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Pathophysiology 1 > Jan 23 - Peptic Ulcer Disease > Flashcards

Jan 23 - Peptic Ulcer Disease Flashcards

1
Q

Name the different layers of the stomach lining from deep to superficial (kinda)

A 
Mucosal layer
Superficial epithelial cells
Parietal cells
Chief cells
G cells
Enterochromaffin-like (ECL) cells
Muscularis mucosa
Blood vessels
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2
Q

Describe the mucosal layer of the stomach lining

A

It faces the stomach

It’s a thick layer of mucous that protects the layer of skin that surrounds the stomach

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3
Q

Describe the superficial epithelial cells of the stomach lining

A

They have a high turnaround time (similar to the skin, they just schluff off). They are critical for producing mucous

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4
Q

What is the role of the parietal cells?

A

They are critical for the production of stomach acid (HCl)

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5
Q

What is the role of the chief cells?

A

They are involved in digestion; they produce digestive enzymes (pepsinogen, chymotrypsin, gastric lipase)

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6
Q

What is the role of G cells?

A

They produce gastrin, a peptide hormone that is most potent in the stimulation of the secretion of gastric acid by parietal cells of the stomach and aids in gastric mobility.

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7
Q

What is the role of enterochromaffin-like cells?

A

ECL cells are critical for the release of histamine, which is important because, upon stimulation, it causes the parietal cells to further increase acid production

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8
Q

Why are blood vessels important

A

Bicarbonate is drawn out from the bloodstream

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9
Q

Name three gastric acid producers

A

Acetylcholine (ACh)
Gastrin
Histamine

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10
Q

Name two gastric acid reducers

A

Prostaglandins

Somatostatin

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11
Q

How does acetylcholine work to produce gastric acid?

A

Cholinergic receptors are located on the parietal cell membranes. Vagal stimulation of muscarinic cholinergic parietal cells via muscarinic receptors activates the parietal cells to secrete gastric HCl

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12
Q

How does gastrin work to produce gastric acid? What stimulates gastrin release?

A

Gastrin binds to cholecystokinin B receptors (CCK2) to stimulate the release of histamines in ECL cells and it induces the insertion of K+/H+ ATPase pumps into apical membrane of the parietal cells (which in turn increases H+ release into the stomach cavity). Its release is stimulated by peptides in the lumen of the stomach.
It also causes chief cells to secrete pepsinogen, the zymogen (inactive) form of the digestive enzyme pepsin
It may impact lower esophageal sphincter (LES) tone, causing it to contract

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13
Q

How does histamine work to produce gastric acid?

A

Receptors located on the parietal cells and when stimulated by histamine, gastric acid secretion occurs. It is the most important gastric acid secretion stimulant and is released from ECL cells by gastric and cholinergic activity

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14
Q

How do prostaglandins work to reduce gastric acid?

A

PGE2, PGI2

Receptors located on parietal cells that when stimulated reduce gastric acid secretion

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15
Q

How does somatostatin work to reduce gastric acid?

A

It inhibits gastric acid secretion as receptors are located on the parietal cells

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16
Q

Besides mucous production, what is the role of superficial epithelial cells?

A

It draw bicarbonate from the blood and transfers it into the intermediate layer and protects superficial epithelial cells by neutralizing the acid

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17
Q

How does mucosal layer protect the stomach lining?

A

It acts as a physical barrier that pepsin and other proteases cannot penetrate and slows the diffusion of H+

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18
Q

What’s so dangerous about gastric acid?

A

It has a pH of 1-2, which denatures and hydrolyzes protein, hydrolyzes TG and carbohydrates. It also has pepsin and other proteases rapidly hydrolyzes protein. If there is an imbalance between gastric acid and mucosal defenses, it can result in inflammation and damage to the stomach lining leading to ulcerations

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19
Q

What are the two stages of of mucosal damage?

A

Erosion and ulcer

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20
Q

Describe erosion

A

Superficial injury of the gastrointestinal mucosa causes by decrease in mucosal defences or increase in gastric acid

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21
Q

Describe an ulcer

A

Complete erosion through the GI mucosa extends through the muscularis mucosa into the submucosa or deeper resulting in a GI bleed

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22
Q

What are the 3 main etiologies/causes peptic ulcer disease (PUD)?

A 
Helicobacter pylori (most common)
NSAID-induced (second most common)
Stress induced (uncommon)
23
Q

What is H pylori?

A

Gram-negative bacterium and 40% of individuals have them colonized in the stomach. It’s spread from person to person by fecal-oral route. Of the 40%, most (90%) have inflammation of the stomach (gastritis) or duodeum (duodenitis), which is usually asymptomatic. Only 15% of these go on to develop ulcers. 85% to 100% of duodenal ulcers and 65% of gastric ulcers are associated with H pylori

24
Q

What are the virulence factors of H pylori?

A

H pylori has genes that make it more capable of colonizing the stomach, penetrating through the mucus layer (to evade the low gastric pH) and causing inflammation and cell death

25
Q

How does H pylori affect the mucus lining?

A

H pylori is a spiral-shaped bacterium commonly found in the stomach. The bacteria’s shape and the way they move allow them to penetrate the stomach’s protective mucus lining, where they produce substances that weaken the lining and make the stomach more susceptible to damage from gastric acid

26
Q

What happens if the H pylori attaches to the cells of the stomach?

A

The bacteria can also attach to cells of the stomach, causing stomach inflammation (gastritis), and can stimulate the production of excess stomach acid. Over time, infection with the bacteria can also increase the risk of stomach cancer

27
Q

What is the mechanism of H pylori infection?

A

H pylori produces urease, which produces ammonia. The ammonia neutralizes gastric acid, allowing transit through stomach to the gastric mucosa. The flagella allows penetration of the mucus layer to the epithelial cell. After, the bacteria starts producing the toxins Vac A and LPS

28
Q

What is Vac A?

A

Vacuolating toxin; it induces inflammation/apoptosis, promotes formation of acidic vacuoles in cells, and it forms pores in the epithelial cell membrane

29
Q

What is LPS?

A

Lipopolysaccharides; it recruits and activates the immune cells resulting in inflammation that kills epithelial cells

30
Q

What is the most common symptom of peptic ulcer disease caused by H pylori?

A

Gnawing or burning abdominal pain, usually in the area just beneath the ribs. This pain typically gets worse when your stomach is empty and improves when you eat food, drink milk or take an antacid

31
Q

What are less common symptoms of peptic ulcer disease caused by H pylori?

A 
Weight loss
Loss of appetite
Bloating
Burping
Nausea
Vomiting (vomit may be bloody or look like coffee grounds)
Black tarry stools
32
Q

Why can H pylori infection lead to stomach cancer?

A

The more repeated damage creates scar tissue and the repeated damage can cause mutation in the stomach cells and eroded area can become cancerous

33
Q

What is more common, duodenal ulcer or gastric ulcer?

A

The duodenal ulcer is 4x more common than a gastric ulcer

34
Q

Describe the duodenal ulcer pathogenesis

A
  1. Antral H pylori infection
  2. Antral inflammation stimulates increased release of gastrin
  3. Gastrin induces acid secretion from the body of the stomach
  4. Increased acid damages the duodenal mucosa, causing ulceration
  5. Duodenal cells change into gastric-like cells (metaplasia)
  6. Metaplastic duodenum becomes colonized by H pylori
35
Q

Describe the gastric ulcer pathogenesis

A
  1. H pylori infection throughout most of the stomach
  2. Inflammation stimulates increased release of gastrin
  3. Gastrin induces increased acid secretion from body of stomach at first
  4. Increased acid and inflammation damages the gastric mucosa, causing ulceration
  5. Infection and inflammation causes loss of parietal and chief cells called atrophy, H+ decreases
36
Q

What are the symptoms of gastric ulceration?

A

Burning pain over a wide area below the breast bone

Precipitated by food (hurts when the patient eat); the food stimulates acid production

37
Q

What are the symptoms of duodenal ulceration?

A

Focal pain between breast bone and umbilicus
Pain relieved by eating but reoccurs 1-3 hours after meals
Pain also worse at night

38
Q

What is the main invasive method to diagnose H pylori PUD?

A

Histology - requires expert pathologist (and a biopsy)

39
Q

What are other invasive methods to diagnose H pylori PUD?

A 
Culture biopsy - allows culture and sensitivity
Rapid urease (CLO) test - cost effective, requires an additional test for confirmation of H pylori infection (still need a biopsy)
40
Q

What the main noninvasive method to diagnose H pylori PUD?

A

Urea breath test - expensive, reliable test to evaluate success of treatment for H pylori

41
Q

What are other noninvasive methods to diagnose H pylori PUD?

A

Fecal antigen test - simple test, not reliable for evaluation of treatment success
Serology - not reliable for routine screening; will test positive even after treatment due to immunological memory

42
Q

What are lifestyle changes are recommended when someone has to make if they have PUD

A

Reduce alcohol consumption (alcohol causes irritation of the cell lining)
Quit smoking (smoking cause larger ulcers, higher recurrence and makes them harder to treat)
Quit cocaine/amphetamine consumption (it reduces blood flow to gastric mucosa, which results in less bicarbonate to be taken up by the superficial epithelial cells)
Stop using NSAIDs (they could be the cause of the ulcer)

43
Q

What are NSAIDs?

A

Nonsteroidal anti-inflammatory drugs

44
Q

What do NSAIDs do?

A

They inhibit prostaglandins synthesis

45
Q

What do prostaglandins do in the stomach?

A

They stimulate bicarbonate secretion and mucus secretion

They stimulate mucosal cell growth and decrease acid production

46
Q

How is H pylori-induced PUD treated?

A

Antibiotics - H-pac: lansoprazole/amoxicillin/clarithromycin. They produce long-term cure in 80% of non NSAID induced ulcers

47
Q

What are other treatment options besides antibiotics for PUD?

A 
Discontinue NSAIDs
Stop smoking
Stop excessive alcohol consumption
Stop eating foods that cause pain
Reduce stress
48
Q

What are PUD complications?

A 
Acute or chronic GI tract bleeding (vomiting blood, rectal bleeding or dark tarry stools, massive loss of blood which results in hypotension, tachycardia and fainting)
Gastric ulcer (gastric cancer)
49
Q

What are three uncommon causes of PUD?

A

Zollinger-Ellison syndrome
Vascular insufficiency
Radiation therapy/chemotherapy

50
Q

What is zollinger-ellison syndrome?

A

A gastrin secreting tumor that produces hyper-activity. It can cause ulcers from stomach to lieum

51
Q

What causes vascular insufficiency?

A

Cocaine/crack use. It reduces gastric blood flow resulting in reduced HCO3- uptake

52
Q

How does radiation therapy/chemotherapy cause PUD?

A

It kills rapidly growing gastric epithelial cells

53
Q

Name some possible pharmacological treatment intervention strategies for PUD

A

Muscarinic antagonists (not really used - they block the muscarinic receptors)
Antibiotics to kill H pylori (main treatment method)
Histamine H2 receptors antagonists (less common - they effect the ECL cells)
Block H+/K+ ATPase (part of treatment of H pylori)
CCK2 receptor antagonists (they would work, but non exist)

Pathophysiology 1 (11 decks)

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