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Pathophysiology - Midterm > Lecture 11: Peptic Ulcer Disease > Flashcards

Lecture 11: Peptic Ulcer Disease Flashcards

1
Q

What are the 3 layers of the stomach?

A

1) Mucosa
2) Submucosa
3) Muscle

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2
Q

What is a part of the mucosa layer of the stomach?

A
  • Gastric pits
  • Mucus layer
  • Superficial epithelial cells
  • Parietal cells
  • Chief cells
  • G cells
  • ECL cell
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3
Q

What is the function of superficial epithelial cells?

A

Produce mucous and bicarbonate to neutralize acid and prevent damage to the lining of the stomach

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4
Q

What is the function of parietal cells?

A

Produce HCl

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5
Q

What is the function of chief cells?

A

Produce digestive enzymes (pepsinogen, chymotrypsin, gastric lipase)

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6
Q

What is the function of G cells?

A

Produce gastrin

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7
Q

What is the function of ECL cells?

A

Release histamine

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8
Q

What are 3 gastric acid producing hormones?

A

Acetylcholine, gastrin, and histamine

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9
Q

How does acetylcholine work to produce gastric acid?

A

Cholinergic receptors located on parietal cell membranes are stimulated by the vagus nerve and the muscarinic receptors activate the parietal cells to secrete HCl

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10
Q

What is gastrin?

A

A peptide hormone that is the most potent in stimulating secretion of gastric acid by parietal cells and aids in gastric motility

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11
Q

Gastrin is released by ___

A

G cells in the pyloric antrum of the stomach, duodenum, and pancreas

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12
Q

How does gastrin work to produce gastric acid?

A

Gastrin binds to cholecystokinin B receptors to stimulate release of histamine in ECL cells and it induces the insertion of K+/H+ ATPase pumps into apical membrane of parietal cells

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13
Q

Gastrin release is STIMULATED by ____

A

Peptides in stomach lumen

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14
Q

What is the ultimate result of gastrin secretion?

A

Causes chief cells to secrete pepsinogen

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15
Q

How does histamine work to produce gastric acid?

A

Histamine stimulates receptors on parietal cells to secrete gastric acid

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16
Q

What is the most important gastric acid secretion stimulant?

A

Histamine

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17
Q

Histamine is released from ____

A

ECL cells by gastric and cholinergic activity

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18
Q

What are 2 hormones that are gastric acid reducers?

A

1) Prostaglandins

2) Somatostatin

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19
Q

How do prostaglandins work to reduce gastric acid?

A

Stimulate receptors on parietal cells to decrease gastric acid secretion

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20
Q

What is a secondary function of prostaglandins?

A

Increase mucous and bicarbonate production

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21
Q

How does somatostatin work to reduce gastric acid?

A

Binds to receptors on parietal cells to inhibit gastric acid secretion

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22
Q

What is mucous?

A
  • Physical barrier that pepsin and other proteases cannot penetrate
  • Slows diffusion of H+ pH gradient from 2-6
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23
Q

What is the function of the bicarbonate layer?

A

Neutralize H+

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24
Q

What type of cells are rapidly replaced?

A

Superficial epithelial cells

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25
Q

What is the function of mucosal blood flow?

A

Supplies HCO3-

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26
Q

What are 2 dangers of gastric acid?

A

1) HCl has pH of 1-2 that denatures and hydrolyzes protein and carbohydrates
2) Has pepsin and other proteases that rapidly hydrolyze protein

27
Q

What can an imbalance between gastric acid and mucosal defenses cause?

A

Inflammation and damage to the stomach, ultimately causing ulcerations

28
Q

What is erosion?

A

Superficial injury of GI mucosa caused by a decrease in mucosal defenses or an increase in gastric acid

29
Q

What is an ulcer?

A

Complete erosion through GI mucosa that extends through muscularis mucosa into submucosa or deeper, causes GI bleeding

30
Q

What are the 3 main causes of peptic ulcers?

A

1) Helicobacter pylori
2) NSAID induced
3) Stress induced

31
Q

What are the 2 kinds of peptic ulcers?

A

Gastric and duodenal

32
Q

What percent of the population is infected with H pylori?

A

40%

33
Q

What percent of people infected with H pylori have inflammation of the stomach?

A

About 90%

34
Q

What percent of people infected with H pylori go on to develop ulcers?

A

15%

35
Q

What percent of duodenal ulcers and what percent of gastric ulcers are caused by H pylori?

A
  • Duodenal – 85-100%

- Gastric – 65%

36
Q

What are virulence factors of H pylori?

A

Genes that make it more capable of colonizing the stomach, penetrating through the mucous layer, and causing inflammation and cell death

37
Q

How can H pylori be contracted?

A

Through food and water or by fecal-oral route

38
Q

Give a broad description on how H pylori causes stomach ulcers

A

A spiral-shaped bacterium that can attach to cells of the stomach and stimulate excess production of stomach acid

39
Q

How is urease produced and what is its function?

A
  • Produced by ammonia

- Neutralizes gastric acid allowing transit through stomach to gastric mucosa

40
Q

What is the function of flagella for H pylori?

A

Allow penetration of the mucous layer to epithelial cells

41
Q

What is vac A?

A

A vacuolating toxin

42
Q

What are 3 functions of vac A in PUD?

A

1) Induces inflammation/apoptosis (programmed cell death)
2) Promotes formation of acidic vacuoles in cells
3) Forms pores in epithelial cell membranes

43
Q

What is the function of LPS in PUD?

A

Recruits and activates immune cells

44
Q

What is the most common symptom of PUD?

A

Gnawing or burning abdominal pain, usually just beneath ribs

45
Q

What are secondary symptoms of PUD?

A

Weight loss, loss of appetite, bloating, burping, nausea, vomiting (may be bloody), or black, tarry stool

46
Q

Describe the pathogenesis of duodenal ulcers

A

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

47
Q

Describe the pathogenesis of gastric ulcers

A

1) H pylori infects most of stomach
2) Inflammation stimulates increased release of gastrin
3) Gastrin induces increased acid secretion from body of stomach
4) Increased acid and inflammation damages gastric mucosa, causing ulceration
5) Infection and inflammation cause loss of parietal and chief cells, causing decreased H+

48
Q

What are symptoms of a gastric ulcer?

A
  • Burning pain over a wide area below breast bone

- Precipitated by food

49
Q

What are symptoms of a duodenal ulcer?

A
  • Focal pain between breast bone and umbilicus
  • Pain relieved by eating, but reoccurs 1-3 hours after meals
  • Pain also worse at night
50
Q

True or false: symptoms are enough to diagnosis a patient with a peptic ulcer

A

False, symptoms alone do not provide a definitive diagnosis

51
Q

True or false: ulcers can be asymptomatic

A

True

52
Q

What are 3 lifestyle choices that cause ulcers?

A

1) Alcohol consumption
2) Smoking
3) Cocaine/amphetamines

53
Q

How does cocaine/amphetamines cause ulcers?

A

Reduces blood flow to gastric mucosa, causing decreased secretion of bicarbonate

54
Q

What is an NSAID?

A

Non-steroidal anti-inflammatory drug

55
Q

What is the function of NSAIDs?

A

Inhibit prostaglandin synthesis

56
Q

What are some complications of PUD?

A
  • Acute or chronic GI bleeding
  • Vomiting blood
  • Rectal bleeding
57
Q

What can a massive loss of blood from PUD cause?

A

Hypotension, tachycardia, or fainting

58
Q

What are 3 less common causes of PUD?

A

1) Zollinger-Ellision syndrome
2) Vascular insufficiency
3) Radiation/chemotherapy

59
Q

How can Zollinger-Ellison syndrome cause PUD?

A
  • Gastrin secreting tumour

- Produces hyper-acidity

60
Q

How can vascular insufficiency cause PUD?

A

Decreased blood flow to stomach means less bicarbonate

61
Q

How can radiation/chemotherapy cause PUD?

A

Kills rapidly growing gastric superficial epithelial cells

62
Q

What are 4 non-pharm treatments for PUD?

A
  • Stop smoking
  • Stop excessive alcohol consumption
  • Stop eating foods that cause pain
  • Decrease stress
63
Q

What are 4 possible pharmacological treatment interventions for PUD?

A

1) Muscarinic antagonists (not really used)
2) Antibiotics to kill H pylori (main treatment method)
3) Histamine H2 receptor antagonists
4) Block K+/H+ ATPase

Pathophysiology - Midterm (11 decks)

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