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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
Q

Prostaglandin Generic and Trade Name (1)

A

-misoprostol (Cytotec)

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26
Q

AEs of Prostaglandin/Misoprostol

A
  • diarrhea in 30-40% (start low and titrate up)
  • uterine contraction (preg cat X)
  • abdominal pain, nausea, flatulence
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27
Q

Drug Interactions of PG

A

-may increase effect of oxytocin (hence uterine contraction and preg cat X)

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28
Q

MOA of Sucralfate

A
  • forms protective barrier in stomach

- weak acid neutralizer

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29
Q

Trade Name of Sucralfate

A

Carafate

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30
Q

AEs of Sucralfate

A
  • constipation

- safe in pregnancy

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31
Q

Drug Interactions of Sucralfate

A

-chelation of phenytoin, warfarin, quinolones, thyroxine

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32
Q

MOA of Bismuth Preparations

A
  • possible local gastroprotective effect
  • stimulation of PGs
  • suppression of H pylori
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33
Q

Trade Name of Bismuth Subsalicylate

A

Pepto Bismol

34
Q

AEs of Bismuth Preparations

A
  • 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
Q

Drug Interactions of Bismuth Preparation

A
  • toxicity of ASA, warfarin or hypoglycemics may be increased
  • may decrease GI absorption and bioavailability of tetracyclines
36
Q

PPI Ulcer Healing Duration

37
Q

H2RA and Sucralfate Ulcer Healing Duration

38
Q

What is the general treatment for PUD management?

not looking for specific meds

A

ulcer healing therapy (eg PPI, H2RA) + specific ulcer type therapy (eg NSAID, H pylori) +/- maintenance therapy

39
Q

What type of dosing is recommended for large gastric ulcers?

A

-higher dose or longer duration

40
Q

When will H2RAs and PPIs start to provide symptom relief?

A

within 1 week

41
Q

H pylori causes what % of ulcers?

A

90% duodenal and 80% gastric

42
Q

What is the H pylori rate of re-infection?

43
Q

How much of the world population is colonized by H pylori?

A

50%, 30% in US

44
Q

Nonendoscopic H pylori Diagnostic Tests

A
  • urea breath test
  • serological testing
  • stool antigen
45
Q

Endoscopic H pylori Diagnostic Tests

A
  • histology
  • culture
  • biopsy (rapid) urease
46
Q

How might H pylori tests result in a false negative?

A
  • abx or bismuth taken within previous 4 weeks

- PPI taken w/in previous 2 weeks

47
Q

Best Regimens for Hy Pylori treatment are…

A
  • simple
  • well-tolerated
  • cost-effective
  • encourage patient compliance
  • eradicate >90%
  • minimize resistance
48
Q

H Pylori PUD regimens must contain what drugs?

A
  • 2 or more abx

- antisecretory drug (H2RA or PPI)

49
Q

What is first line H pylori PUD therapy?

A
  • 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
Q

What is second line H pylori PUD therapy?

A

-quadruple therapy
-bismuth subsalicylate 2 tabs qid plus
tetracycline 500 mg qid plus
metronidazole 500 mg tid plus
PPI bid

51
Q

How can we avoid H pylori resistance? How can H pylori cure be confirmed?

A
  • 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
Q

NSAID GI Adverse Effects

A
  • nuisance sxs, eg dyspepsia
  • mucosal lesions
  • serious GI complications (>100,000 hospitalizations, >20,000 deaths/yr)
53
Q

How do NSAIDs cause mucosal damage>

A
  • direct or topical irritation of gastric epithelium

- systemic inhibition of endogenous GI mucosal PG synthesis

54
Q

What are the established risk factors for NSAID induced ulcers?

A
  • 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
Q

What are possible risk factors for NSAID induced ulcers?

A
  • NSAID-related dyspepsia
  • H pylori infection
  • rheumatoid arthritis
  • EtOH use
56
Q

What are the nonsalicylates?

A
  • nonselective NSAIDs: ibuprofen, naproxen
  • partially selective NSAIDs: etodolac, meloxicam
  • COX2 inhibitors: celecoxib
57
Q

What are the salicylates?

A
  • acetylated: aspirin

- non-acetylated: salsalate, trisalicylate

58
Q

NSAIDs with the Lowest GI Toxicity

A

COX2 inhibitors (celcoxib - celebrex)

59
Q

NSAIDs with Low GI Toxicity

A

ibuprofen and meloxicam

60
Q

NSAIDs with Intermediate GI Toxicity

A

naproxen
indomethacin
ketoprofen
diclofenac

61
Q

NSAIDs with High GI Toxicity

A

ketorolac

piroxicam

62
Q

What is considered a low risk GI patient for NSAID therapy?

A
  • no risk factors
  • age < 60
  • no aspirin
  • no prior ulcer or hx of ulcer-related GI complication
63
Q

What NSAID therapy should a low risk GI patient have?

A

N-NSAID or P-NSAID

64
Q

What is considered a moderate risk GI patient for NSAID therapy?

A

-1-2 risk factors

65
Q

What NSAID therapy should a moderate risk GI patient have?

A

N-NSAID or P-NSAID plus PPI or misoprostol therapy; COX-2

66
Q

What is considered a high risk GI patient for NSAID therapy?

A
  • 3+ risk factors or concomitant use of low dose aspirin and either corticosteroids, warfarin or clopidogrel
67
Q

What NSAID therapy should a high risk GI patient have?

A

N-NSAID or P-NSAID or COX-2 plus PPI or misoprostol therapy

68
Q

What is considered a very high risk GI patient for NSAID therapy?

A

-prior ulcer or ulcer-related GI complication plus additional risk factors (age, concomitant use of low dose aspirin, warfarin, corticosteroids, or clopidogrel)

69
Q

What NSAID therapy should a very high risk GI patient have?

A

N-NSAID or P-NSAID or COX-2 plus PPI or misoprostol therapy

consider doing PPI and misoprostol

70
Q

Target Dose of Misoprostol Therapy

A

200 mcg TID

71
Q

What type of ulcer prevention can H2RAs be used for?

72
Q

What treatments are not effective for preventing NSAID-induced PUD in high risk patients?

A
  • COX-2 inhibitors
  • sucralfate
  • antacids
73
Q

How should NSAID-induced ulcers be treated?

A
  • PPI, H2RA, or sucralfate

- STOP NSAIDs! (or at least reduce dose), switch to acetaminophen for analgesia

74
Q

Who might have stress-related mucosal damage (SRMD)?

A

-critically ill patients with risk factors including multiple trauma or multi system organ failure

75
Q

What is the primary pathogenic factor with stress-related mucosal damage?

A

-mucosal ischemia due to decreased gastric blood flow

76
Q

Prevention Options for Stress-Related Mucosal Damage

A
  • PPI
  • H2RA
  • antacids
  • sucralfate
77
Q

Dosing for Zollinger-Ellison Syndrome

A

-omeprazole, lansoprazole, or rabeprazole 60mg/day

78
Q

What is the second line therapy for Zollinger-Ellison syndrome?

A

-octreotide

79
Q

Indications for PUD Maintenance Therapy

A
  • frequent ulcer recurrence
  • hx of ulcer-related bleeding
  • healed refractory ulcer
  • failed H pylori eradication
  • heavy smokers
  • continuous NSAID therapy
80
Q

PUD Treatment Monitoring

A
  • ulcer symptoms
  • alarm signs and symptoms
  • medication adverse effects

Fall 2014 - Pharm GI/ENT (14 decks)

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