Peptic Ulcer Disease Flashcards

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1
Q

Where in the body can ulcers develop? Where can they not develop?

A

They can develop anywhere in the body.

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2
Q

Where do most ulcers occur?

A

~80% occur in the duodenum

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3
Q

Other than the duodenum, where else do ulcers commonly form?

A

~20% in the stomach.

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4
Q

T or F:

An increased amount of acid will cause ulcers

A

F, acid irritates the ulcers but does not cause them.

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5
Q

What tissue layer do ulcers primarily affect? Can they go deeper than this layer?

A

The mucosa, yes they can go deeper than this.

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6
Q

Is PUD common?

A

~10% prevalence.

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7
Q

What is the pattern of recovery from PUD?

A

People with PUD may suffer from remissions and exacerbations .

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8
Q

Can PUD ever be completely cured?

A

Yes, but it may return even if it has been completely cured. Bleak :/

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9
Q

What is the main factor in the Et of PUD?

A

Helicobacter Pylori.

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10
Q

How does the stomach protect itself from acid damage?

A

The mucosa provides protection.

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11
Q

There is no mucosa in the duodenum, how does this structure withstand damage from acid?

A

The duodenum has by-chemical protection from the buffers in the pancreas.

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12
Q

T or F:

The mucosa is able to regenerate itself after damage has occurred.

A

T

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13
Q

Can perfusion be considered a defensive factor?

A

Yes.

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14
Q

If the protective forces of the mucosa and duodenum are so effective, when does PUD occur?

A

When the offensive factors outweigh the defensive.

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15
Q

Things to know about Helicobacter Pylori’s role in PUD:

3

A
  • Needs a site
  • Secretes adhesion proteins to adhere to site
  • Secretes urease
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16
Q

What does urease do?

A

Converts urea into CO2 and NH2

17
Q

What are some risk factors that contribute to the development of PUD?

A
  • Helicobacter Pylori duh
  • HCl and biliary acid
  • NSAIDs
  • Chronic gastritis
  • Smoking, alcohol
18
Q

Explain how NSAIDs contribute to PUD:

A

Because of the decrease in prostaglandin synthesis, the mucosa’s ability to repair itself is hindered and it is more susceptible to damage.

19
Q

2 things caused by the presence of Helicobacter Pylori that contribute to the patho of PUD:

A
  • Inflm -> tissue damage
  • Hypergastrinemia -> increase in gastric secretions ->
    tissue damage
20
Q

What is gastrin?

A

A peptide hormone that stimulates secretion of HCl by the parietal cells of the stomach and aids in gastric motility.

21
Q

Where is gastrin released from?

A

G cells in the pyloric antrum of the stomach, duodenum, and the pancreas

22
Q

Mnfts of PUD:

A
  • Burning/cramping abdm pain

- Nausea/vomiting

23
Q

With PUD, is nausea/vomiting a local or systemic mnft?

A

Local

24
Q

What are some complications that may arise d/t PUD?

A
  • Hemorrhage
  • Perforation
    • Peritonitis
  • Obstruction
25
Q

What is used to Dx PUD?

A
  • Urea breath test (based on the presence of urease)
  • Serology (specifically looking for Ags against
    Helicobacter Pylori, not routine)
  • Fecal Ags (not routine)
  • Gastroscopy (long wait)
  • Barium swallow
26
Q

What is used in the management of PUD?

A
  • Antacids for short term
  • Triple regimen:
    • H2RA + 2 Abx
      - Zantac + Amoxil + Biaxin
    • PPI + 2 Abx
      - Losec + Flagyl + Biaxin
27
Q

What does a H2RA do to manage PUD?

A

Blocks acid secretion

28
Q

What does histamine stimulate?

A

The secretion of HCl acid

29
Q

What does a PPI do to manage PUD?

A

Blocks H secretion