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PHM 604- GI Therapeutics > Peptic Ulcer Disease > Flashcards

Peptic Ulcer Disease Flashcards

1
Q

Kinds of ulcers

A

Gastric and duodenal

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2
Q

What does ulcer severity tell you?

A

The deeper the ulcer, the more severe the damage is

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3
Q

How can you determine the ulcer severity?

A

ENDOSCOPY

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4
Q

Main symptom of PUD

A

DYSPEPSIA

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5
Q

PUD’s association with food

A

Duodenal ulcers- food helps the pain

Gastric ulcer- food makes it worse

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6
Q

Patients with duodenal ulcers will describe what symptom?

A

Pain that wakes them up at midnight-3 AM

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7
Q

The #1 cause of PUD is due to what?

A

H. pylori bacteria

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8
Q

H. pylori tends to cause what kind of ulcers?

A

Duodenal ulcers

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9
Q

Features of H. pylori

A

Spiral shape with flagellum
Adherence pedestals
Protective mechanisms against stomach acid

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10
Q

Protective mechanisms of H. pylori

A

Convert urea to ammonia and bicarb
Produces lipases and proteases to degrade mucus later
Toxin production
Induces inflammatory immune response

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11
Q

Diagnosis methods of PUD

A

Endoscopy and blood tests

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12
Q

Tests used to determine eradication of H. pylori infection

A

Breath tests and fecal antigen tests

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13
Q

What class of drugs is the #1 cause of drug-related toxicity in the US?

A

NSAIDs

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14
Q

How can NSAIDs cause ulcers?

A

Decreases prostaglandin effects
Epithelial cell turnover
Weak acids crossing into epithelial cells and getting trapped

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15
Q

Risk factors for NSAID-induced PUD

A 
>65 years
Past history of an ulcer or PUD
Concomitant steroid use with NSAID (mostly non-selective NSAIDs)
Anticoagulants (warfarin, DOACs)
Antiplatelets (ASA, Plavix, P2Y12is)
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16
Q

How many risk factors do you need to start on PPI prophy for NSAID-induced PUD?

A

≥1

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17
Q

Diagnosis of NSAID-induced PUD

A

Patients describing dyspepsia symptoms
NSAID taking history
ENDOSCOPY

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18
Q

Alcohol use and PUD

A

Usually causes superficial gastritis and nothing life-threatening

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19
Q

What patients are at risk for stress-related mucosal bleeding due to illness PUD?

A

Patients who are in the hospital ICU with sepsis, mechanical ventilation, etc.

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20
Q

Altered defense mechanisms in patients with critical illness PUD

A

No acid in stomach
Decreased blood flow to GI tract due to hypotension
Release of damaging mecanisms

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21
Q

Major risk factors for critical illness PUD

A 
Respiratory failure (mechanical ventilation for ≥48 hours or planning to be for ≥48h)
Coagulopathy: INR >1.5 or platelets <50
22
Q

How many major risk factors do you need to be at risk for critical illness PUD?

A

1

23
Q

Minor risk factors for critical illness PUD

A

Sepsis, hypotension/requiring pressors, history of GI bleeding, use of high dose steroids

24
Q

How many minor risk factors do you need to be at risk for critical illness PUD?

A

≥2

25
Q

What disease can also cause critical illness PUD?

A

Zollinger Ellison Syndrome (gastrin-producing tumor)

26
Q

Symptom of Zollinger-Ellison Syndrome

A

Diarrhea

27
Q

PPI dosing in Zollinger-Ellison Syndrome

A

Dosed q8-12h!

28
Q

When to suspect upper GI bleeding

A

Haematemesis, melina
Patients who use NSAIDs
History of PUD

29
Q

Presentation of UGIB

A

Vomiting blood, jet black stools, epigastric pain (dyspepsia), high heart rate, low blood pressure, low hemoglobin and hematocrit

30
Q

Treatment of UGIB

A

IV bolus of LR or NS STAT
Blood products for plasma expansion (packed RBCs)
Supplemental O2
Fresh frozen plasma for reverse anticoagulation
Epinephrine, cauterization
80mg bolus of pantoprazole or esomeprazole, then 8mg/hr infusion x72 hours OR IV pantoprazole 40mg IV BID

31
Q

Target Hgb

A

7

32
Q

Target Osat

A

92%

33
Q

Complication of PUD

A

GI BLEEDING

34
Q

Treatment goals of PUD

A

Relieve pain, heal ulcer, prevent recurrence, eliminate H. pylori if it’s the cause

35
Q

How long should H. pylori treatment last?

A

10-14 days

36
Q

H. pylori treatment: triple therapy

A

PPI of choice BID
Clarithromycin 500mg BID
Amoxicillin 1g BID

37
Q

H. pylori treatment: bismuth quadruple therapy

A

PPI of choice BID
Bismuth subsalicylate or subcitrate QID
Tetracycline 500mg QID
Metronidazole 250mg QID or 500mg TID

38
Q

H. pylori treatment: levofloxacin triple therapy

A

PPI of choice BID
Levofloxacin 500mg QD
Amoxicillin 1g BID

39
Q

When to use bismuth quad therapy

A

FIRST-LINE!

40
Q

When to use levofloxacin triple therapy

A

If quad therapy fails

41
Q

What to use in patients with a PCN allergy but need H.pylori treatment

A

Bismuth quad therapy, can also use metronidazole for the ampicillin instead in triple therapy

42
Q

H. pylori eradication tests

A

Wait 4 weeks after treatment is done, then use urea breath test or fecal antigen test

43
Q

What happens if there’s no eradication?

A

Treatment continues

If triple therapy was used the first time, go to bismuth quad therapy

44
Q

Treatment for NSAID-induced PUD

A

PPI for 4 weeks, but can extend to 8 weeks or longer if NSAID use continues

45
Q

Prevention of NSAID-induced PUD

A

Switch to APAP if possible, switch to selective COX-2 NSAID if possible (celecoxib (Celebrex)), add on PPI as prophy, add prostaglandin analog (misoprostol)

46
Q

Treatment for NSAID-induced PUD in patients that require both an antiplatelet and NSAID

A

Use celecoxib (Celebrex) when possible, add PPI to regimen

47
Q

Prophylaxis for stress ulcer

A

H2RAs!

Ranitidine (Zantac)

48
Q

Duration of prophy for stress ulcer

A

Continue until risk factors are gone

49
Q

Management of ASA or P2Y12i (secondary prevention)

A

Evaluate risk vs. benefit –> risk of having a post-stent cardiac event outweighs the GI bleeding risk

Make sure bleeding stops, check hemoglobin multiple times a day. Restart antiplatelet within 1-3 days after hemoglobin stabilizes

50
Q

What happens if a patient is taking ASA with no cardiac history?

A

D/C the ASA because the risk of GI bleeding outweighs the benefit

51
Q

Selective NSAIDs

A

Celecoxib, meloxicam, etodolac, nabumetone

PHM 604- GI Therapeutics (10 decks)

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