๐‘ท๐’†๐’‘๐’•๐’Š๐’„ ๐‘ผ๐’๐’„๐’†๐’“ ๐‘ซ๐’Š๐’”๐’†๐’‚๐’”๐’† Flashcards

(72 cards)

1
Q

What are the four main aggravating factors for peptic ulcer disease?

A

NSAIDs, H. pylori infection, alcohol, and stress

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2
Q

Which organism produces urease in peptic ulcer disease, and what does it do?

A

H. pylori produces urease, which breaks down urea into CO2 and ammonia, creating an alkaline environment

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3
Q

How does the pain pattern differ between duodenal and gastric ulcers?

A

Duodenal ulcer pain is relieved by eating, while gastric ulcer pain worsens with eating

โ€œDuodenal Digests, Gastric Gnaws.โ€

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4
Q

What is the characteristic timing of gastric ulcer pain?

A

Burning sensation that occurs after meals

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5
Q

What are the three main diagnostic tests for peptic ulcer disease?

A

Endoscopy (definitive diagnosis), H. pylori test, and urea breath test

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6
Q

What is the standard triple therapy for H. pylori-associated ulcers?

A

Proton pump inhibitor (PPI) + Clarithromycin + Amoxicillin

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7
Q

What is an alternative triple therapy regimen for H. pylori eradication?

A

PPI + Amoxicillin + Metronidazole

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8
Q

What are the four major complications of peptic ulcer disease?

A

Bleeding, perforation, obstruction (due to fibrosis), and malignancy

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9
Q

What does epigastric pain radiating to the back suggest in ulcer disease?

A

Possible penetration into the pancreas

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10
Q

What protective factors help prevent ulcer formation?

A

Bicarbonate
Mucus
Mucosal blood flow
Epithelial renewal
Tight intercellular junction

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11
Q

How does severe stress contribute to ulcer formation?

A

It disrupts the balance between mucosal defense mechanisms and aggravating factors

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12
Q

What is Zollinger-Ellison syndrome, and how does it relate to ulcers?

A

A condition characterized by excessive gastric acid production, leading to ulcers

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13
Q

What are the two main scoring systems for assessing bleeding risk in ulcer disease?

A

Rockall score (0-11) and Blatchford score (0-23)

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14
Q

What is the endoscopic appearance of Type 3 ulcers?

A

Lesions without bleeding
(appearing as a flat spot with a clean ulcer base)

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15
Q

What are the signs of active bleeding in peptic ulcer disease?

A

Spurting or oozing from visible vessels

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16
Q

What is the role of cimetidine in ulcer treatment?

A

An H2 receptor blocker that reduces acid secretion

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17
Q

How does metaplasia contribute to ulcer disease?

A

Duodenal mucosa transforms into gastric mucosa, reducing bicarbonate secretion

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18
Q

What distinguishes Type 1 from Type 2 ulcers?

A

Type 1: Located at the angularis incisura; Type 2: Includes both incisura and duodenal ulcers

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19
Q

What is the significance of the AIMS65 score?

A

A risk assessment tool for upper gastrointestinal bleeding

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20
Q

What symptoms suggest ulcer complications?

A

Water brash, chest discomfort, and hematemesis

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21
Q

Why is endoscopy the gold standard for diagnosing peptic ulcers?

A

It provides direct visualization and allows for biopsy if needed

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22
Q

How does H. pylori stimulate acid production?

A

It induces parietal cell hyperplasia through an inflammatory response

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23
Q

What lifestyle modifications help manage peptic ulcers?

A

Avoid smoking, alcohol, and NSAIDs

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24
Q

What characterizes NSAID-induced ulcers (Type 5)?

A

Ulcers caused by prolonged NSAID use, requiring discontinuation of NSAIDs

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25
What is the significance of prepyloric ulcers (Type 3)?
They occur near the pylorus and can affect gastric emptying
26
Why is the combination of NSAIDs and H. pylori particularly dangerous?
They synergistically weaken mucosal defenses, increasing ulcer risk
27
What role does gastrin play in ulcer formation?
It stimulates enterochromaffin-like (ECL) cells to release histamine, increasing acid production
28
How does smoking contribute to ulcer formation?
It increases acid secretion and reduces mucosal blood flow
29
What is the endoscopic appearance of an adherent clot on an ulcer?
It appears as a Type 2b lesion, indicating recent bleeding
30
Why are Type 4 ulcers (gastroesophageal junction) clinically significant?
They can affect both esophageal and gastric function
31
What causes the alkaline tide in ulcer disease?
H. pylori's urease activity, which generates ammonia and increases pH
32
How do parietal cells contribute to ulcer formation?
They produce hydrochloric acid (HCl), which can damage the mucosa if protective mechanisms fail
33
When should surgical intervention be considered for ulcers?
For complications like uncontrolled bleeding, perforation, or obstruction
34
What is the role of the Meissner plexus in ulcer disease?
It regulates mucosal secretion and blood flow, affecting mucosal defense
35
Why is pain worse at night in duodenal ulcers?
Increased acid secretion and reduced food buffering during fasting
36
How does chronic ulcer disease affect gastric motility?
It can lead to fibrosis and gastric outlet obstruction
37
What role do chief cells play in ulcer formation?
They produce pepsinogen, which is converted to pepsin, contributing to mucosal damage
38
Why is timely treatment of H. pylori important?
To prevent chronic inflammation and potential malignant transformation
39
What makes the antrum particularly susceptible to ulcers?
Its location and exposure to acid and pepsin
40
What is a peptic ulcer?
A defect in the mucosa of the esophagus, stomach, duodenum, or Meckelโ€™s diverticulum that occurs in the presence of acid and pepsin.
41
What is the underlying cause of peptic ulcers?
An imbalance between mucosal defense mechanisms and aggressive factors like acid and pepsin.
42
How has the management of peptic ulcer disease evolved over time?
The development of PPIs, H2 blockers, effective antibiotics against H. pylori, and endoscopic treatment has reduced the need for surgery.
43
Why has the role of open surgery in peptic ulcer disease declined?
Due to the availability of effective medical and endoscopic treatments.
44
What part of the stomach secretes acid?
The parietal cells in the gastric mucosa.
45
What role do nerves play in gastric acid secretion?
The vagus nerve stimulates acid secretion through acetylcholine release.
46
What infection is strongly linked to peptic ulcer disease?
Helicobacter pylori infection.
47
How do NSAIDs contribute to peptic ulcer formation?
By inhibiting prostaglandin synthesis, which reduces mucosal protection.
48
What lifestyle factors increase the risk of peptic ulcers?
Smoking, excessive alcohol consumption, and stress.
49
What genetic conditions are associated with peptic ulcer disease?
Zollinger-Ellison syndrome and G-cell hyperplasia.
50
How does physiological stress contribute to peptic ulcer formation?
By increasing acid secretion and impairing mucosal defense mechanisms.
51
What are the two main types of peptic ulcers?
Gastric ulcers and duodenal ulcers.
52
Where do most duodenal ulcers occur?
In the first part of the duodenum.
53
What is a stress ulcer?
An ulcer that occurs due to severe physiological stress, such as in critically ill patients.
54
What is the most common cause of peptic ulcer disease?
H. pylori infection.
55
What is Zollinger-Ellison syndrome?
A condition characterized by excessive gastric acid production due to gastrin-secreting tumors.
56
How does G-cell hyperplasia contribute to peptic ulcer disease?
By increasing gastrin levels, leading to excessive acid secretion.
57
How does H. pylori survive in the acidic environment of the stomach?
It produces urease, which converts urea into ammonia, creating a protective alkaline environment.
58
What effect does H. pylori infection have on acid secretion?
It stimulates acid production by inducing parietal cell hyperplasia.
59
What happens when excess acid reaches the duodenum?
It leads to gastric metaplasia and reduced bicarbonate secretion, making the duodenum more susceptible to ulceration.
60
What are the long-term complications of surgery for peptic ulcer disease?
Duodenogastric reflux, diarrhea, weight loss, osteomalacia, iron deficiency anemia, gallstones, gastric stump carcinoma, and colonic carcinoma.
61
Why does gastric stump carcinoma occur after surgery?
Chronic irritation from duodenogastric reflux increases cancer risk, typically developing 20 years post-surgery.
62
Why is the incidence of gallstones increased after truncal vagotomy?
Due to decreased gallbladder motility.
63
What is afferent loop syndrome?
A complication where the afferent limb of a gastrojejunostomy becomes obstructed, leading to pain and vomiting.
64
What is a gastrojejunocolic fistula?
An abnormal connection between the stomach, jejunum, and colon, often resulting from chronic ulceration.
65
Why are patients at increased risk of infections post-surgery?
Due to altered gastric physiology and impaired immune response, leading to conditions like pulmonary tuberculosis and gastric mycosis.
66
What are the common symptoms of peptic ulcer disease?
Epigastric pain, nausea, vomiting, bloating, and melena.
67
How does the pain of gastric ulcers differ from duodenal ulcers?
Gastric ulcer pain worsens with food intake, while duodenal ulcer pain improves with food.
68
What is the gold standard for diagnosing peptic ulcer disease?
Upper gastrointestinal endoscopy.
69
What tests can be used to detect H. pylori infection?
Urea breath test, stool antigen test, and biopsy with urease testing.
70
What are the main medical treatments for peptic ulcer disease?
Proton pump inhibitors (PPIs), H2 blockers, and H. pylori eradication therapy (antibiotics).
71
When is surgical treatment indicated for peptic ulcer disease?
In cases of life-threatening complications, perforation, obstruction, or refractory ulcers.
72
How does the prognosis of peptic ulcer disease change with effective treatment?
Most cases resolve with medical therapy, but complications like perforation or bleeding may require surgical intervention.