PEPTIC ULCER DISEASE Flashcards

(76 cards)

1
Q

What is an ulcer?

A

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

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

What are erosions?

A

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

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

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

What does pepsin do?

A

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

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

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

What are gastric glands and what varies?

A

Gastric glands’ makeup varies with anatomical location.

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

What is the gastric cardia?

A

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

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

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

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

Where are parietal (oxyntic) cells found?

A

In the neck or isthmus of the oxyntic gland.

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

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

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

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

What does mucus in the stomach contain?

A

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

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

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

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

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

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

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

What conditions are necessary for restitution?

A

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

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

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

What is the subepithelial defense layer?

A

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

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

What does the subepithelial layer provide?

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the central role of prostaglandins in gastric epithelial defense?
Prostaglandins regulate the release of mucosal bicarbonate and mucus, inhibit parietal cell secretion, and maintain mucosal blood flow and epithelial restitution.
26
What enzyme is the rate-limiting factor in prostaglandin synthesis?
Cyclooxygenase (COX), present in two isoforms: COX-1 and COX-2.
27
Which COX enzyme is involved in housekeeping functions and found in the stomach, kidney, platelets, and endothelium?
COX-1
28
What are the functions of COX-2?
COX-2 mediates inflammation, mitogenesis, bone formation, and other inflammatory functions.
29
Name four non-specific NSAIDs that inhibit both COX-1 and COX-2.
Ibuprofen, Naproxen, Naloxone, and Diclofenac
30
How does nitric oxide contribute to gastric mucosal defense?
Nitric oxide stimulates gastric mucus production, increases mucosal blood flow, and maintains epithelial cell barrier function.
31
What are the principal gastric secretory products that can induce mucosal injury?
HCl and pepsinogen
32
When are basal acid production levels highest and lowest?
Highest at night and lowest in the morning hours.
33
What initiates the cephalic phase of gastric acid secretion?
The thought, sight, or smell of food, stimulating acid secretion via the vagus nerve.
34
Which hormone provides negative feedback inhibition of gastric acid secretion?
Somatostatin
35
What cell type releases somatostatin in response to HCl?
D cells in the gastric mucosa
36
What is the role of somatostatin in gastric acid inhibition?
Somatostatin inhibits acid production by acting directly on parietal cells and indirectly by reducing histamine, ghrelin, and gastrin release.
37
What are the three main receptors on parietal cells that stimulate acid secretion?
Histamine (H2), Gastrin (cholecystokinin 2/gastrin receptor), and Acetylcholine (muscarinic, M3)
38
Which enzyme controls the acid-secreting pump (H+, K+-ATPase)?
The H+, K+-ATPase enzyme, regulated by signaling pathways from histamine, gastrin, and acetylcholine receptors.
39
Why are proton pump inhibitors (PPIs) effective acid suppressants?
PPIs block the H+, K+-ATPase pump, which is the main generator of H+ ions for acid secretion.
40
What is the primary function of chief cells in the stomach?
Chief cells synthesize and secrete pepsinogen, the inactive precursor of pepsin.
41
What is the optimal pH for pepsin activity?
pH < 2
42
What are the principal risk factors for peptic ulcer disease (PUD)?
H. pylori infection and NSAID use
43
Which drug class increases the odds of gastrointestinal bleeding 5-6x?
NSAIDs
44
Name three substances or conditions that contribute to mucosal ischemia in the GI tract.
Cocaine, methamphetamine, and bisphosphonates
45
How does smoking affect peptic ulcer disease in H. pylori-infected patients?
Smoking increases the risk of PUD in H. pylori-infected patients.
46
List some other risk factors for PUD aside from H. pylori and NSAID use.
Older age, COPD, chronic renal insufficiency, coronary heart disease, and stress.
47
What are some pathogens that can cause ulcers aside from H. pylori?
Cytomegalovirus and Herpes simplex virus
48
Name a few drugs or toxins, other than NSAIDs, that can cause ulcers.
Bisphosphonates, chemotherapy, clopidogrel, crack cocaine, and glucocorticoids (when combined with NSAIDs)
49
List a few miscellaneous causes of ulcers not related to H. pylori or NSAIDs.
Radiation therapy, Crohn's disease, ischemia, and eosinophilic infiltration.
50
Principal agents in peptic ulcer disease
Gastric acid and Pepsin
51
What physiologic role do gastric acid and pepsin play?
Protein digestion; absorption of iron, calcium, magnesium, and Vitamin B12
52
Effect of H. pylori predominant gastritis
Reduced somatostatin in the antrum, increased basal and meal-stimulated acid secretion
53
Acid secretion in duodenal ulcer vs gastric ulcer
Duodenal ulcer: increased acid secretion; Gastric ulcer: normal or decreased acid production
54
Gastric mucosa defense mechanisms
Gastric surface epithelium, mucus/phospholipid and bicarbonate barrier, epithelial cell renewal and regeneration, mucosal blood flow, alkaline tide, prostaglandin production
55
Role of prostaglandin in gastric mucosa
Stimulates mucus, bicarbonate, and phospholipid production
56
Effect of COX1 inhibition
Reduces prostaglandin synthesis, compromising gastric mucosa integrity
57
NSAIDs effect on COX enzymes
Inhibit both COX 1 and COX 2, which contributes to gastric injury
58
Non-H. pylori causes of peptic ulcers
Crohn's disease, Lymphoma, Gastrin-secreting tumors, Systemic Mastocytosis
59
Location of duodenal ulcers
D1/First portion of duodenum (>95%)
60
Typical characteristics of benign duodenal ulcers
Usually < 1 cm, sharply demarcated, high recurrence without H. pylori eradication
61
Reduction in duodenal ulcer recurrence post H. pylori eradication
>80% reduction
62
Why biopsy gastric ulcers upon discovery
Potential malignancy
63
Histopathology of NSAID-related gastric ulcers
Foveolar hyperplasia, lamina propria edema, epithelial regeneration, absence of H. pylori
64
Peak incidence age for gastric ulcers
6th decade
65
Primary causes of duodenal ulcers
H. pylori and NSAID-induced injuries
66
Acid production in gastric vs duodenal ulcers
Gastric ulcer: normal or decreased acid; Duodenal ulcer: increased acid secretion
67
Helicobacter pylori characteristics
Gram-negative, microaerophilic rod, spiral shape, unipolar flagella, urease production
68
Helicobacter pylori's diagnostic feature
Urease enzyme hydrolyzes urea to ammonia and CO2
69
Risk factors for H. pylori infection
Low socioeconomic status, less education, birth or residence in developing country, crowding, unsanitary conditions
70
Modes of H. pylori transmission
Person-to-person (oral-oral, fecal-oral, gastro-oral), contaminated water
71
Interplay determining H. pylori-induced gastrointestinal disease
Bacterial and host factors
72
Virulence factors associated with H. pylori
y-glutamyl transpeptidase (GGT), cagA, vacA, adhesins
73
Role of cag-PAI in H. pylori pathogenicity
Encodes CagA and other factors increasing risk of PUD, premalignant lesions, gastric cancer
74
H. pylori's effect on gastric epithelial cells
Apoptosis due to interaction with T cells and pro-inflammatory cytokines
75
Result of antral-predominant gastritis from H. pylori
Duodenal ulcer formation or asymptomatic infection
76
Potential outcomes of chronic corpus-predominant atrophic gastritis
Gastric ulcer, intestinal metaplasia, dysplasia, and potential gastric cancer