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)
17
Q
PPI chronic use
A
- Increases gastrin level 2-4-fold
- Gastrin has proliferative effects on both oxyntic enterochromaffin like (ECL) cells and parietal cells
- Results is ECL and parietal cell hyperplasia and/or hypertrophy (rebound hypersecretion)
- Fear of cancers hasn’t been seen in humans
18
Q
PPI side effects
A
- Concerns raid w/ -> infections upon early initiation of PPI, osteoporosis, hypomagnesemia
- Retrospective database studies have linked PPI use to many AEs including infections (community acquired pneumonia and C difficile), fractures, and interaction w/ clopidogrel (increased cardiac events)
19
Q
Gastroesophageal reflux disease (GERD)
A
- Retrograde spilling of the gastric contents into the esophagus
- Occurs in everyone but is pathogenic only in some
- Both structural and symptomatic pathology which often don’t coincide w/ each other (bad correlation between level of damage and level of sx; often mismatched)
20
Q
Sx of GERD
A
- Classical -> regurgitation, heartburn, dysphagia, odynophagia (pain on swallowing)
- Atypical -> coughing, wheezing, globus sensation, laryngitis, chest pain, dental erosions
21
Q
Risk factors for GERD
A
- Pregnancy or obesity
- Increased age
- Disease states (ex: Sjogren’s)
- Hiatus hernia
22
Q
Complications of GERD
A
- Esophagitis and (much less commonly) esophageal bleeding
- Esophageal stricture
- Barrett’s esophagus
- Esophageal cancer
23
Q
GERD diagnosis
A
- Endoscopy
- Barium swallowing
- pH monitoring
- Impedance monitoring
- Anti-secretory therapy (PPI test) -> done for most people
24
Q
Subgroups of GERD
A
- Non-erosive reflux disease (NERDs)
- Erosive esophagitis (EE)
- Barrett’s esophagus (BE) and esophageal cancer
25
Q
Tx goals for GERD
A
- *Same as PUD
- Sx relief
- Accelerate healing
- Prevent and treat complications
- Prevent recurrence
26
Q
GERD – lifestyle modifications
A
- Smaller, more frequent meals
- Avoid foods that precipitate events
- Avoid smoking
- Reduce alcohol and caffeine
- Obtain ideal weight
- Stress reduction
- Reassurance
27
Q
Surgery options for GERD
A
- Number of open and laparoscopic techniques
- Mostly reserved for those w/ severe lower esophageal sphincter problems or reluctance to use medications
28
Q
Antacids for GERD
A
- Provides sx relief
- Give 1 and 3 h post meals and at HS or as needed
29
Q
H2 blockers for GERD
A
- Can go up to twice the PUD dose (ex: ranitidine 300 mg BID); b/c of cost this is rarely done now (PPIs around the same price)
- Commonly employed for OTC use, step out and step-down GERD regimens
30
Q
Prokinetics for GERD
A
- Increase LESP, accelerate gastric emptying
- Cisapride, domperidone, metoclopramide studied -> most data w/ cisapride (best agent, but very difficult to get now b/c of risk of Torsades)
- Metoclopramide has CNS adverse effects but is a great anti-emetic
31
Q
PPIs for GERD
A
- Gold standard -> heals EE quicker than H2 blockers
- Key role in Barrett’s esophagus; everyone w/ BE gets high dose PPI for life
- Rationale for step up or step down or on demand therapy
- Equivalence amongst agents -> likely all the same
32
Q
GERD recurrence
A
- Considered chronic disease or chronically relapsing disorder
- Questions remain on who requires continuous therapy
33
Q
Functional dyspepsia
A
- Dyspepsia of at least 3 months w/ no clearly identifiable pathology (structural or biochemical)
- Both motor and sensitivity changes in the GI tract are postulated mechanisms; increased sensitivity to organ distension
- Poor correlation between actual delayed gastric emptying, pt sx, and response to prokinetics
- Contribution of psychosocial issues in prevalence and severity of FD is of considerable debate
- Sx subgroups can include:
- Ulcer-like dyspepsia
- Dysmotility-like dyspepsia
- Reflux-like dyspepsia
- Poor predictive value for endoscopic diagnosis
- Tx goal = sx relief
34
Q
Approach to FD
A
- HP – test and treat
- HP negative px:
- Endoscopy vs. PPI
- PPI vs. H2 blocker
- PPI vs. prokinetics
- TCAs/SSRIs
- CBT and other psychological approaches
35
Q
Lifestyle modifications for FD
A
- Same as GERD
- Eat healthier, lose weight, quit smoking
- *No evidence this works
36
Q
Acid suppression therapy in FD
A
- Antacids appear to be of limited to no benefit
- Appears OTC H2 blockers used more for GERD and PUD than dyspepsia
- Approx. 1/2 of studies published find a beneficial effect on sx
- Very little outcome validation and studies of short duration (few weeks)
37
Q
PPI therapy in FD
A
- Do have a significant benefit over placebo, but is less than overwhelming
- Net therapeutic gain around 10%
- PPIs much more beneficial for ulcer & reflux like sx
- Limit to once daily -> don’t increase to BID for FD (might do this for GERD)
38
Q
Alternative therapies in FD
A
- Theory of sx related to psychiatric disorders (depression, anxiety, somatic)
- SSRIs, anxiolytics -> no controlled trials establishing benefit; probably best to avoid
- Best evidence w/ TCAs (amitriptyline and imipramine) -> some benefit over placebo
- Recommendation is for px w/ no sx relief to PPI to consider a TCA (over a prokinetic)
- This recommendation (TCA over prokinetic) doesn’t apply to other indications (ex: diabetic gastroparesis)
39
Q
Prokinetic therapy in FD
A
- Most studies find metoclopramide, domperidone, and cisepride all more effective than placebo
- Concern w/ long-term risk w/ these agents
- Limiting metoclopramide use to 12 weeks is recommended
- Limit domperidone daily dose to max of 30 mg (10 mg TID)
40
Q
Tx of FD
A
- Few trials indicate any therapy is proven very effective for FD (prokinetics, H2 blockers, PPIs, antacids, bismuth, sucralfate)
- Despite this, up to 98% of px who seek medical help for FD will get a drug prescribed
- Important to review therapy after initiation -> optimal dose, sx relieved & their frequency
- 4 weeks should be plenty of time to determine benefits of therapy
41
Q
FD prognosis
A
Commonly relapses w/ up to 2/3 of px having the same sx 3 years later
