Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI Review by Minnie (she/her) > 138b/139b - Pathology of Gastric Disorders, PUD, H. Pylori > Flashcards

138b/139b - Pathology of Gastric Disorders, PUD, H. Pylori Flashcards

1
Q

Do benign gastric ulcers occur in pernicious anemia?

A

No!

  • Pernicious anemia is often caused by autoimmune destruction of parietal cells
    • ​=> decreased gastric acid
  • Any ulcer that forms in the setting of pernicious anemia should be considered for malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which stimulants of parietal cell gastric acid secretion act through the IP3/Ca2+ pathway?

A
  • ACh
    • Released when we think about food (cephalic phase) or secondary to antral distention (gastric phase)
  • Gastrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which part of the stomach is affected by H. pylori gastritis?

A

Antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the pathophysiology of diarrhea in patinets with Zollinger-Ellison syndrome

A

ZE = gastrin-secreting tumor

  • Increased HCl secretion
  • HCL spills into duodenum
    • Denatures pancreatic enzymes
      • Maldigestion of fat and protein
      • Diarrhea
    • Directly damages the small intestinal epithelium
      • Secretory diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment for Zollinger-Ellison Syndrome?

A

High dose PPI

  • Resect tumor if you can, but they can be hard to find!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the pathophysiology of chronic autoimmune gastritis

A
  • Antibodies against parietal cells and intrinsic factor
    • -> Destruction of parietal cells
  • -> Hypochlorhydria, high serum gastrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does H. pylori cause an increase in gastric acid release?

A

H. Pylori preferentially destroys D cells

  • D cells normally secrete somatostatin
    • Normally inhibits gastrin secretion from G cells
    • Results in decreased gastric acid release
  • No D cells = no brakes on gastrin secretion
    • Lots of gatrin -> lots of gastric acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the pathophysiology of H. pylori infection in the gastric epithelium

(Starting with ingestion of H. pylori)

A
  • Ingestion of H. pylori
  • H. pylori lodges into the mucus using adhesins
    • Protected from acid by urease (Urea -> CO2 + NH3)
    • NH3 is converted to NH4+ in the acidic stomach; NH4+ cloud protcts H. pylori
  • H. pylori multiplies
  • Immune response
    • Cytokine release
    • Damage to mucosa
    • H. pylori internalizes in the epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the pathophysiology of a Curling ulcer

A

Severe burns/trauma -> hypovolemia -> ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the eradication rate for H. pylori after antibiotic treatment?

A

~75% and decreasing due to abx resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most common cause of benign peptic ulcer disease?

A

H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the two subtypes of gastric adenocarcinoma?

How do you tell them apart?

A
  • Intestinal
    • Ulcer with raised borders
    • Composed of glands
  • Diffuse
    • Diffusely thickened gastric wall
    • Signet ring cells are present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List two hypertrophic gastropaties

How do you tell them apart histologically?

A
  • Menetrier disease (excess TGF-alpha)
    • Foveolar hyperplasia
  • Zollinger-Ellison syndrome (gastrin-secreting tumor)
    • Parietal cell hyperplasia

Endoscopically, both will have enlarged folds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

H. pylori typically colonizes in gastric epithelium

How, then, does it caue duodenal ulcers?

A
  • H. pylori colonization in the stomach results in increased post-prandial gastrin release, resulting in increased gastric acid
    • Due to destruction of D cells (no brakes on gastrin release)
  • Gastric acid spills into the duodenum
  • -> Gastric metaplasia
  • -> H. pylori colonizes in the gastric metaplasia in the duodenum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the effect of somatostatin on gastric acid secretion?

A

Somatostatin inhibits gastric acid secretion

  • Inhibits gastrin secretion from G cells, histamine secretion from HCL cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the pathophysiology of a Cushing ulcer

A
  • Increased intracranial pressure
  • -> Vagal stimulation
  • -> Acid production
  • -> Ulcer formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which of the following mechanisms plays an important role in the development of a gastric ulcer in a 32 year old patient with rheumatoid arthritis taking ibuprofen 800 mg three times daily for one month?

  1. Reduction in blood flow to the gastric mucosa
  2. Ion trapping and low pKa of ibuprofen
  3. Excessive production of acid induced by ibuprofen
  4. Concomitant infection with H.pylori
  5. Autoimmune damage to the gastric epithelium
A

a. Reduction in blood flow to the gastric mucosa

  • Ibuprofen is a nonselective COX inhibitor
  • -> Decreased prostaglandins production
  • -> Decreased blood flow

Ishcemic damage = nidus for ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which protein is elevated in Menetrier disease?

What endoscopic changes will occur?

Histologic changes?

Clinical signs?

A

TGF-alpha

  • Prominent gastric folds
  • Diffuse, foveolar hyperplasia
  • Weight loss, diarrhea, peripheral edema, hypoproteinemia
19
Q

Are NSAIDs more likely to cause gastric ulcers or duodenal ulcers?

A

Gastric ulcers

  • But, H. pylori is the most ocmmon cause of both gastric and duodenal ulcers
20
Q

What percent of patinets infected with H. pylori develop clinical disease?

Should patinets without clinical disease be treated?

A

1-10%

  • Many people are affected asymptomatically!!
  • Treat asymptomatic infections if the backround prevalence of H. pylori is >20%
21
Q

What are the possible sequelae of untreated H. pylori infection?

A
  • Chronic active gastritis (antrum)
    • -> Duoenal ulcer
  • Chronic active pangastritis
    • -> Gastric ulcer
  • Chronic atrophic pangastritis
    • -> Cancer

​

22
Q

What causes Zollinger-Ellison syndrome?

A

Gastrinoma

  • Tumor that secretes gastrin
  • -> Parietal cells stimulation
    • -> HCL secretion
    • -> Parietal cell hyperplasia -> large folds
23
Q

What gastric pathology would you suspect if fasting gastrin levels are >1000 pg/mL?

What test can you use to confirm?

A

Zollinger-Ellison syndrome

Secretin test
(positive result = increase in gastrin after secretin administration)
24
Q

Which inhibitors of parietal cell gastric acid secretion act through the cAMP pathway?

A
  • Somatostatin
  • Prostaglandins
25
Q

What etiologies are implicated in H pylori-negative ulcers?

A
  • Medications
    • Aspirin, NSAIDs
  • Zollinger-Ellison syndrome
26
Q

Which stimulant of parietal cell gastric acid secretion act through the cAMP pathway?

27
Q

What are the endoscopic findings of Zolinger-Ellison syndrome?

A

What medications are implicated in H pylori-negative ulcers?

  • ZE is caused by a gastrin-secreting tumor
  • -> Stimulates parietal cells
  • -> hyperplasia
28
Q

List the two most common causes of chronic gastritis

A
  • H. pylori gastritis (most common)
  • Autoimmune gastritis
29
Q

Where is the prevalence of H pylori highest?

A

Places with worse sanitation (underdeveloped countries)

Transmitted through fecal-oral route

30
Q

A patient with previously well documented duodenal ulcer and gastrointestinal bleeding was treated for H.pylori infection with 14 days of omeprazole 20 mg BID, amoxicilin 1 gm BID, clarithromycin 500 mg BID. He presents with recurrent epigastric pain 2 months after completion of therapy.

What is the best next step?

A

Urea breath test or stool antigen assay for H. pylori

  • Need to figure out if H. pylori persists before treating symptoms
  • Urea breath test and stool antigen are sensitive for active H. pylori infection
31
Q

What genetic mutation is associated with gastric adenocarcinoma?

A

CDH1 mutation

  • Tumor suppressor gene
  • Encodes E-cadherin
32
Q

What gastric pathology is confirmed by a secretin stimulation test?

What results would constitute a postiive test?

A

Zolinger Ellison Syndrome

  • Positve result: gastrin levels increase after secretin stimulation

Explanation

  • Normally, secretin stimulates D cells > G cells
  • D cells secrete somatostatin, inhibit gastrin release from G cells
  • However, it does stimulate G cells a little bit
    • In ZE, G cells greatly outnumber D cells. So even though D cells are more strongly stimulated, there are so many G cells that the G cells response (-> gastrin release) overwhelms the somatostatin secreted by D cells
33
Q

How is an active H. pylori infection diagnosed?

A

Urea breath test OR stool antigen assay

But: will only be accurate >4 weeks after stopping eradication therapy

34
Q

What is the most common tumor of the stomach?

A

Gastric adenocarcinoma

35
Q

Which cancers are associated with H. pylori? (2)

A

MALT lymphoma

Gastric adenocarcinoma (both intestinal and diffuse)

36
Q

Where in the body does H pylori colonize?

A

Gastric epithelium (stomach)

  • If gastric epithelium is elsewhere, H. pylori can colonize elsewhere
    • Barrett’s esophagus
    • Duodenal ulcers
    • Meckel’s diverticulum
37
Q

Describe the pathogenesis of an NSAID-induced ulcer

A

Usually a chronic process, after weeks of NSAID use

  • Inhibition of COX1 (when using nonspecific COX inhibitor) for weeks
  • -> Depletion of prostaglandins
    • PGEs are important for mucous, HCO3- production, blood flow
  • -> Decreased blood flow, less HCO3-
  • -> Ischemia, necrosis
  • -> Ulcer

(Single dose of ibuprofen -> superfiical damage, but usually resolves)

38
Q

What cells types mediate the inflamation caused by H. pylori gastritis?

A

Neutrophils AND lymphocytes

H. pylori gastritis is a chornic, active gastritis

39
Q

Describe the typical presentation of Zollinger-Ellison Syndrome (3)

A
  • Intractable or multiple ulcers
  • Diarrhea
    • High acid content spilling into duodenum
      • Denatures pancreatic enzymes
      • Cannot digest food
    • Also secretory due to direct mucosal damage
  • Enlarged gastric folds
40
Q

Which medications are associated with the development of fundic gland polyps?

A

PPIs

  • Fundic glands contain parietal cells, G cells, and D cells
  • Inhibited HCL secretion -> gastrin
    • ​-> G cell hyperplasia
    • -> Polyp formation
41
Q

What virulence factor helps H. pylori survive in the acidic gastric environment?

42
Q

What histologic changes occur in chronic autoimmune gastritis?

A
  • Lymphocyte infiltration
  • Loss of fundic glands
  • Extensive metaplasia
    • Will see goblet cells and pancreatic acinar cells
43
Q

What is the msot common cause of peptic ulcer disese?

A

H. pylori gastritis

44
Q

Which cancer is most likely to be cured by antibiotics?

A

MALT lymphoma

  • H. pylori plays a role in MALT lymphoma pathogenesis
  • Antibiotics that kill H. pylori cause regression of MALT lymphoma

GI Review by Minnie (she/her) (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions