16 - Dyspepsia Flashcards Preview

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Flashcards in 16 - Dyspepsia Deck (41)
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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