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GI Exam 3 > PUD > Flashcards

PUD Flashcards

1
Q

Duodenal Ulcer Clinical Presentation

A

Most present before age of 40
Some NSAID association
Pain on empty stomach
Food alleviates pain (always snacking)

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2
Q

Gastric Ulcer Clinical Presentation

A

Usually seen after age 40
Strong association with NSAID use
Pain after eating

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3
Q

Common Presentation with both Gastric and Duodenal Ulcer

A

Diffuse epigastric pain
May be painless with NSAIDs
Dyspepsia
May lead to significant bleeding, hemorrhage or obstruction

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4
Q

*** Alarm Symptoms of Peptic Ulcer Disease

A

Weight loss
Vomiting
Back pain
Signs of bleeding (coffee ground emesis, black/tarry stool)

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5
Q

Main cause of Duodenal Ulcers and Gastric Ulcers =

A

H. Pylori (90% vs 70%)

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6
Q

Aggressive Factors are:

A 
Acid
Pepsin
Smoking 
H. pylori
NSAID
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7
Q

Defensive Factors are:

A

Prostaglandins
Bicarbonate
Mucus

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8
Q

So PUD is:

A

an imbalance between aggressive factors and defensive factors

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9
Q

H. Pylori

A

Gram negative
Produces urease to keep local pH at 7.0
Produces gastrin-releasing peptide

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10
Q

Risk Factors for H. pylori Infection

A 
Age (older)
Institutionalization (LTCF)
Crowded living conditions
Poor socioeconomic status
Infected family members
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11
Q

H. pylori + Inflammation

A

Turns on the parietal cells to release acid and inhibits bicarbonate secretion
Duodenum doesn’t have much mucus and without the bicarbonate to protect itself = ulcer

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12
Q

**If you have an ulcer…

A

You ALWAYS test for H. pylori

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13
Q

So when do you test?

A

If ulcer is present

Post-treatment (4 weeks post eradication)

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14
Q

Best H. Pylori Test?

A

Focal antigen test

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15
Q

H. Pylori Test that is sensitive and specific? And how does it work?

A

Urea breath test
Radio labeled urea
If urease is present it will break it down into ammonia and CO2 (means there is H. pylori producing the urease)
- Can still be positive up to 4 weeks after treatment

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16
Q

Stool antigen testing

A

Test on day 7 to see if you have eradicated the H. pyrlori

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17
Q

PUD Treatment Goal

A

Eradicate the H. pylori and you won’t have to treat again.

Don’t eradicate it and it will come back

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18
Q

Standard Therapy (PAC) =

A 
PPI (pantoprazole 40 mg BID)
Amoxicillin 1 g BID
Clarithrmycin 500 mg BID 
X 14 days
(active ulcer: PPI continued for 6-8 weeks)
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19
Q

Concomitant Therapy

A 
PPI
Amoxicillin
Clarithromycin
Metronidazole
X 5-7 days
20
Q

LAP Therapy

A

Levofloxacin 500 mg BID
Amoxicillin 1 gram BID
PPI BID for
X 10-24 days days

21
Q

COX1 function

A

Regulates homeostatis

House keeping enzyme

22
Q

COX2 function

A

Pro-inflammatory inducible COX

23
Q

COX3 function

A

Affects pain and fever

Acetaminophen target

24
Q

Effects of PGs in the GI tract

A

Thicken protective mucus layer
Stimulate acid neutralizing bicarbonate secretion
Maintain microcirculation and prevent ischemia

25
Q

How do NSAIDs cause mucosal injury

A

Decrease PG synthesis
Alter the mucus
Decrease bicarbonate
Decrease blood flow

26
Q

Define Epidemiology

A

Relationship for the occurrence, how common is it, what makes it better or worse, characteristics of the disease

27
Q

Epidemiology of Ulcers

A

75% are gastric
25% are duodenal independent of H. pylori
Risk of NSAID induced ulcers are based on the potency of the drug and the dose of the drug
Typically pts are asymptomatic until the ulcer is severe

28
Q

Extremely potent NSAID?

A

Piroxicam

29
Q

RA + NSAIDS

A

Risk of ulcer was 5.5 times higher if on NSAID

Risk of death was 4 times higher if on NSAID

30
Q

Risk Factors for NSAID associated Bleeding

A 
PUD history/complications
Age > 60 years
History of cardiac disease (aspirin therapy)
H. pylori
Corticosteroids
Anticoagulants or antiplatelets (SSRI)
High NSAID dose
BISPHOSPHONATES!!
31
Q

Treatment of NSAID induced Ulcer

A

Determine the etiology of the ulcer (H.pylori test!!!)

Histology normal with negative H. pylori - NSAID induced used PPI for 6-8 weeks and stop NSAID

32
Q

Prevention of NSAID induced Ulcer

A

Avoidance (OA: acetaminophen 40 mg/kg/day is just as effective as NSAIDs; RA)
H2RAs (prevent duodenal ulcers

33
Q

Misoprostol + NSAID Induced Ulcers

A

Increases mucosal blood flow and mucus (diarrhea)
Better than PPI but lots of diarrhea so patients prefer PPI
- Found out that if you do 300 mg BID it works as well as QID dosing but doesn’t have diarrhea!!!

34
Q

Celecoxib

A

Only COX2 selective agent still available

Effect in combination with PPI in HIGH RISK patients

35
Q

High Risk of NSAID GI toxicity

A

History of a previously complicated ulcer

Multiple RF

36
Q

Moderate Risk of NSAID GI Toxicity

A

1-2 RF
Age greater than 60
High dose NSAID
A previous history of uncomplicated ulcer
Concurrent use of aspirin, corticosteroids or anticoagulants

37
Q

Low Risk of NSAID GI toxicity

A

No risk factors

38
Q

Low CV risk + Low GI Risk

A

NSAID alone at lowest possible dose

39
Q

Low CV risk + Moderate GI Risk

A

NSAID + PPI/Misoprostal

40
Q

Low CV risk + High GI Risk

A

Alterantive therapy if possible or COX 2 inhibitor + PPI/misoprostal

41
Q

High CV risk + Low GI Risk

A

Naproxen + PPI/misoprostal

42
Q

High CV risk + Moderate GI Risk

A

Naproxen + PPI/misoprostal

43
Q

High CV risk + High GI Risk

A

Avoid NSAIDs or COX2 inhibitors

Use alternative

44
Q

High CV risk =

A

Low dose aspirin required

45
Q

DAT and Ulcer Risk

A

DAT + history of upper GI bleed
Consider PPI if DAT + at least one of the following (advanced age, warfarin/steroid/NSAID concomitant use or H. pylori infection)
Avoid PPI: DAT and none of above RF adn no history of upper GI bleed

46
Q

***When do you use around the clock acetaminophen or tramadol?

A

High GI risk
On warfarin
With severe OA
Dose: 40 mg/kg/day

GI Exam 3 (9 decks)

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