Module- Drugs for Peptic Ulcers Flashcards
1
Q
Which ulcers are more common duodenal or gastric?
A
duodenal
2
Q
T/F: It is rare to develop ulcers before the age of 30
A
true
3
Q
T/F: Males and females are just as likely to get ulcers as eachother
A
true
4
Q
T/F: signs and symptoms depend on location of ulcer
A
true
5
Q
Duodenoal ulcers present with what two factors in what location?
A
- burning or gnawing pain
- abdomen btw breastbone and navel
6
Q
What is duodenal burning more commonly reported as and how long after meals?
A
- heartburn; 1-3hrs after meal
7
Q
t/f: Nausea and vomiting are prominent in duodenal ulcers
A
false; rarely present
8
Q
When is pain with duodenal ulcers often relieved?
A
after meals
9
Q
What are duodenal ulcers most commonly associated with?
A
- chronic NSAID use
- helicobacter pylori infections
- smoking
10
Q
t/f: duodenal ulcers can heal on their own
A
true
11
Q
Severe duodenal ulcers
A
- erode deep layers of stomach
- causes bleeding
12
Q
What signs are associated with severe duodenal ulcers?
A
- black tarry stool
- anemia
13
Q
T/F: gastric ulcers occur less frequently than duodenal ulcers
A
true
14
Q
Gastric ulcers occur with
A
- chronic NSAID use
- stress
- H.pylori infections
15
Q
T/F: pain is often relived after eating with GASTRIC ULCERS
A
false; rarely
16
Q
Patients with gastric ulcers often experience what?
A
- anorexia
- weight loss
17
Q
Which type of ulcer commonly has vomitting?
A
gastric
18
Q
In which population are gastric ulcers more commonly found in?
A
elderly
19
Q
T/F: gastric ulcers can sometimes become cancerous
A
true
20
Q
T/F: gastric ulcers can sometimes become cancerous
A
true
21
Q
is monitoring required in the long term for gastric ulcers?
A
yes
22
Q
How do NSAIDS effect peptic ulcer diseases
A
- mask pain and discomfort
23
Q
Peptic ulcer pathophysiology
A
- attributed to imbalance between mucosal destructive and muscosal protective factors
24
Q
What is gastric acid secreted by?
A
parietal cells in the mucosa of the stomach
25
What is the pH of gastric?
2; can digest stomach wall when mucosal defences are disrupted
26
Gastric acid has receptors for; function
- Ach
- Gastrin
- Histamine
- stimulate gastric acid production
27
In what periods are gastric acid produced and secreted?
physiological and psychological stress
28
Those with peptic ulcer hyper or hypo secrete gastric acid?
hypersecrete
29
Pepsin: what is its function?
- helps digest proteins in food
30
What features can pepsin also digest?
- stomach and duodenal wall
31
In what environment is pepsinogen converted to pepsin?
high acidic
32
In what period is pepsin secreted?
times of physiological and psychological stress
33
Helicobacter pylori is found in what percent of people with gastric ulcers
60-80%
34
Helicobacter pylori is found in what percent of people with duodenal ulcers?
80-85%
35
What is considered to be the primary cause of peptic ulcers?
Helicobacter pylori
36
How is the infection of Helicobacter pylori spread?
oral to oral; ingestion of infected feces
37
How does Helicobacter pylori cause ulcers?
- penetrates stomach lining
| - produced gastritis and ulcerations of mucosal linings
38
Function of NSAIDS
- inhibit prostaglandins synthesis
- inhibits mucosal secretion
- increase gastric acid production
- leave gastric and duodenal mucosa vulnerable to ulcerations
39
What is the second most common cause of peptic ulcers?
NSAIDS
40
T/F: cigarette smoking increases chances of peptic ulcers
true
41
T/F: Cigarrette smoking decreases pancreatic bicarbonate production
true
42
How to prevent autodigestion of stomach and duodenal tissues and inhibit ulcer formation
- synthesis of mucous and bicarb
- production of prostaglandins E
- alkalinisation of gastric secretions by pancreatic juices and bile
43
What is the main role of prostaglandin E in keeping individuals healthy?
- prostaglandin E inhibits gastric acid release by blocking the stimulatory effects of histamine on parietal cell proton pumps
44
Peptic ulcer disease (4) steps
- 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
T/F: One is advised to change lifestyle before pharma therapy
true
46
Life style changes for remission
- quit smoking
- no alcohol
- reduce stress
47
Goals of pharmacotherapy
- symptom relief
- promotion of ulcer healing
- prevention of peptic ulcer reoccurrence
48
t/f: most treatment involves combination drug therapy
true
49
What is the gold standard for diagnosis of peptic ulcer disease
- endoscopy; inspecting lining of gastric and duodenal mucosa for erosion and ulceration
50
Once the peptic ulcer is identified what occurs?
- biopsy of stomach and duodenum collected to determine cause
51
Possible causes for peptic ulcers
- Helicobacter pylori
- inflammation r/t NSAIDS or stress
- cancer
52
Histological examination is the gold standard because
tells us which organism is present in the tissue
53
Rapid urease test is used for
- based on ability of Helicobacter pylori to produce urease
| - provides rapid testing
54
Culture is used for
- biopsy of Helicobacter
54
Culture is used for
- biopsy of Helicobacter
55
t/f: culture is rarely performed unless antimicrobial susceptibility testing is required
true
56
t/f: all patients with Helicobacter pylori develop peptic ulcers
false
57
What are the four main drug classes prescribed?
- antiacids
- antimicrobials
- histamine H2 receptor antagonists
- proton pump inhibitor
58
Antacids
- alkaline substance
- neutralize acid in stomach
- increase pH
- inhibit pepsinogen to pepsin
- alters rate of absorption
59
How much do antacids increase pH levels by
2. 5 to 3
| - neutralizes more than 90% of gastric acid
60
Antacids inhibit absorption of
- benzos
- coricosteroids
- digoxin
- histamin H2 receptor antagonists
- iron supplements
- antipsychotic drugs
- antibiotics
61
Antiacids increase absorption of
● Levodopa
● Valproic acid
***administer 1-2 hours after or before
62
What are antiacids normally used for?
relieve abdominal discomfort
63
T/F: antiacids can heal peptic ulcers as single therapy
false; should be used with other medications
64
antiaicds are or are not cost effective
are cost effective
65
Antacids w/ calcium, aluminum, and magnesium = first choice; What does aluminum do? and what does magnesium do?
Aluminum minimizes constipation
| Magnesium minimizes diarrhea
66
Antimicrobials
Treat H.pylori and heal ulcers → 2 antibiotics and proton pump inhibitor is GOLD STANDARD
67
Antimicrobials: Antibiotic drugs
- Amoxicillin
- Clarithromycin
- Metronidazole
- Tetracycline
68
Addition of proton pump inhibitor OR histamine H2 receptor does what?
accelerates symptoms relief and ulcer healing
69
Bismuth or pepto bismol
- 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
Histamine H2 Receptor Antagonists
- 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
How long does ulcer healing take
- 6/8 weeks after drug therapy
| - associated pain typically stops 1-2 weeks of therapy
72
If you're treating acute ulcers how long of therapy would it take?
- full 8 weeks
| - once healed its reduced by 50% for maintenance therapy to prevent recurrence
73
T/F: Histamine H2 antagonists have been replaced by proton pump inhibitor drugs as first line therapy
true
74
T/F: you can take antacids and HRA's together (if F, correct)
- F
| - antacids reduce absorption of HRA
75
MOA of Proton Pump Inhibitors (PPIs)
Inhibits parietal cell H/K ATP pump (bind irreversibly)
| - • Inhibits both daytime (stimulated) and nocturnal (unstimulated) gastric acid secretion
76
T/F: PPIs block effect of all gastric stimuli on secretion (if F, correct)
True
77
How long after administration are effects normally seen?
72 hours
78
MOA of misoprostol
Synthetic form of prostaglandin E
• Inhibits gastric acid secretion
• Increases mucous and bicarbonate secretion
• Enhances mucosal blood flow and repair
79
T/F: chronic NSAID use block synthesis of prostaglandin E2 (if F, correct)
true
80
Contraindications of misprostol
women in childbearing age
81
MOA of sucralfate
* 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
T/F: sucralfate has no effect on H. pylori (if F, correct)
true
83
What can you not co-administer sucralfate with? Why?
- antacid
- PPI
- HRA
- may bind to the other drugs and inhibit their absorption
84
What nutrient deficiencies can occur due to prolonged use of HRAs or PPIs? Why?
- folate, calcium, iron, B12
| - these nutrients are best absorbed in an acidic environment, these drugs increase gastric pH
