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Gastroenterology > PUD > Flashcards

PUD Flashcards

1
Q

What does PUD encompass?

A

Gastric ulcers (GUs) and duodenal ulcers (DUs)

PUD stands for Peptic Ulcer Disease.

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2
Q

How are ulcers defined in terms of size and depth?

A

Breaks in the mucosal surface >5 mm in size, with depth to the submucosa

This definition applies to both gastric and duodenal ulcers.

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3
Q

What are the most common risk factors for PUD?

A
  • H. pylori
  • NSAIDs

These factors have estimated odds ratios of 3.7 and 3.3, respectively.

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4
Q

What is the odds ratio for chronic obstructive lung disease as a risk factor for PUD?

A

2.34

This indicates a significant association with PUD risk.

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5
Q

List additional risk factors for PUD along with their odds ratios.

A
  • Chronic renal insufficiency (2.29)
  • Current tobacco use (1.99)
  • Former tobacco use (1.55)
  • Older age (1.67)
  • Three or more doctor visits in a year (1.49)
  • Coronary heart disease (1.46)
  • Former alcohol use (1.29)
  • African American race (1.20)
  • Obesity (1.18)
  • Diabetes (1.13)

These factors contribute to the risk of developing PUD.

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6
Q

What medications and procedures are associated with an increased incidence of PUD?

A
  • Selective serotonin reuptake inhibitors (SSRIs)
  • Gastric bypass surgery

Both have been linked to a higher incidence of peptic ulcers.

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7
Q

True or False: DUs and GUs share many common features in terms of pathogenesis, diagnosis, and treatment.

A

True

Despite their differences, GUs and DUs have similar underlying mechanisms.

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8
Q

When do gastric ulcers (GUs) typically occur in life?

A

GUs tend to occur later in life, with a peak incidence reported in the sixth decade.

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9
Q

What is the gender distribution for gastric ulcers?

A

More than one-half of GUs occur in males.

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10
Q

Where do duodenal ulcers (DUs) most often occur?

A

In the first portion of the duodenum (>95%)

DUs are usually located within 3 cm of the pylorus

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11
Q

What is the typical diameter of duodenal ulcers?

A

≤1 cm, but can reach 3–6 cm (giant ulcer)

Giant ulcers are a rare occurrence

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12
Q

What is the characteristic appearance of duodenal ulcers?

A

Sharply demarcated with depth reaching the muscularis propria

The base often consists of eosinophilic necrosis with surrounding fibrosis

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13
Q

What distinguishes gastric ulcers (GUs) from duodenal ulcers?

A

GUs can represent a malignancy and should be biopsied upon discovery

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14
Q

Where are benign gastric ulcers most often found?

A

Distal to the junction between the antrum and the acid secretory mucosa

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15
Q

What association do benign gastric ulcers have with H. pylori?

A

Associated with antral gastritis

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16
Q

What may be observed in NSAID-related gastric ulcers instead of chronic active gastritis?

A

Chemical gastropathy, typified by foveolar hyperplasia, edema of the lamina propria, and epithelial regeneration

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17
Q

What are the primary causes of duodenal ulcers (DUs)?

A

H. pylori and NSAID-induced injuries

These account for the majority of DUs.

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18
Q

How does gastric acid secretion in DU patients compare to control subjects?

A

Average basal and nocturnal gastric acid secretion appears to be increased

There is substantial overlap between DU patients and control subjects.

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19
Q

What is the significance of bicarbonate secretion in DU patients?

A

Bicarbonate secretion is significantly decreased in the duodenal bulb

This is compared to control subjects.

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20
Q

What are the main causes of gastric ulcers (GUs)?

A

H. pylori or NSAID-induced mucosal damage

The majority of GUs can be attributed to these factors.

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21
Q

What tends to be the gastric acid output in gastric ulcer patients?

A

Normal or decreased

This applies to both basal and stimulated gastric acid output.

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22
Q

Where do Type I gastric ulcers occur and what is their association with gastric acid production?

A

In the gastric body; associated with low gastric acid production

They are classified as Type I ulcers.

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23
Q

Where do Type II gastric ulcers occur and what is their association with gastric acid production?

A

In the antrum; gastric acid can vary from low to normal

They are classified as Type II ulcers.

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24
Q

Where do Type III gastric ulcers occur and what is their gastric acid production status?

A

Within 3 cm of the pylorus; commonly associated with DUs and normal or high gastric acid production

They are classified as Type III ulcers.

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25
Q

Where are Type IV gastric ulcers found and what is their association with gastric acid production?

A

In the cardia; associated with low gastric acid production

They are classified as Type IV ulcers.

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26
Q

What dose of aspirin may lead to serious GI ulceration?

A

75 mg/d

This indicates that even low doses of aspirin can be risky for gastrointestinal health.

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27
Q

What infection increases the risk of PUD-associated GI bleeding in chronic users of low-dose aspirin?

A

H. pylori infection

This infection is a significant risk factor for gastrointestinal complications.

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28
Q

List established risk factors for NSAID-induced morbidity.

A
  • Advanced age
  • History of ulcer
  • Concomitant use of glucocorticoids
  • High-dose NSAIDs
  • Multiple NSAIDs
  • Concomitant use of anticoagulants or clopidogrel
  • Serious or multisystem disease

These factors increase the likelihood of serious complications from NSAID use.

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29
Q

List possible risk factors for NSAID-induced morbidity.

A
  • Concomitant infection with H. pylori
  • Cigarette smoking
  • Alcohol consumption

These factors may contribute to the risk of complications when using NSAIDs.

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30
Q

What effect do SSRIs have on NSAID-induced GI bleeding?

A

Synergistic effect

SSRIs may increase the risk of GI bleeding due to their impact on platelet aggregation.

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31
Q

What is the role of prostaglandins in the gastroduodenal mucosa?

A

Maintaining mucosal integrity and repair

Prostaglandins are essential for protecting the gastric mucosa from injury.

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32
Q

What role do neutrophils play in NSAID-induced mucosal injury?

A

Initiation of mucosal injury via adherence to gastric microcirculation

Neutrophil adherence is crucial in the early stages of injury.

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33
Q

What are single nucleotide polymorphisms (SNPs) associated with in NSAID-induced mucosal injury?

A

Genes including cytochrome P450 subtypes, IL-1β, angiotensinogen, and SLCO1B1

These SNPs need confirmation in larger studies.

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34
Q

How does topical use of NSAIDs affect the mucosa?

A

Increases epithelial surface permeability

This can lead to mucosal injury through various mechanisms.

35
Q

Why do aspirin and many NSAIDs cause cell injury in the stomach?

A

They remain in a nonionized lipophilic form in the acidic environment

This allows NSAIDs to cross lipid membranes and become trapped intracellularly.

36
Q

What is one consequence of NSAIDs altering the surface mucous layer?

A

Permitting back diffusion of H + and pepsin

This leads to further epithelial cell damage.

37
Q

What is a risk associated with enteric-coated or buffered NSAID preparations?

A

Risk of peptic ulceration

These preparations can still contribute to mucosal injury.

38
Q

How do NSAIDs produce additional proinflammatory mediators?

A

Through activation of the lipoxygenase pathway

This results in increased levels of TNF and leukotrienes.

39
Q

What is the relationship between H. pylori and NSAIDs in the pathogenesis of PUD?

A

Complex interplay as independent and synergistic risk factors

Both factors can increase the risk of PUD and complications.

40
Q

What effect does the eradication of H. pylori have on NSAID-induced complications?

A

Reduces likelihood of GI complications in high-risk individuals

This brings their risk levels closer to those of average-risk individuals.

41
Q

What role does cigarette smoking play in the pathogenesis of PUD?

A

Cigarette smoking is implicated in increased frequency of ulcers, decreased healing rates, impaired response to therapy, and increased ulcer-related complications

The exact mechanism is unknown, but theories include altered gastric emptying and increased risk for H. pylori infection.

42
Q

What is the genetic predisposition related to peptic ulcer disease (PUD)?

A

First-degree relatives of DU patients are three times as likely to develop an ulcer

Increased frequencies of blood group O and nonsecretor status are also implicated.

43
Q

Which blood group is preferentially bound by H. pylori?

A

Blood group O

This binding may be a factor in ulcer development among those with this blood type.

44
Q

What are potential susceptibility genes for NSAID-induced PUD?

A

Genes encoding cytochrome P450 2C9 and 2C8 (CYP2C9 and CYP2C8)

Studies have not consistently demonstrated this association.

45
Q

How does psychological stress relate to PUD?

A

Psychological stress has been thought to contribute to PUD, but studies have shown conflicting results

Certain personality traits like neuroticism are associated with PUD and nonulcer dyspepsia.

46
Q

What dietary factors are associated with peptic diseases?

A

No convincing studies indicate a specific diet associated with ulcer formation

Certain foods and beverages may cause dyspepsia.

47
Q

List chronic disorders strongly associated with PUD.

A
  • Advanced age
  • Chronic pulmonary disease
  • Chronic renal failure
  • Cirrhosis
  • Nephrolithiasis
  • α1-antitrypsin deficiency
  • Systemic mastocytosis

These conditions have a strong correlation with PUD.

48
Q

What disorders have a possible association with PUD?

A
  • Hyperparathyroidism
  • Coronary artery disease
  • Polycythemia vera
  • Chronic pancreatitis
  • Former alcohol use
  • Obesity
  • African-American race
  • Three or more doctor visits in a year

These associations are less definitive than those of strong association.

49
Q

What are the two predominant causes of PUD?

A
  • H. pylori infection
  • NSAID ingestion

PUD not related to these causes is on the rise.

50
Q

What is the common symptom in many GI disorders, including DU and GU?

A

Abdominal pain

Abdominal pain has a poor predictive value for the presence of either DU or GU.

51
Q

What percentage of patients with PUD do not have abdominal pain?

A

Approximately two-thirds

Up to 87% of patients with NSAID-induced mucosal disease can present with complications without antecedent symptoms.

52
Q

How is epigastric pain in DU and GU typically described?

A

Burning or gnawing discomfort

It can also be described as an ill-defined, aching sensation or as hunger pain.

53
Q

When does typical pain in DU occur after a meal?

A

90 minutes to 3 hours

This pain is frequently relieved by antacids or food.

54
Q

What symptom is most discriminating for DU patients?

A

Pain that awakes the patient from sleep (between midnight and 3 a.m.)

Two-thirds of DU patients describe this complaint.

55
Q

How do elderly patients typically present with PUD?

A

They are less likely to have abdominal pain and may present with a complication

Complications include ulcer bleeding or perforation.

56
Q

How may the pain pattern in GU patients differ from DU patients?

A

Discomfort may be precipitated by food

Nausea and weight loss occur more commonly in GU patients.

57
Q

What does constant dyspepsia that is no longer relieved by food or antacids suggest?

A

A penetrating ulcer

This may involve the pancreas.

58
Q

What does sudden onset of severe, generalized abdominal pain indicate?

A

Perforation

This is a critical symptom that requires immediate attention.

59
Q

What symptoms suggest gastric outlet obstruction?

A

Pain worsening with meals, nausea, and vomiting of undigested food

These symptoms can indicate a blockage in the stomach.

60
Q

What do tarry stools or coffee-ground emesis indicate?

A

Bleeding

These symptoms are associated with gastrointestinal bleeding.

61
Q

What is the most frequent finding in patients with GU or DU?

A

Epigastric tenderness

GU refers to gastric ulcer, and DU refers to duodenal ulcer.

62
Q

What signs suggest dehydration secondary to vomiting or active GI blood loss?

A

Tachycardia and orthostasis

These vital sign changes are critical indicators of fluid loss.

63
Q

What does a severely tender, board-like abdomen suggest?

A

Perforation

This finding is a serious complication that requires immediate medical attention.

64
Q

What does the presence of a succussion splash indicate?

A

Retained fluid in the stomach

This suggests a potential gastric outlet obstruction.

65
Q

What is the most common complication observed in PUD?

A

GI bleeding

PUD stands for peptic ulcer disease.

66
Q

In which age group does bleeding and complications of ulcer disease occur more often?

A

> 60 years of age

67
Q

What is a likely reason for the higher incidence of GI bleeding in the elderly?

A

Increased use of NSAIDs

68
Q

What percentage of mortality in PUD-related bleeding is due to nonbleeding causes?

A

Up to 80%

69
Q

List three nonbleeding causes of mortality in PUD-related bleeding.

A
  • Multiorgan failure (24%)
  • Pulmonary complications (24%)
  • Malignancy (34%)
70
Q

What percentage of patients with ulcer-related hemorrhage bleed without any preceding warning signs or symptoms?

A

> 50%

71
Q

What is the second most common ulcer-related complication?

A

Perforation

Reported in 6–7% of PUD patients with an estimated 30-day mortality of >20%

72
Q

What are the classic symptoms associated with perforation?

A

Acute abdominal pain, tachycardia, abdominal rigidity

This classic triad may not be present in elderly or immunosuppressed patients

73
Q

Which organ do DUs typically penetrate into?

A

Pancreas

This can lead to pancreatitis

74
Q

Which organ do GUs typically penetrate into?

A

Left hepatic lobe

Gastrocolic fistulas associated with GUs have also been described

75
Q

What is gastric outlet obstruction? The least common ulcer-related complication, occurring in 1–2% of patients.

A

Gastric outlet obstruction

76
Q

What can cause relative obstruction in gastric outlet obstruction?

A

Ulcer-related inflammation and edema in the peripyloric and duodenal region.

77
Q

What happens to relative obstruction after ulcer healing?

A

It often resolves.

78
Q

What is a fixed, mechanical obstruction in gastric outlet obstruction caused by?

A

Scar formation in the peripyloric areas.

79
Q

What interventions may be required for fixed mechanical obstruction?

A

Endoscopic (balloon dilation with or without placement of a biodegradable stent) or surgical intervention (stricturoplasty or gastrojejunostomy).

80
Q

How may signs and symptoms of mechanical obstruction develop?

A

Insidiously.

81
Q

What are some signs and symptoms of gastric outlet obstruction?

A
  • New onset of early satiety
  • Nausea
  • Vomiting
  • Increase of postprandial abdominal pain
  • Weight loss
82
Q

True or False: Gastric outlet obstruction is a common ulcer-related complication.

A

False.

83
Q

Fill in the blank: Gastric outlet obstruction occurs in _______ of patients.

A

1–2%

Gastroenterology (10 decks)

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