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Spring PNT exam 4 > PUD > Flashcards

PUD Flashcards

1
Q

3 common forms of PUD

A

H. pylori positive
NSAID-induced
Stress related mucosal damage

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2
Q

H. pylori site of damage

A

duodenum

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3
Q

NSAID site of damage

A

stomach

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4
Q

stress related site of damage

A

stomach

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5
Q

which type of PUD is more dependent on pH

A

H. pylori

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6
Q

which type/s of PUD are asymptomatic

A

NSAID

stress related

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7
Q

which type of PUD has deep ulcers

A

NSAID

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8
Q

Describe GI bleeding associated with H. pylori

A

less severe

single vessel

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9
Q

describe GI bleeding associated with NSAID

A

more severe

single vessel

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10
Q

describe GI bleeding associated with stress

A

more severe

superficial mucosal capillaries

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11
Q

PUD risk factors

A 
H. pylori 
NSAIDs
Stress
Gastric acid hypersecretion 
Cigarette smoking
Diet
Chronic diseases
Vascular insufficiency
Chemo/radiation
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12
Q

Risk factors for NSAID induced ulcer

A 
age >65
previous peptic ulcer, ulcer-related complications
high dose NSAIDs
Multiple NSAIDs
Selection of NSAID
Use of ASA, bisphosphonates, corticosteroids, anticoagulants, antiplatelets, SSRIs
chronic debilitating disorders
H. pylori infection
Smoking
Alcohol
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13
Q

Name nonselective NSAIDs

A 
indomethacin
piroxicam
ibuprofen 
naproxen
sulindac
ketoprofen
ketorolac
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14
Q

name partially selective NSAIDs

A

etodolac
meloxicam
nabumetone
diclofenac

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15
Q

PUD complications

A

Upper GI bleed
Perforation
Obstruction

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16
Q

PUD complications

A

Upper GI bleed
Perforation
Obstruction

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17
Q

PUD clinical presentation

A

Epigastric pain
Nocturnal pain
Duodenal ulcer (1-3 hours after eating, aggrevated by food)
Gastric ulcer (resolved by food)

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18
Q

Urease test requirements

A

Endoscopic
no PPIs x 2 weeks
no antibiotics/bismuth salts x 4 weeks

19
Q

4 non-pharm treatments for PUD

A

reduce stress
smoking cessation
d/c NSAIDs
avoid aggrevating food/beverages

20
Q

H2RA MOA

A

reversible inhibition of histamine receptor on parietal cells - acid production reduced 70%

21
Q

Famotidine dosing

A

20 mg IV/PO BID or 40 mg HS

22
Q

Famotidine dosing renal

A

CrCl

23
Q

Ranitidine dosing

A

150 mg PO BID or 300 mg HS

50 mg IV Q6-8 hours

24
Q

Ranitidine dosing renal

A

CrCl

25
Q

H2RA AEs

A

Tolerance develops quickly
Thrombocytopenia
Neuro effects: somnolence, HA

26
Q

PPI MOA

A

irreversibly inhibit proton pump, reduce acid up to 99%

27
Q

Omeprazole dosing

A

20-40 mg PO daily

28
Q

Esomeprazole dosing

A

40 mg PO/IV daily

29
Q

Pantoprazole dosing

A

40 mg PO/IV daily

30
Q

PPI AEs

A 
Fractures
C. diff
Pneumonia
Thrombocytopenia
GI upset (N/V/D)
31
Q

Antacids MOA

A

neutralize gastric acid
inhibit action of peptin
no effect on acid production

32
Q

Antacids AEs

A

GI upset - diarrhea (magnesium), constipation (calcium)
Accumulation in renal dysfunction -> toxicity
frequent administration
drug interactions

33
Q

Antacids AEs

A

GI upset - diarrhea (magnesium), constipation (calcium)
Accumulation in renal dysfunction -> toxicity
frequent administration
drug interactions

34
Q

Sucralfate MOA

A

forms polyvalent bonds with damaged tissue and normal GI mucosa

35
Q

Sucralfate AEs

A 
Aluminum toxicity 
Cheap
Decreased risk of pneumonia
PO only 
Drug interactions
Constipation
Frequent administration
36
Q

Misoprostol MOA

A

inhibits gastric acid secretion, increase in mucosal defense

synthetic prostaglandin analog

37
Q

Misoprostol AEs

A

diarrhea
abdominal cramping
N/V

38
Q

Misoprostal preg cat

A

X

39
Q

Bismuth subsalicylate MOA

A

antibacterial effect
local gastroprotective effect
stimulation of endogenous prostaglandins

40
Q

Bismuth subsalicylate AEs

A

Discoloration of the tongue
Gray/Black stools
tinnitus

41
Q

Bismuth subsalicylate AEs

A

Discoloration of the tongue
Gray/Black stools
tinnitus

42
Q

When is 14 day therapy for treatment of H. pylori preferred

A

1st line 3 drug regimen and recurrence

43
Q

duration of therapy for treatment of H. pylori

A

10-14 days

Spring PNT exam 4 (3 decks)

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