Neutrophilic infiltration resolves
– Lymphocytic infiltration may persist

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10
Q

Epidemiology of H.Pylori

A

Infects ½ of world population
• Increased in developing countries
• Increased with crowding, poverty
• Increased with age (age < 12:10% vs age > 60: 50%)

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11
Q

How and when is H.pylori aquired?

A
  • Usually acquired in infancy/childhood
  • Transmission like fecal/oral or oral/oral
  • Acquisition 1%/year after childhood
  • Declining in developed countries
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12
Q

How do you Dx H.pylori infection

A
  • Serology: Persists even after eradication (false positive)
  • Endoscopic gastric mucosa biopsy
  • Urea breath testing
  • Stool antigen testing
  • False negative with recent antibiotics or PPI therapy
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13
Q

Adverse effects of H.pylori infection

A
  • Peptic ulcer
  • Enteric infections
  • Malnutrition/iron & B12 deficiency
  • Gastric neoplasia
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14
Q

What type of gastric neoplasias

A

-Adenocarcinoma
– MALT lymphoma
– Carcinoid

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15
Q

Adverse consequences of eradication of H.pylori

A

– GERD/adenocarcinoma of esophagus
– Weight gain?
– Atopic diseases?

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16
Q

Inherited form associated with
immune response in the oxyntic
mucosa against parietal cells and
intrinsic factor (IF)

A

Autoimmune Gastritis

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17
Q

In Autoimmune Gastritis; Inherited form associated with immune response in the oxyntic mucosa against

A

parietal cells and intrinsic factor (IF)

18
Q

Pt population we usually see autoimmune gastritis in?

What type of cells inflitrate the parietal cells?

A 
• Three times more common in women
• Lymphocytic inflammation with
destruction of parietal cells
• Associated with other autoimmune
considers (Thyroid, celiac, Type I DM)
19
Q

Causes Achlorhydria (increased gastrin) and see reduced or absent IF

A

Atrophic metaplastic gastritis

20
Q

Consequences of Atrophic Metaplastic Gastritis

A
  • Those of reduced acid secretion
  • Pernicious anemia
  • Gastric cancer
  • Gastric carcinoid
21
Q 
Inflammatory destruction of normal
mucosa with replacement by
metaplastic elements (commonly
intestinal type with goblet cells)
A

Atrophic metaplastic gastritis

22
Q

Difference between Type A and Type B atrophic metaplastic gastritis

A

Type A: body and fundus
– Autoimmune
• Type B: antrum (can extend proximally)
– H. pylori (may be absent at this stage)

23
Q

Define Gastritis

A

inflammation associated mucosal injury

• Infectious, autoimmune

24
Q

Define Gastropathy

A

epithelial cell damage and regeneration with minimal or no associated inflammation
• Bile, alcohol, aspirin, NSAIDs, ischemia

25
Q

inflammation associated mucosal injury

• Infectious, autoimmune

A

Gastritis

26
Q

epithelial cell damage and regeneration with minimal or no associated inflammation
• Bile, alcohol, aspirin, NSAIDs, ischemia

A

Gastropathy

27
Q

Affects of NSAIDS on stomach

A
  • Trapped in epithelial cells
  • Uncoupling of oxidative phosphorylation
  • Reduced energy production
  • Increased cell permeability
  • Rapid cell death and superficial mucosal injury
28
Q

What is a systemic effect of NSAIDS

A

• Inhibit COX-1 prostaglandin

synthesis,

29
Q

What is the result of inhibited COX-1 prostaglandin synthesis from NSAIDS?

A 
REDUCES:
• Mucosal blood flow and oxygen delivery
• Mucin, bicarbonate, and phospholipid
secretion
• Epithelial cell proliferation and migration
30
Q

destructive breach of mucosa that extends below muscularis mucosa

A

ulcer

31
Q

destruction superficial to muscularis mucosa

A

erosion

32
Q

Prevalance and risk factors of peptic ulcer disease

A

• Prevalence of 2%
– Risk increases with age, smoking
• H. pylori associated decreasing

33
Q

NSAID/aspirin and peptic ulcer disease correlation

A 
• Among NSAID/aspirin users
– 50% develop erosions
– 25% of chronic users develop PUD
– 2-4% have complications, resulting in
100,000 hospitalizations each year in U.S.
34
Q

Three most common causes of Peptic ulcer disease

A

– Aspirin/NSAIDs
– Helicobacter pylori
– Surreptitious/unaware NSAID use

35
Q

Risk Factors for NSAID/ASA

PUD and Complications

A
  • Age > 65
  • Dose and duration of therapy
  • Prior PUD/complication
  • Concurrent use of: • Aspirin/another NSAID
  • Glucocorticoids• Anticoagulants,• Clopidogrel
  • Selective serotonin reuptake inhibitors
36
Q

Less common causes of Peptic ulcer diesease

A 
– Gastric malignancy
• Adenocarcinoma
• Lymphoma
– Viral infection (Herpes/CMV)
– Bisphosphonates
– Anastomotic ulceration (gastric bypass)
– Stress ulceration
37
Q

Rare causes of Peptic ulcer disease

A 
– Zollenger-Ellison syndrome
– Other hypersecretory states
– Crohn’s disease
– Mesenteric ischemia (incl. cocaine)
– Radiation therapy
– Treponema pallidum
– Hepatic artery infusion of 5-fluorouracil
38
Q

Complications of peptic ulcer disease

A
  • Acute GI hemorrhage
  • Chronic GI blood loss/iron deficiency anemia
  • Perforation/peritonitis/pancreatitis
  • Gastric outlet obstruction
  • Gastrointestinal fistula
  • Malabsorption/malnutrition/weight loss
  • Iatrogenic complications
39
Q

Difference and simularity between symptoms in Duodental ulcer vs gastric ulcer

A 
Chronic dyspeptic epigastric pain
– DU: 2-3 hours after meals/night
– GU: worse with meals
– Waxes/wanes over weeks
• Nausea
• Anorexia/weight loss
40
Q

Acute pain in pt with peptic ulcer is concerning because?

A

may be d/t perforation

41
Q

Below are symptoms of?
• Hematemesis (loss of 25% of total blood volume)
• Melena, red blood per rectum
(loss of 33% blood volume)
• Recurrent post-prandial vomiting(obstruction)
• Diarrhea (fistula)
• May have no symptoms

A

Peptic ulcer disease

GI (14 decks)

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