16 - Dyspepsia Flashcards
1
Q
Definition of dyspepsia
A
- “Bad digestion”
- Predominant epigastric pain lasting at least 1 month
- Can be associated w/ any other upper GI sx such as epigastric fullness, N/V, or heartburn, provided epigastric pain is the px primary concern
2
Q
Categories of dyspepsia
A
- Organic (~40%) -> peptic ulcer disease, GERD, cancer
- Functional (~60%) -> non-ulcer
3
Q
Other causes of dyspepsia
A
- Gastritis – bile reflux, viral infection
- Parasites
- Pancreatitis or other abdominal cancers
- Carb malabsorption (lactose, sorbitol, fructose, mannitol)
- Systemic diseases – diabetes, thyroid, connective tissue
- Drugs (ex: antibiotics, iron, NSAIDs)
- Herbs (ex: garlic, saw palmetto, feverfew)
4
Q
Define peptic ulcer disease and give common sx
A
- Group of ulcerative disorders that are dependent on both acid and pepsin for their production
- Primarily refer to gastric (GU) & duodenal (DU) ulcers
- Common sx = episodic epigastric pain and heartburn
5
Q
PUD pathology
A
- Imbalance between mechanisms of injury and protection/repair
- Sources of injury = acid, enzymes, toxins (ex: bacteria, viruses, drugs)
6
Q
PUD complications
A
- Perforation
- Penetration
- Hemorrhage
- Gastric outlet obstruction
7
Q
PUD risk factors
A
- *H pylori
- *NSAIDs (also anticoagulants)
- Genetic
- Smoking, EtOH, caffeine – minor causes
8
Q
PUD diagnosis
A
- Endoscopy and (much less commonly) diagnostic imaging
- Barium swallow (very rare now)
- H pylori – test and treat
- PPI test
9
Q
PUD tx goals
A
- Sx relief
- Accelerate healing of ulcer
- Prevent and treat complications
- Prevent recurrence
10
Q
PUD non-drug tx
A
- Nutrition -> avoid large bedtime meals (increase HS acid production)
- Avoid precipitants and factors affecting healing -> drugs (NSAIDs, ASA), smoking, EtOH (> 20% proof), excess caffeine
- Surgery (rarely needed, only if someone is actively bleeding)
11
Q
Antacids for PUD
A
- For sx relief due to compliance issues
- Equivalence based on acid neutralizing capacity
- Give 1 and 3 h post meal and at HS
- SE = constipation/diarrhea, drug interactions
- Things to watch for –> sodium bicarb in CHF/cirrhosis px**, magnesium-based salts in dialysis px (occasional dose is fine, but chronic use is bad; use aluminum or calcium instead)
12
Q
H2 blockers for PUD
A
- Decrease acid production by 50-75%
- All agents the same at appropriate dosage; all can be given 1 or 2x/day
- SE = very low except for drug interactions w/ cimetidine
13
Q
PPIs for PUD
A
- Decrease acid 80% at 2 h, 50% by 24 h, effects last 3 days
- Increasing omeprazole dose from 20 to 40 mg only decreases acid by further 6%
- Efficacy -> gold standard, heals ulcers quicker than H2 blockers, also have key role in H pylori eradication regimens
- Equivalence amongst agents = likely all the same
14
Q
PUD recurrence
A
- Unhealed ulcers at 4 weeks ~20% w/ H2 blocker, decreases to < 10% w/ 8-week therapy
- Considered refractory if fail 8-week therapy in DU, 12 week in GU; most will use a BID PPI for recurrences
- Always look for a reason for recurrence:
- Non-adherence
- H pylori (retest all serious bleeders to ensure eradication)
- NSAIDs
15
Q
H pylori eradication
A
- Based on a very limited sample size, MB clarithromycin resistance rates are > 15% threshold
- Therefore, recommendation is to treat w/ a quad based regimen (triple therapy no longer recommended)
16
Q
Chronic prophylaxis in PUD
A
- Up to 20% of px w/ complications cured of HP will have an ulcer recurrence in 6 months
- Most px don’t need chronic therapy but in those w/ a severe PUD complication or significant co-morbidity, case can be made for placing these a once daily PPI indefinitely (ex: dialysis pt w/ a PUD bleed that required hospitalization)
