Module- Drugs for Peptic Ulcers Flashcards

1
Q

Which ulcers are more common duodenal or gastric?

A

duodenal

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2
Q

T/F: It is rare to develop ulcers before the age of 30

A

true

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3
Q

T/F: Males and females are just as likely to get ulcers as eachother

A

true

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4
Q

T/F: signs and symptoms depend on location of ulcer

A

true

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5
Q

Duodenoal ulcers present with what two factors in what location?

A
  • burning or gnawing pain

- abdomen btw breastbone and navel

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6
Q

What is duodenal burning more commonly reported as and how long after meals?

A
  • heartburn; 1-3hrs after meal
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7
Q

t/f: Nausea and vomiting are prominent in duodenal ulcers

A

false; rarely present

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8
Q

When is pain with duodenal ulcers often relieved?

A

after meals

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9
Q

What are duodenal ulcers most commonly associated with?

A
  • chronic NSAID use
  • helicobacter pylori infections
  • smoking
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10
Q

t/f: duodenal ulcers can heal on their own

A

true

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11
Q

Severe duodenal ulcers

A
  • erode deep layers of stomach

- causes bleeding

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12
Q

What signs are associated with severe duodenal ulcers?

A
  • black tarry stool

- anemia

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13
Q

T/F: gastric ulcers occur less frequently than duodenal ulcers

A

true

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14
Q

Gastric ulcers occur with

A
  • chronic NSAID use
  • stress
  • H.pylori infections
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15
Q

T/F: pain is often relived after eating with GASTRIC ULCERS

A

false; rarely

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16
Q

Patients with gastric ulcers often experience what?

A
  • anorexia

- weight loss

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17
Q

Which type of ulcer commonly has vomitting?

A

gastric

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18
Q

In which population are gastric ulcers more commonly found in?

A

elderly

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19
Q

T/F: gastric ulcers can sometimes become cancerous

A

true

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20
Q

T/F: gastric ulcers can sometimes become cancerous

A

true

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21
Q

is monitoring required in the long term for gastric ulcers?

A

yes

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22
Q

How do NSAIDS effect peptic ulcer diseases

A
  • mask pain and discomfort
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23
Q

Peptic ulcer pathophysiology

A
  • attributed to imbalance between mucosal destructive and muscosal protective factors
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24
Q

What is gastric acid secreted by?

A

parietal cells in the mucosa of the stomach

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25
Q

What is the pH of gastric?

A

2; can digest stomach wall when mucosal defences are disrupted

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26
Q

Gastric acid has receptors for; function

A
  • Ach
  • Gastrin
  • Histamine
  • stimulate gastric acid production
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27
Q

In what periods are gastric acid produced and secreted?

A

physiological and psychological stress

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28
Q

Those with peptic ulcer hyper or hypo secrete gastric acid?

A

hypersecrete

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29
Q

Pepsin: what is its function?

A
  • helps digest proteins in food
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30
Q

What features can pepsin also digest?

A
  • stomach and duodenal wall
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31
Q

In what environment is pepsinogen converted to pepsin?

A

high acidic

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32
Q

In what period is pepsin secreted?

A

times of physiological and psychological stress

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33
Q

Helicobacter pylori is found in what percent of people with gastric ulcers

A

60-80%

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34
Q

Helicobacter pylori is found in what percent of people with duodenal ulcers?

A

80-85%

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35
Q

What is considered to be the primary cause of peptic ulcers?

A

Helicobacter pylori

36
Q

How is the infection of Helicobacter pylori spread?

A

oral to oral; ingestion of infected feces

37
Q

How does Helicobacter pylori cause ulcers?

A
  • penetrates stomach lining

- produced gastritis and ulcerations of mucosal linings

38
Q

Function of NSAIDS

A
  • inhibit prostaglandins synthesis
  • inhibits mucosal secretion
  • increase gastric acid production
  • leave gastric and duodenal mucosa vulnerable to ulcerations
39
Q

What is the second most common cause of peptic ulcers?

A

NSAIDS

40
Q

T/F: cigarette smoking increases chances of peptic ulcers

A

true

41
Q

T/F: Cigarrette smoking decreases pancreatic bicarbonate production

A

true

42
Q

How to prevent autodigestion of stomach and duodenal tissues and inhibit ulcer formation

A
  • synthesis of mucous and bicarb
  • production of prostaglandins E
  • alkalinisation of gastric secretions by pancreatic juices and bile
43
Q

What is the main role of prostaglandin E in keeping individuals healthy?

A
  • prostaglandin E inhibits gastric acid release by blocking the stimulatory effects of histamine on parietal cell proton pumps
44
Q

Peptic ulcer disease (4) steps

A
  • Helicobacter pylori and chronic NSAID can induce erosion of gastric or duodenal mucosa
  • hyper secrete gastric acid
  • gastric juices present in stomach further break down the mucosal lining of stomach/duodenom
  • produces ulcer
45
Q

T/F: One is advised to change lifestyle before pharma therapy

A

true

46
Q

Life style changes for remission

A
  • quit smoking
  • no alcohol
  • reduce stress
47
Q

Goals of pharmacotherapy

A
  • symptom relief
  • promotion of ulcer healing
  • prevention of peptic ulcer reoccurrence
48
Q

t/f: most treatment involves combination drug therapy

A

true

49
Q

What is the gold standard for diagnosis of peptic ulcer disease

A
  • endoscopy; inspecting lining of gastric and duodenal mucosa for erosion and ulceration
50
Q

Once the peptic ulcer is identified what occurs?

A
  • biopsy of stomach and duodenum collected to determine cause
51
Q

Possible causes for peptic ulcers

A
  • Helicobacter pylori
  • inflammation r/t NSAIDS or stress
  • cancer
52
Q

Histological examination is the gold standard because

A

tells us which organism is present in the tissue

53
Q

Rapid urease test is used for

A
  • based on ability of Helicobacter pylori to produce urease

- provides rapid testing

54
Q

Culture is used for

A
  • biopsy of Helicobacter
54
Q

Culture is used for

A
  • biopsy of Helicobacter
55
Q

t/f: culture is rarely performed unless antimicrobial susceptibility testing is required

A

true

56
Q

t/f: all patients with Helicobacter pylori develop peptic ulcers

A

false

57
Q

What are the four main drug classes prescribed?

A
  • antiacids
  • antimicrobials
  • histamine H2 receptor antagonists
  • proton pump inhibitor
58
Q

Antacids

A
  • alkaline substance
  • neutralize acid in stomach
  • increase pH
  • inhibit pepsinogen to pepsin
  • alters rate of absorption
59
Q

How much do antacids increase pH levels by

A
  1. 5 to 3

- neutralizes more than 90% of gastric acid

60
Q

Antacids inhibit absorption of

A
  • benzos
  • coricosteroids
  • digoxin
  • histamin H2 receptor antagonists
  • iron supplements
  • antipsychotic drugs
  • antibiotics
61
Q

Antiacids increase absorption of

A

● Levodopa
● Valproic acid

***administer 1-2 hours after or before

62
Q

What are antiacids normally used for?

A

relieve abdominal discomfort

63
Q

T/F: antiacids can heal peptic ulcers as single therapy

A

false; should be used with other medications

64
Q

antiaicds are or are not cost effective

A

are cost effective

65
Q

Antacids w/ calcium, aluminum, and magnesium = first choice; What does aluminum do? and what does magnesium do?

A

Aluminum minimizes constipation

Magnesium minimizes diarrhea

66
Q

Antimicrobials

A

Treat H.pylori and heal ulcers → 2 antibiotics and proton pump inhibitor is GOLD STANDARD

67
Q

Antimicrobials: Antibiotic drugs

A
  • Amoxicillin
  • Clarithromycin
  • Metronidazole
  • Tetracycline
68
Q

Addition of proton pump inhibitor OR histamine H2 receptor does what?

A

accelerates symptoms relief and ulcer healing

69
Q

Bismuth or pepto bismol

A
  • Possess antimicrobial effect on H.pylori
  • Disrupts bacterial cell walls
  • Prevents organism from adhering to gastric epithelium
  • Inhibits bacterial enzymatic activity
  • Increases secretion of mucous and bicarbonate
  • Inhibits pepsin activity
  • Accumulates in ulcer craters
  • Not sufficient to eradicate H.pylori
70
Q

Histamine H2 Receptor Antagonists

A
  • Inhibit basal secretion of gastric acid
  • Inhibit secretion of gastric acid stimulated by histamines, ACh, and gastrin
  • Decrease the amount of acidity and pepsin content of gastric juices
  • Lasts for 6-12 hrs post administration
71
Q

How long does ulcer healing take

A
  • 6/8 weeks after drug therapy

- associated pain typically stops 1-2 weeks of therapy

72
Q

If you’re treating acute ulcers how long of therapy would it take?

A
  • full 8 weeks

- once healed its reduced by 50% for maintenance therapy to prevent recurrence

73
Q

T/F: Histamine H2 antagonists have been replaced by proton pump inhibitor drugs as first line therapy

A

true

74
Q

T/F: you can take antacids and HRA’s together (if F, correct)

A
  • F

- antacids reduce absorption of HRA

75
Q

MOA of Proton Pump Inhibitors (PPIs)

A

Inhibits parietal cell H/K ATP pump (bind irreversibly)

- • Inhibits both daytime (stimulated) and nocturnal (unstimulated) gastric acid secretion

76
Q

T/F: PPIs block effect of all gastric stimuli on secretion (if F, correct)

A

True

77
Q

How long after administration are effects normally seen?

A

72 hours

78
Q

MOA of misoprostol

A

Synthetic form of prostaglandin E
• Inhibits gastric acid secretion
• Increases mucous and bicarbonate secretion
• Enhances mucosal blood flow and repair

79
Q

T/F: chronic NSAID use block synthesis of prostaglandin E2 (if F, correct)

A

true

80
Q

Contraindications of misprostol

A

women in childbearing age

81
Q

MOA of sucralfate

A
  • Binds to ulcerated tissue, Creates a barrier between gastric acids and peptic ulcers
  • No effect on gastric acid secretion or pH of gastric acid
82
Q

T/F: sucralfate has no effect on H. pylori (if F, correct)

A

true

83
Q

What can you not co-administer sucralfate with? Why?

A
  • antacid
  • PPI
  • HRA
  • may bind to the other drugs and inhibit their absorption
84
Q

What nutrient deficiencies can occur due to prolonged use of HRAs or PPIs? Why?

A
  • folate, calcium, iron, B12

- these nutrients are best absorbed in an acidic environment, these drugs increase gastric pH