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GASTROENTEROLOGY > PEPTIC ULCER DISEASE > Flashcards

PEPTIC ULCER DISEASE Flashcards

1
Q

What is an ulcer?

A

A break through in the lining of the mucosa with appreciable depth at endoscopy.

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2
Q

What are erosions?

A

Superficial breaks in the mucosa that do not have perceptible depth.

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3
Q

What is a peptic ulcer?

A

Includes ulcers and erosions in the stomach and duodenum, involving mucosal integrity disruption and resulting in local defects due to active inflammation.

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4
Q

What does pepsin do?

A

Causes mucosal breaks regardless of the cause of the inciting agent.

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5
Q

What does the epithelial lining of the stomach contain?

A

Rugae or folds with microscopic gastric pits branching into 4 or 5 gastric glands.

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6
Q

What are gastric glands and what varies?

A

Gastric glands’ makeup varies with anatomical location.

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7
Q

What is the gastric cardia?

A

Comprises less than 5% of the gastric gland area and contains mucous and endocrine cells.

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8
Q

Where are most gastric glands found?

A

75% are found in oxyntic mucosa and contain mucous neck, parietal, chief, endocrine, enterochromaffin, and enterochromaffin-like (ECL) cells.

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9
Q

What are pyloric glands and where are they found?

A

Similar to the cardia, they contain mucous and endocrine cells, and are found in the antrum of the stomach.

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10
Q

Where are parietal (oxyntic) cells found?

A

In the neck or isthmus of the oxyntic gland.

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11
Q

What happens to parietal cells in the resting state?

A

They contain prominent cytoplasmic tubulovesicles and short microvilli along the apical surface; H+ K+-ATPase is expressed in the tubulovesicle membrane.

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12
Q

What happens to parietal cells in the stimulated state?

A

Microvilli in the canaliculi lengthen, and the tubulovesicle membrane moves to the apical portion, forming a dense network of long microvilli.

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13
Q

What is the pre-epithelial barrier in the gastroduodenal defense system?

A

It is the most superficial barrier, composed of a mucus-bicarbonate-phospholipid bilayer.

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14
Q

What does mucus in the stomach contain?

A

Mainly water (95%) and a mixture of phospholipids and glycoproteins (mucin).

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15
Q

What role does the mucus gel play in protection?

A

Impeding diffusion of ions (e.g., hydrogen ion) and molecules (e.g., pepsin).

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16
Q

What is the role of bicarbonate in gastric protection?

A

It forms a pH gradient from 1-2 at the gastric luminal surface to 6-7 along the epithelial surface, stabilizing clots in ulcers.

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17
Q

What are the components of the epithelial barrier in gastric protection?

A

Mucus production, ionic transporters for intracellular pH maintenance, and intracellular tight junctions.

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18
Q

What is the purpose of heat shock proteins in the stomach?

A

They prevent protein denaturation and protect cells from increased temperature, cytotoxic agents, and oxidative stress.

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19
Q

What is restitution in gastric epithelial defense?

A

The process by which gastric epithelial cells migrate to restore a damaged region if the pre-epithelial barrier is breached.

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20
Q

What conditions are necessary for restitution?

A

Uninterrupted blood flow and an alkaline pH in the surrounding environment.

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21
Q

Why are ICU patients prone to develop stress-related mucosal injuries?

A

Due to ischemia and reduced blood flow to the GI tract during states like hypotension and shock.

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22
Q

What is the subepithelial defense layer?

A

The deeper mucosal layer with a microvascular system supporting mucosal defense.

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23
Q

What does the subepithelial layer provide?

A

HCO3 for acid neutralization, micronutrient supply, oxygen, and removal of toxic by-products.

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24
Q

What local factors in the stomach promote blood flow?

A

Nitric oxide (NO), hydrogen sulfide, and prostacyclin, which cause vasodilation of the microcirculation.

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25
Q

What is the central role of prostaglandins in gastric epithelial defense?

A

Prostaglandins regulate the release of mucosal bicarbonate and mucus, inhibit parietal cell secretion, and maintain mucosal blood flow and epithelial restitution.

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26
Q

What enzyme is the rate-limiting factor in prostaglandin synthesis?

A

Cyclooxygenase (COX), present in two isoforms: COX-1 and COX-2.

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27
Q

Which COX enzyme is involved in housekeeping functions and found in the stomach, kidney, platelets, and endothelium?

A

COX-1

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28
Q

What are the functions of COX-2?

A

COX-2 mediates inflammation, mitogenesis, bone formation, and other inflammatory functions.

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29
Q

Name four non-specific NSAIDs that inhibit both COX-1 and COX-2.

A

Ibuprofen, Naproxen, Naloxone, and Diclofenac

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30
Q

How does nitric oxide contribute to gastric mucosal defense?

A

Nitric oxide stimulates gastric mucus production, increases mucosal blood flow, and maintains epithelial cell barrier function.

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31
Q

What are the principal gastric secretory products that can induce mucosal injury?

A

HCl and pepsinogen

32
Q

When are basal acid production levels highest and lowest?

A

Highest at night and lowest in the morning hours.

33
Q

What initiates the cephalic phase of gastric acid secretion?

A

The thought, sight, or smell of food, stimulating acid secretion via the vagus nerve.

34
Q

Which hormone provides negative feedback inhibition of gastric acid secretion?

A

Somatostatin

35
Q

What cell type releases somatostatin in response to HCl?

A

D cells in the gastric mucosa

36
Q

What is the role of somatostatin in gastric acid inhibition?

A

Somatostatin inhibits acid production by acting directly on parietal cells and indirectly by reducing histamine, ghrelin, and gastrin release.

37
Q

What are the three main receptors on parietal cells that stimulate acid secretion?

A

Histamine (H2), Gastrin (cholecystokinin 2/gastrin receptor), and Acetylcholine (muscarinic, M3)

38
Q

Which enzyme controls the acid-secreting pump (H+, K+-ATPase)?

A

The H+, K+-ATPase enzyme, regulated by signaling pathways from histamine, gastrin, and acetylcholine receptors.

39
Q

Why are proton pump inhibitors (PPIs) effective acid suppressants?

A

PPIs block the H+, K+-ATPase pump, which is the main generator of H+ ions for acid secretion.

40
Q

What is the primary function of chief cells in the stomach?

A

Chief cells synthesize and secrete pepsinogen, the inactive precursor of pepsin.

41
Q

What is the optimal pH for pepsin activity?

A

pH < 2

42
Q

What are the principal risk factors for peptic ulcer disease (PUD)?

A

H. pylori infection and NSAID use

43
Q

Which drug class increases the odds of gastrointestinal bleeding 5-6x?

A

NSAIDs

44
Q

Name three substances or conditions that contribute to mucosal ischemia in the GI tract.

A

Cocaine, methamphetamine, and bisphosphonates

45
Q

How does smoking affect peptic ulcer disease in H. pylori-infected patients?

A

Smoking increases the risk of PUD in H. pylori-infected patients.

46
Q

List some other risk factors for PUD aside from H. pylori and NSAID use.

A

Older age, COPD, chronic renal insufficiency, coronary heart disease, and stress.

47
Q

What are some pathogens that can cause ulcers aside from H. pylori?

A

Cytomegalovirus and Herpes simplex virus

48
Q

Name a few drugs or toxins, other than NSAIDs, that can cause ulcers.

A

Bisphosphonates, chemotherapy, clopidogrel, crack cocaine, and glucocorticoids (when combined with NSAIDs)

49
Q

List a few miscellaneous causes of ulcers not related to H. pylori or NSAIDs.

A

Radiation therapy, Crohn’s disease, ischemia, and eosinophilic infiltration.

50
Q

Principal agents in peptic ulcer disease

A

Gastric acid and Pepsin

51
Q

What physiologic role do gastric acid and pepsin play?

A

Protein digestion; absorption of iron, calcium, magnesium, and Vitamin B12

52
Q

Effect of H. pylori predominant gastritis

A

Reduced somatostatin in the antrum, increased basal and meal-stimulated acid secretion

53
Q

Acid secretion in duodenal ulcer vs gastric ulcer

A

Duodenal ulcer: increased acid secretion; Gastric ulcer: normal or decreased acid production

54
Q

Gastric mucosa defense mechanisms

A

Gastric surface epithelium, mucus/phospholipid and bicarbonate barrier, epithelial cell renewal and regeneration, mucosal blood flow, alkaline tide, prostaglandin production

55
Q

Role of prostaglandin in gastric mucosa

A

Stimulates mucus, bicarbonate, and phospholipid production

56
Q

Effect of COX1 inhibition

A

Reduces prostaglandin synthesis, compromising gastric mucosa integrity

57
Q

NSAIDs effect on COX enzymes

A

Inhibit both COX 1 and COX 2, which contributes to gastric injury

58
Q

Non-H. pylori causes of peptic ulcers

A

Crohn’s disease, Lymphoma, Gastrin-secreting tumors, Systemic Mastocytosis

59
Q

Location of duodenal ulcers

A

D1/First portion of duodenum (>95%)

60
Q

Typical characteristics of benign duodenal ulcers

A

Usually < 1 cm, sharply demarcated, high recurrence without H. pylori eradication

61
Q

Reduction in duodenal ulcer recurrence post H. pylori eradication

A

> 80% reduction

62
Q

Why biopsy gastric ulcers upon discovery

A

Potential malignancy

63
Q

Histopathology of NSAID-related gastric ulcers

A

Foveolar hyperplasia, lamina propria edema, epithelial regeneration, absence of H. pylori

64
Q

Peak incidence age for gastric ulcers

A

6th decade

65
Q

Primary causes of duodenal ulcers

A

H. pylori and NSAID-induced injuries

66
Q

Acid production in gastric vs duodenal ulcers

A

Gastric ulcer: normal or decreased acid; Duodenal ulcer: increased acid secretion

67
Q

Helicobacter pylori characteristics

A

Gram-negative, microaerophilic rod, spiral shape, unipolar flagella, urease production

68
Q

Helicobacter pylori’s diagnostic feature

A

Urease enzyme hydrolyzes urea to ammonia and CO2

69
Q

Risk factors for H. pylori infection

A

Low socioeconomic status, less education, birth or residence in developing country, crowding, unsanitary conditions

70
Q

Modes of H. pylori transmission

A

Person-to-person (oral-oral, fecal-oral, gastro-oral), contaminated water

71
Q

Interplay determining H. pylori-induced gastrointestinal disease

A

Bacterial and host factors

72
Q

Virulence factors associated with H. pylori

A

y-glutamyl transpeptidase (GGT), cagA, vacA, adhesins

73
Q

Role of cag-PAI in H. pylori pathogenicity

A

Encodes CagA and other factors increasing risk of PUD, premalignant lesions, gastric cancer

74
Q

H. pylori’s effect on gastric epithelial cells

A

Apoptosis due to interaction with T cells and pro-inflammatory cytokines

75
Q

Result of antral-predominant gastritis from H. pylori

A

Duodenal ulcer formation or asymptomatic infection

76
Q

Potential outcomes of chronic corpus-predominant atrophic gastritis

A

Gastric ulcer, intestinal metaplasia, dysplasia, and potential gastric cancer

GASTROENTEROLOGY (3 decks)

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