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Fall 2014 - Pharm GI/ENT > PUD > Flashcards

PUD Flashcards

1
Q

How many in the US population develop PUD in their lifetime?

A

10%

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2
Q

What are the causes of PUD?

A
  • H pylori
  • NSAIDs
  • stress related mucosal damage
  • Zollinger-Ellison syndrome
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3
Q

What is a potential risk factor for PUD?

A

smoking

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4
Q

Pathophysiology of PUD

A

-imbalance between factors in GI tract that break down food and factors that protect and repair the mucosa

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5
Q

How do duodenal ulcers present?

A
  • pain 1-3 hours after meals

- pain may be relieved by food

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6
Q

How do gastric ulcers present?

A
  • pain immediately after meals

- food often aggravates pain

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7
Q

What are the goals of PUD treatment?

A
  • resolve symptoms
  • reduce acid secretion
  • promote epithelial healing
  • prevent ulcer-related complications and recurrence
  • eradicate H pylori if present
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8
Q

What is the non-pharmacologic treatment for PUD?

A

Eliminate or reduce:

  • psychological stress
  • cigarette smoking
  • EtOH consumption
  • NSAID or aspirin use
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9
Q

MOA Histamine Blockers

A

-inhibit gastric acid secretion

competitive inhibition of histamine at H2 receptors of gastric parietal cells

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10
Q

Histamine Blockers Generic Names

A
  • “tidine”
  • Cimetidine
  • Ranitidine
  • Famotidine
  • Nizatidine
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11
Q

Cimetidine Trade Name

A

Tagamet

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12
Q

Famotidine Trade Name

A

Pepcid

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13
Q

Nizatidine Trade Name

A

Axid

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14
Q

Ranitidine Trade Name

A

Zantac

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15
Q

Histamine Blockers Adverse Effects

A
  • well tolerated
  • N/V/D
  • rare bone marrow suppression, hepatotoxicity
  • confusion, hallucinations, seizures w/ IV cimetidine (rare)
  • gynecomastia, impotence w/ prolonged or high cimetidine doses
  • reduce does w/ renal impairment
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16
Q

Drug Interactions of Histamine Blockers

A
  • cimetidine increases plasma concentration of anticoagulants, theophylline, phenytoin
  • others do not have significant interactions
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17
Q

MOA of Proton Pump Inhibitors

A
  • decrease acid secretion (more than H2RAs)

- inhibit H+/K+ ATPase (proton pump) of parietal cells

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18
Q

Generic Names of PPIs

A
  • “prazole”

- Omeprazole

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19
Q

Omeprazole Trade Name

A

Prilosec

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20
Q

PPIs Adverse Effects

A
  • well-tolerated
  • N/D, HA, dizziness, skin rash
  • rebound acid hypersecretion
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21
Q

Why must overuse of PPIs be avoided?

A
  • fracture risk due to decreased calcium absorption
  • increased risk of pneumonia of C diff
  • decreased magnesium
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22
Q

PPI Drug Interactions

A
  • CYP450 2C19 inhibitor
  • decreases clopidogrel’s active metabolite levels and anti-platelet activity by half (worse cardiovascular outcomes)
  • alters absorption of some medications (due to hi pH)
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23
Q

When should PPIs be dosed?

A

30-60 min before AM meal

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24
Q

Prostaglandin MOA

A

-replaces protective PGs (NSAIDs decrease PG production)

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25
Prostaglandin Generic and Trade Name (1)
-misoprostol (Cytotec)
26
AEs of Prostaglandin/Misoprostol
- diarrhea in 30-40% (start low and titrate up) - uterine contraction (preg cat X) - abdominal pain, nausea, flatulence
27
Drug Interactions of PG
-may increase effect of oxytocin (hence uterine contraction and preg cat X)
28
MOA of Sucralfate
- forms protective barrier in stomach | - weak acid neutralizer
29
Trade Name of Sucralfate
Carafate
30
AEs of Sucralfate
- constipation | - safe in pregnancy
31
Drug Interactions of Sucralfate
-chelation of phenytoin, warfarin, quinolones, thyroxine
32
MOA of Bismuth Preparations
- possible local gastroprotective effect - stimulation of PGs - suppression of H pylori
33
Trade Name of Bismuth Subsalicylate
Pepto Bismol
34
AEs of Bismuth Preparations
- black stool or tongue - may cause salicylate sensitivity - caution in older pts or renal failure - caution in kids, flu, herpes zoster (Reye's syndrome)
35
Drug Interactions of Bismuth Preparation
- toxicity of ASA, warfarin or hypoglycemics may be increased - may decrease GI absorption and bioavailability of tetracyclines
36
PPI Ulcer Healing Duration
4 weeks
37
H2RA and Sucralfate Ulcer Healing Duration
6-8 weeks
38
What is the general treatment for PUD management? | not looking for specific meds
ulcer healing therapy (eg PPI, H2RA) + specific ulcer type therapy (eg NSAID, H pylori) +/- maintenance therapy
39
What type of dosing is recommended for large gastric ulcers?
-higher dose or longer duration
40
When will H2RAs and PPIs start to provide symptom relief?
within 1 week
41
H pylori causes what % of ulcers?
90% duodenal and 80% gastric
42
What is the H pylori rate of re-infection?
1%/year
43
How much of the world population is colonized by H pylori?
50%, 30% in US
44
Nonendoscopic H pylori Diagnostic Tests
- urea breath test - serological testing - stool antigen
45
Endoscopic H pylori Diagnostic Tests
- histology - culture - biopsy (rapid) urease
46
How might H pylori tests result in a false negative?
- abx or bismuth taken within previous 4 weeks | - PPI taken w/in previous 2 weeks
47
Best Regimens for Hy Pylori treatment are...
- simple - well-tolerated - cost-effective - encourage patient compliance - eradicate >90% - minimize resistance
48
H Pylori PUD regimens must contain what drugs?
- 2 or more abx | - antisecretory drug (H2RA or PPI)
49
What is first line H pylori PUD therapy?
- sequential therapy - PPI plus amoxicillin 1 gm PO BID x 5 days - then PPI plus clarithromycin 500 mg and tinidazole 500 mg BID x 5 days - PPI continues for 2-4 more weeks
50
What is second line H pylori PUD therapy?
-quadruple therapy -bismuth subsalicylate 2 tabs qid plus tetracycline 500 mg qid plus metronidazole 500 mg tid plus PPI bid
51
How can we avoid H pylori resistance? How can H pylori cure be confirmed?
- full course of therapy 10-14 days is best | - confirm cure with urea breath test or stool antigen >8 weeks after end of treatment
52
NSAID GI Adverse Effects
- nuisance sxs, eg dyspepsia - mucosal lesions - serious GI complications (>100,000 hospitalizations, >20,000 deaths/yr)
53
How do NSAIDs cause mucosal damage>
- direct or topical irritation of gastric epithelium | - systemic inhibition of endogenous GI mucosal PG synthesis
54
What are the established risk factors for NSAID induced ulcers?
- age >60 - prior PUD or GI bleed - high dose or more toxic NSAIDs - concomitant use of corticosteroids, oral bisphosphanates, SSRIs, antiplatelets (ASA, clopidogrel), anticoagulants - chronic illness (eg cardiovascular dz)
55
What are possible risk factors for NSAID induced ulcers?
- NSAID-related dyspepsia - H pylori infection - rheumatoid arthritis - EtOH use
56
What are the nonsalicylates?
- nonselective NSAIDs: ibuprofen, naproxen - partially selective NSAIDs: etodolac, meloxicam - COX2 inhibitors: celecoxib
57
What are the salicylates?
- acetylated: aspirin | - non-acetylated: salsalate, trisalicylate
58
NSAIDs with the Lowest GI Toxicity
COX2 inhibitors (celcoxib - celebrex)
59
NSAIDs with Low GI Toxicity
ibuprofen and meloxicam
60
NSAIDs with Intermediate GI Toxicity
naproxen indomethacin ketoprofen diclofenac
61
NSAIDs with High GI Toxicity
ketorolac | piroxicam
62
What is considered a low risk GI patient for NSAID therapy?
- no risk factors - age < 60 - no aspirin - no prior ulcer or hx of ulcer-related GI complication
63
What NSAID therapy should a low risk GI patient have?
N-NSAID or P-NSAID
64
What is considered a moderate risk GI patient for NSAID therapy?
-1-2 risk factors
65
What NSAID therapy should a moderate risk GI patient have?
N-NSAID or P-NSAID plus PPI or misoprostol therapy; COX-2
66
What is considered a high risk GI patient for NSAID therapy?
- 3+ risk factors or concomitant use of low dose aspirin and either corticosteroids, warfarin or clopidogrel
67
What NSAID therapy should a high risk GI patient have?
N-NSAID or P-NSAID or COX-2 plus PPI or misoprostol therapy
68
What is considered a very high risk GI patient for NSAID therapy?
-prior ulcer or ulcer-related GI complication plus additional risk factors (age, concomitant use of low dose aspirin, warfarin, corticosteroids, or clopidogrel)
69
What NSAID therapy should a very high risk GI patient have?
N-NSAID or P-NSAID or COX-2 plus PPI or misoprostol therapy | consider doing PPI and misoprostol
70
Target Dose of Misoprostol Therapy
200 mcg TID
71
What type of ulcer prevention can H2RAs be used for?
duodenal
72
What treatments are not effective for preventing NSAID-induced PUD in high risk patients?
- COX-2 inhibitors - sucralfate - antacids
73
How should NSAID-induced ulcers be treated?
- PPI, H2RA, or sucralfate | - STOP NSAIDs! (or at least reduce dose), switch to acetaminophen for analgesia
74
Who might have stress-related mucosal damage (SRMD)?
-critically ill patients with risk factors including multiple trauma or multi system organ failure
75
What is the primary pathogenic factor with stress-related mucosal damage?
-mucosal ischemia due to decreased gastric blood flow
76
Prevention Options for Stress-Related Mucosal Damage
- PPI - H2RA - antacids - sucralfate
77
Dosing for Zollinger-Ellison Syndrome
-omeprazole, lansoprazole, or rabeprazole 60mg/day
78
What is the second line therapy for Zollinger-Ellison syndrome?
-octreotide
79
Indications for PUD Maintenance Therapy
- frequent ulcer recurrence - hx of ulcer-related bleeding - healed refractory ulcer - failed H pylori eradication - heavy smokers - continuous NSAID therapy
80
PUD Treatment Monitoring
- ulcer symptoms - alarm signs and symptoms - medication adverse effects

Fall 2014 - Pharm GI/ENT (14 decks)

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