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Therapeutics Y2 Sem 2 > Peptic Ulcer Disease Management > Flashcards

Peptic Ulcer Disease Management Flashcards

1
Q

What is the incidence of gastric ulcers/Duodenal ulcers?

A

2-2.9%

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2
Q

What are the main alarm symptoms?

A

VBAD

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3
Q

Who should receive an endoscopy? (4)

A
  • New onset symptoms >50 (>60) years of age
  • Any alarm symptoms
  • Refractory symptoms
  • At risk for Barrett’s esophagus
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4
Q

What are the systematic approach in patients presenting wit hdyspepsia?

A

1) Other possible causes?
2) Upper GI location?
3) New onset >50 (>60) or red flag symptoms?
4) NSAID use?
6) H. Pylori present?

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5
Q

What is the definition of Peptic Ulcer Disease?

A

Any breach in the mucosa of the digestive tract

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6
Q

What are the majority of PUD?

A

Gastric duodenal ulcers and differ from gastric erosions

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7
Q

What are the aggressive factors of PUD?

A
  • H. Pylori ● Acid
  • NSAIDs ● Ethanol
  • Pepsin ● Smoking?
  • Physiologic stress ● Psychologic stress?
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8
Q

What are the protective factors of PUD?

A
  • Gastric mucous
  • HCO3
  • Prostaglandins
  • Mucosal blood flow
  • Epithelial cell regeneration
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9
Q

What is NSAID-Induced PUD?

A

↓ COX-1 activity = ↓ prostaglandins = predispose mucosa to injury
* Dose and duration an important determinant of risk
* Presence of dyspeptic symptoms and severity poorly correlated to PUD

There is no topical effect, hence when we even recieve NSAIDS via IV, we have these same issues

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10
Q

Which NSAIDs have the lowest risk profile for PUD?

A

Celecoxib and Ibuprofen

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11
Q

What NSAID have the highest risk?

A

Piroxicam and Ketorolac

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12
Q

What high dose of Celecoxib reduces the Cox-2 selectivity?

A

> 400mg/day

Concomitant ASA or anticoagulant increases ulcer risk

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13
Q

What is the determining risk of NSAID-induced ulcers?

A
  • History of an uncomplicated ulcer
  • Age >60 (++ risk >70)
  • High-dose or multiple NSAID use
  • Concomitant ASA, glucocorticoids, anticoagulants, antiplatelets, SSRI
  • History of CVD
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14
Q

What is H.pylori induced PUD?

A
  • A gram-negative rod bacteria spread by fecal – oral route
  • Exclusively colonizes gastric epithelium
  • Risk factors for colonization:
  • Crowded living conditions
  • Unclean water
  • Raw vegetables
  • Produces urease, which converts urea → ammonia
  • Also produces phospholipase and catalase
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15
Q

How does H.pylori woork?

A

Renders underlying mucosa more vulnerable to acid damage and high levels of ammonia
(Prevents detection of acidity, and direct toxic effect on epithelial cells)

Promotes cytokine and inflammation

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16
Q

What is the general symptom difference between dueodenal ulcer and gastric ulcer?

A

Duodenal ulcer is initially relievs pain then pain 2-5 hours after a meal and at night

Gastric ulcer is immediately worsened by food

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17
Q

Complicaitons of PUD?

A
  • Quality of life decrease
  • GI Bleeds
  • Perforations or fistulation
  • Gastric outlet obstructions
  • Mortality increase
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18
Q

What are the clinical symptoms of PUD complications with respect to bleeding?

A
  • Nausea and vomiting
  • Hematemesis
  • Melena
  • Orthostatic hypotension
  • Red blood in stool if massive bleed (hematochezia)
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19
Q

What are the clinical symptoms of PUD complications with respect to obstruction?

A
  • Nausea and vomiting
  • Early satiety
  • Bloating
  • Indigestion
  • Anorexia and weight loss
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20
Q

What are the clinical symptoms of PUD complications with respect to perforation or fistulas?

A
  • Sudden change in symptom pattern
  • Halitosis
  • Post-prandial diarrhea
  • Weight loss
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21
Q

What is the establishment of the cause of PUD?

A

H.Pylori testing and NSAID assessment use

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22
Q

What is the evaluation of other causes for PUD?

A
  • Smoking history
  • Acid hypersecretion
  • Local ischemia
  • Other ulcerogenic drugs
  • H. Pylori false negative
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23
Q

What are the indications of H.pylori testing?

A
  • Active or past history of PUD
  • History of H. Pylori infection and recurrent symptoms
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24
Q

What are the methods for H.Pylori testing?

A

Endoscopy
Urea breath testing
Stool antigen assay
Serology

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25
Q

What are the risk of recurrence of PUD?

A
  • NSAIDs
  • H. Pylori suboptimal eradication or reinfection
  • Smoking
  • Alcohol use
  • Long-standing PUD
26
Q

What are the goals of therapy with respect to PUD?

A
  • Relieve dyspepsia
  • Heal the ulcer
  • Prevent complications
  • Prevent recurrence
  • Implement lifestyle changes
  • Avoid foods that trigger symptoms
  • Eliminate alcohol intake
  • Smoking cessation
27
Q

What is the txtmnt of NSAID-induced ulcer?

A

Stop NSIAD
PPI standard dose
Duration (Variable)
H.Pylori testing

28
Q

What is the duration of therapy for gastric ulcer healing?

A

8 to 12 weeks

29
Q

What is the duration of therapy for Duodenal ulcer healing?

A

4 to 8 weeks

30
Q

What are some secondary prevention of NSAID-induced PUD strategies?

A

Lower NSAID dose
Switch to celecoxib
Add long-term PPI
Add misoprostol

31
Q

What is the secondary prevention of NSAID-induced PUD-indications?* Continued NSAID use

A
  • Continued NSAID use
  • Giant ulcer and age >50 years
  • H. Pylori resistance
  • Refractory peptic ulcer
  • Recurrent peptic ulcer
32
Q

What is the primary prevention of NSAID-Induced PUD?

A
  • History of an uncomplicated ulcer
  • Age >60 (++ risk >70)
  • High-dose or multiple NSAIDs
  • Concomitant ASA, corticosteroids, antiplatelet agents, anticoagulants, SSRIs
  • History of CVD
33
Q

What is the pharmacology of misoprostol?

A
  • A prostaglandin analogue leading to an increase in:
  • Gastric mucous
  • Bicarbonate secretion
  • Inhibition of basal and nocturnal gastric acid secretion
34
Q

What is the indications of Misoprostol?

A

Treatment of duodenal ulcer
Prevention of NSAID-induced ulcers

35
Q

What are the ADRs of misoprostol?

A

Mg+ antacids

36
Q

What are the current first line drugs used for eradication regimens for H.pylori?

A
  • PBMT - bismuth quadruple therapy
  • PAMC – non-bismuth quadruple therapy
37
Q

What is PBAMTCLF?

A
  • PPIs standard doses
  • Bismuth (subsalicylate, subcitrate)
  • Amoxicillin
  • Metronidazole
  • Tetracycline
  • Clarithromycin
  • Levofloxacin
  • Rifabutin
38
Q

What is PBMT therapy?

A

PPI
Bismuth
Metronidazole
Tetracycline

39
Q

What is PAMC therapy?

A

PPI
Amoxicillin
Metronidazole
Clarithromycin

40
Q

When should triple therapy be used?

A

Only if resistance is less then 15% (Data not available(

41
Q

What are the advantages of PBMT therapy?

A
42
Q

What are the disadvantages of PBMT therapy?

A
43
Q

What is the overall dosing regiment of PBMT?

A

14 days

44
Q

What is the advantages of PAMC?

A
45
Q

What is the disadvantages of PAMC?

A
46
Q

What is the dosing regimen of PAMC?

A
47
Q

What are the disadvantages of three regimen?

A
48
Q

What is generally used if PAMC or PBMT failure?

A

PAL

PPI
Amoxicillin
Levofloxacin

49
Q

What is the regimen details for sequential therapy?

A

Pa –> PMC

PPI BID + Amoxicillin 1000mg BID for 5 days followed by

PPI BID + clarithromycin 500mg BID + Metronidazole 500mg BID for 5 days

50
Q

What is the benefit for sequential therapy for sequential therapy?

A

May reduce GI ADRs

51
Q

What is the disadvantages for sequential therapy for sequential therapy?

A

Complexity
High failures rate similar to triple therapy

52
Q

What are common reasons for H. Pylori induced ulcer txtmnt failure

A

Adherence
Incorrect regimen used
High local resistance

53
Q

Confirmation of eradication for H.pylori-induced ulcer management?

A
  • Test four weeks after completion of therapy
  • Fecal stool antigen test is optimal to confirm
54
Q

What is the maintenance therapy with PPIs afer H. Pylori eradication?

A
  • Duodenal ulcer: generally not indicated…possibly 2 weeks
  • Gastric ulcer: continue PPI for 8 weeks
  • If continuing, reduce PPI to once daily
55
Q

What are some other options for H. Pylori-induced ulcer management?

A

Probiotics and maybe sucralafate

56
Q

Non-H. Pylori and non-NSAID ulcers

A
  • Poor prognosis
  • PPI x 4-8 weeks only option to treat
  • Increase dose and duration if initial trial fails
  • Reassess and consider alternate diagnosis if little improvement
  • Consider long-term PPI
57
Q

PUD during pregnancy and lactation

A

Treat as usual

PPI use: Lansoprazole, omeprazole, pantoprazole

Lactation: prefer pantoprazole

58
Q

When should we defer H. Pylori eradication in pregnancy?

A

Untill delivery as the antibiotics, avoid tetracycline and bismuth

59
Q

Refractory PUD can be defined as those

A

Risk of refractory disease increased by:
* Continued NSAID use
* Poor compliance
* Inadequate H.Pylori testing/eradication
* Smoking
* Genetic rapid metabolizer of PPIs
* Hypersecretory disease

60
Q
A

Therapeutics Y2 Sem 2 (17 decks)

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