Brainscape's Knowledge GenomeTM

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


See full index

GASTROENTEROLOGY > PEPTIC ULCER DISEASE 1.2 > Flashcards

PEPTIC ULCER DISEASE 1.2 Flashcards

1
Q

What is the spectrum of morbidity in NSAID-induced disease?

A

Nausea and dyspepsia (50-60%), peptic ulcer (15-30%), bleeding (melena, hematemesis), perforation (1.5%/year)

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

What is the effect of proton pump inhibitors on NSAID-induced complications?

A

Proton pump inhibitors have decreased the complications over the years.

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

Do dyspeptic symptoms correlate with NSAID-induced pathology?

A

No, dyspeptic symptoms do not correlate with NSAID-induced pathology.

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

What are established risk factors for NSAID-induced ulcers?

A

Advanced age, history of ulcer, concomitant use of GCs, high dose NSAIDs, multiple NSAIDs, anticoagulant use, clopidogrel, serious multisystem disease.

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

What are possible risk factors for NSAID-induced ulcers?

A

Concomitant H. pylori infection, cigarette smoking, alcohol consumption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the pathophysiology of NSAID-induced mucosal injury?

A

Mucosal injury occurs through interruption of prostaglandin synthesis and neutrophil adherence to gastric microcirculation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why are NSAIDs a common cause of pill-induced gastritis?

A

NSAIDs are large acids that remain non-ionized and lipophilic, allowing them to migrate across epithelial membranes, causing intracellular injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Is it safe to shift a rheumatoid arthritis patient to topical NSAIDs?

A

No, topical NSAIDs can lead to back diffusion of H+ and pepsin, causing epithelial damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the effects of enteric-coated or buffered NSAID preparations?

A

Enteric-coated or buffered NSAIDs are also associated with the risk of peptic ulceration.

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

What are the additional pro-inflammatory mediators produced by NSAIDs?

A

TNF and leukotrienes, via activation of the lipoxygenase pathway.

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

What role does H. pylori play in NSAID-induced PUD?

A

H. pylori and NSAIDs act as independent and synergistic risk factors for PUD and complications like GI bleeding.

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

How does cigarette smoking affect ulcer healing?

A

Cigarette smoking decreases healing rates, impairs therapy response, and increases ulcer complications.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does genetic predisposition affect peptic ulcer disease risk?

A

First-degree relatives of DU patients are three times more likely to develop an ulcer. Blood Type O+ is also a risk factor.

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

What are chronic disorders strongly associated with PUD?

A

Advanced age, chronic pulmonary disease, chronic renal failure, cirrhosis, nephrolithiasis, a1-antitrypsin deficiency, systemic mastocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are common clinical features of PUD history?

A

Abdominal pain, classic burning pain in the epigastrium, nausea, vomiting, tarry stools, or coffee-ground emesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the classic pain pattern in duodenal ulcers (DU)?

A

Pain occurs 90 minutes to 3 hours postprandial and is often relieved by food or antacids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the classic pain pattern in gastric ulcers (GU)?

A

Pain may be precipitated by food; nausea and weight loss are more common.

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

What are common physical exam findings in PUD?

A

Epigastric tenderness, tachycardia, orthostasis, severe tenderness, board-like abdomen (perforation), succussion splash (gastric outlet obstruction).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the complications of PUD?

A

Hemorrhage, perforation, and gastric outlet obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does PUD-related hemorrhage present?

A

Melena, hematemesis, or hematochezia in the case of brisk bleeding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the triad for perforation in PUD?

A

Acute abdominal pain, tachycardia, and abdominal rigidity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the typical complication of posterior duodenal ulcers?

A

Penetration into the pancreas, causing pancreatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the management for gastric outlet obstruction in PUD?

A

Endoscopic dilation with a balloon, or surgical intervention like myotomy or gastrectomy if needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the main diagnostic tests for PUD?

A

Barium meal, endoscopy, biopsy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the limitations of using barium meal for diagnosing PUD?

A

Barium meal is rarely used as a first test and has decreased sensitivity for small ulcers (<0.5 cm).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does endoscopy compare to barium meal in detecting PUD?

A

Endoscopy is the current reference standard and more sensitive and specific than barium meal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are alarm features in PUD patients?

A

Age >55, family history of GI cancer, GI bleeding, jaundice, supraclavicular lymphadenopathy, palpable abdominal mass, persistent vomiting, progressive dysphagia, unintended weight loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does a positive alarm feature mean in PUD diagnosis?

A

Presence of alarm features should prompt referral to a gastroenterologist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How are H. pylori infections diagnosed?

A

Via rapid urease test, histology, culture, urea breath test, and stool antigen test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why is the rapid urease test for H. pylori sometimes false negative?

A

Recent use of PPIs, antibiotics, or bismuth can cause false negatives.

31
Q

What is the most sensitive test for diagnosing H. pylori?

A

Endoscopy with biopsy is the most sensitive test.

32
Q

How does the urea breath test help in diagnosing H. pylori?

A

It is simple, rapid, and useful for early follow-up, but may have false negatives after recent therapy.

33
Q

Why is serology for H. pylori not ideal for early follow-up?

A

Serology tests for antibodies, which are not useful for early follow-up or monitoring.

34
Q

What are the risks of NSAID-induced ulcers in elderly patients?

A

The elderly may have absent pain and present with complications like bleeding, perforation, or obstruction.

35
Q

What is the most commonly used agent combination in acid neutralizing inhibitory drugs?

A

Aluminum hydroxide and magnesium hydroxide

36
Q

What side effects are associated with aluminum hydroxide?

A

Constipation and phosphate depletion

37
Q

What side effects are associated with magnesium hydroxide?

A

Loose stools; should not be used in chronic renal failure (CRF) or renal insufficiency

38
Q

What is a side effect of long-term calcium carbonate use in antacids?

A

Mild-alkali syndrome (hypercalcemia, hyperphosphatemia, renal calcinosis)

39
Q

What condition can sodium bicarbonate induce?

A

Systemic alkalosis

40
Q

What is the purpose of combining PPIs with sodium bicarbonate?

A

To provide faster relief, as PPIs have delayed onset of action

41
Q

What is milk-alkali syndrome?

A

A rare side effect from excessive calcium carbonate intake

42
Q

What are the H2 receptor antagonists (H2RAs) commonly used for?

A

Inhibit basal and stimulated acid secretion

43
Q

What are common H2RAs?

A

Cimetidine, ranitidine, famotidine, nizatidine

44
Q

What side effects are associated with cimetidine?

A

Reversible gynecomastia, impotence, inhibition of cytochrome P450

45
Q

What side effect is seen in patients using cimetidine long-term?

A

Malignancy (not well-established)

46
Q

What is the most potent H2RA?

A

Famotidine and nizatidine

47
Q

What adverse effects can H2 receptor antagonists cause?

A

Pancytopenia, neutropenia, anemia, thrombocytopenia

48
Q

Which H2RA is most commonly linked to liver enzyme inhibition?

A

Cimetidine

49
Q

Which H2RAs do not bind to CYP450?

A

Famotidine and nizatidine

50
Q

What should be avoided when administering PPIs and clopidogrel together?

A

Potential competition with cytochrome P450 (CYP2C19)

51
Q

What are common PPIs used in treatment?

A

Omeprazole, Esomeprazole, Lansoprazole, Rabeprazole, Pantoprazole

52
Q

What is the difference between esomeprazole and omeprazole?

A

Esomeprazole is the S-enantiomer of omeprazole

53
Q

Why is dexlansoprazole more effective for GERD with nighttime acid?

A

It has a dual delayed-release system

54
Q

How do PPIs work in terms of absorption?

A

They are protonated in the acidic environment and trapped within the parietal cell’s tubulovesicular system

55
Q

What is the duration of action for PPIs?

A

72-96 hours

56
Q

What are some long-term side effects of PPIs?

A

Community-acquired pneumonia, Clostridium difficile, diarrhea, hip fractures, vitamin deficiencies

57
Q

How do PPIs affect vitamin B12 absorption?

A

They inhibit intrinsic factor production, potentially leading to vitamin B12 deficiency

58
Q

What is a known side effect of PPIs related to magnesium?

A

Magnesium deficiency

59
Q

How does a PPI + clopidogrel interaction work?

A

PPIs and clopidogrel compete for CYP2C19 metabolism, reducing clopidogrel efficacy

60
Q

What are potassium-competitive acid pump antagonists (P-CAPs)?

A

Newest drug class, including revaprazan, venoprazan, and tegoprazan

61
Q

What does sucralfate treat?

A

Active ulcers, by binding to ulcerated tissue and forming a protective barrier

62
Q

What are the common side effects of sucralfate?

A

Constipation, aluminium-induced neurotoxicity, gastric bezoar formation

63
Q

What is the primary action of prostaglandin analogs?

A

Enhancement of mucosal defense and repair

64
Q

What is a common side effect of prostaglandin analogs?

A

Diarrhea

65
Q

Which prostaglandin analog can induce uterine contractions and bleeding?

A

Misoprostol

66
Q

What is the recommended dose for misoprostol?

A

200 µg QID

67
Q

Why is H. pylori treatment important?

A

To decrease ulcer recurrence and recurrent ulcer bleeding

68
Q

What are first-line treatments for H. pylori infection?

A

Combination therapy (e.g., proton pump inhibitor + antibiotics) for 14 days

69
Q

Which patient population is considered for H. pylori testing and treatment?

A

Patients with dyspepsia, previous gastric cancer, long-term NSAID use, unexplained IDA, and ITP

70
Q

What is a common side effect of bismuth-containing preparations?

A

Black stools, constipation, darkening of the tongue

71
Q

What are common side effects of tetracycline?

A

Rashes, hepatotoxicity (monitor SGPT and SGOT)

72
Q

Why is antibiotic resistance a concern in H. pylori treatment?

A

Antibiotic-resistant strains are the most common cause of treatment failure

73
Q

What is a proposed innovative approach for H. pylori treatment?

A

N-acetylcysteine (NAC) to destroy H. pylori biofilm

GASTROENTEROLOGY (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions