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GI and liver > GERD > Flashcards

GERD Flashcards

1
Q

GERD definition

A

heart burn

“symptoms or complications resulting from the reflux of gastric contents into the esophagus, oral cavity, or lung”

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2
Q

epidemiology of GERD

A

prevalence of 14-20% (1/5)
men = women (except during pregnancy)
obese = increased risk

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3
Q

pathophysiology of GERD

A

abnormal reflux of gastric contents
lower esophageal sphincter (LES) must be relaxed and there must be a pressure difference
defective LES pressure - spontaneous LES relaxations not associated with swallowing (vomiting, belching, retching), increased intraabdominal pressure, atonic LES
other factors: pregnancy (hormonal effects, LES tone, increased abdominal pressure, usually resolves after delivery), foods, medications
anatomic factors - hiatal hernia
delayed gastric emptying - increased gastric volume may increase intragastric pressure, emptying may be slowed by high fat meals, smoking, diabetic gastroparesis
esophageal clearance - how long acid stays in contact with mucosa, primary - swallowing, saliva production, secondary - disention, gravity
mucosal resistance - esophagus has limited protective mechanisms
reluxate composition - pH and volume

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4
Q

Drugs that can decrease LES pressure

A

AChs, barbiturates, caffeine, DHP CCBs, dopamine, estrogen, ethanol, nicotine, nitrates, progesterone, tetracycline, theophylline

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5
Q

drugs that are direct irritants to esophageal mucosa

A

alendronate, aspirin, NSAIDs, iron, quinidine, potassium chloride

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6
Q

typical clinical presentation

A

heartburn, acid brash (hypersalivation), regurgitation/belching - not concerning
chest pain - always concerning
may be aggravated by activities - recumbent position, bending over, high-fat meal

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7
Q

atypical clinical presentation

A

aka extraesophageal symptoms
have an association with GERD
should only be considered if a typical symptom is present as well
Sxs: chronic cough, hoarseness, non-allergic asthma, dental enamel erosion

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8
Q

ALARMing clinical presentation

A

may be indicative of GERD complications
requires further diagnostic evaluation
Sxs**:
dysphagia, odynophagia, bleeding, unexplained weight loss, continual pain

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9
Q

esopagitis

A

GERD complication
inflammation as a result of repeated insult and irritation
may cause erosions over time
Sxs: painful swallowing, difficulty swallowing, chest pain, food impaction
can be as a result of other mechanisms: eosinophilic, drug-induced, infections

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10
Q

stricture

A

GERD complication
narrowing of the esophagus
common in distal esophagus
usually 1-2 cm in length
can cause obstruction and difficulty swallowing
occurs in up to 23% of untreated GERD patients

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11
Q

Barrett’s esophagus

A

GERD complication
replacement of squamous epithelial lining of the esophagus by columnar-type epithelium
inc incidence of stricture
inc risk of developing esophageal cancer

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12
Q

adenocarcinoma

A

GERD complication
usually occurs in the distal esophagus
involves cells of the mucus-secreting glands
most commonly seen in white men

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13
Q

clinical history of GERD

A

most useful tool for diagnosis
avoids use of invasive procedures
typical mild symptoms: clinical history + response to treatment = diagnosis
PPI trial of 8 weeks is the best diagnostic tool
consider other tests in those who do not respond to therapy OR who have alarming symptoms

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14
Q

Diagnosis of GERD

A

endoscopy - visualization and biopsy of the mucosa, reserved for PPI refractory GERD, routine endoscopies are not recommended, useful for complications of GERD
capsular endoscopy - uses a small, swallowed capsule for imaging

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15
Q

“other” diagnostic methods

A

reserved for PPI refractory GERD
manometry - measures pressures and muscle contraction during swallowing, useful prior to antireflux surgery
ambulatory reflux monitoring - measures esophageal acid exposure via pH probe, useful prior to antireflux surgery
do not recommend: barium radiograph

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16
Q

GERD treatment desired outcomes

A

alleviate or eliminate symptoms, decreased the frequency and duration, promote healing of the injured mucosa, prevent the development of complications

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17
Q

targets of GERD therapy

A

decrease acidity of refluxate (increase pH), decrease gastric volume to be refluxed, improve gastric emptying, increase LES pressure/tone, enhance esophageal acid clearance, protect esophageal mucosa

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18
Q

nonpharmacologic treatment of GERD

A

Weight loss, Increase exercise, Elevate head of bed, Consume smaller meals and no food within 3 hours of sleeping, ***Avoid foods/medications that exacerbate GERD, Smoking cessation, Avoid alcohol, Take medications in an upright position w/plenty of liquid

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19
Q

lifesytle changes help to:

A

decrease symptoms, decrease doctor visits, decrease use of drugs

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20
Q

overview of antacids

A

short-term relief, Efficacy and safety not well studied, Chronic use not recommended, Require direct delivery to site of action (must be taken PO)
work by binding and neutralizing protons that will be released into the stomach
May be used concomitantly with other acid suppressing therapies, Increases LES pressure via neutralization of
gastric fluid, Used FIRST LINE for intermittent symptoms* (LESS THAN twice weekly*), NOT appropriate for healing established esophageal lesions

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21
Q

antacid agents

A

Aluminum, Calcium carbonate, Magnesium, Alginic acid, Combination
Doses range from PRN to hourly
Similar efficacy at equipotent doses

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22
Q

antacid adverse effects

A

Most common: diarrhea and constipation
Magnesium: Diarrhea, hypermagnesemia
Aluminum: Neurotoxicity**, anemia, constipation
Calcium: Milk-Alkali syndrome - Headache, nausea, irritability, weakness

23
Q

antacid drug interactions

A

pH becomes less acidic - alteration in oral
absorption of other drugs - Digoxin, iron salts, ketoconazole
Chelation and adsorption to other medications - Tetra/doxycycline, isoniazid, quinidine, sulfonylureas, cipro/levofloxacin; Separate from other medications by at least 2 - 4 hours (take other meds 2 hours before or 4 hours after antacid)

24
Q

general info on H2 receptor antagonists

A 
Mild to moderate GERD
Symptomatic improvement in around 60%
Variable efficacy: Severity of disease, Dosage regimen used, Duration of therapy 
Must be absorbed
systemically for effects
25
Q

H2RA pearls **

A

Should NOT be used in patients with erosive disease
May be used for night-time reflux in combination with daytime PPI
Longer acting than antacid therapy

26
Q

OTC H2RA dosing**

A

cimetidine: 200 mg BID
famotidine: 10 mg BID
nizatadine: 75 mg BID
ranitidine: 75 mg BID

27
Q

non erosive GERD H2RA dosing**

A

cimetidine: 400 mg BID
famotidine: 20 mg BID
nizatadine: 150 mg BID
ranitidine: 150 mg BID

28
Q

H2RA dose adjustments

A

Moderate-severe renal insufficiency

*General rule of thumb: decrease dose by 50% when creatinine clearance less than 50 ml/min

29
Q

H2RA drug interactions

A

Affect absorption of drugs which have pH sensitive absorption or pH dependent dosage forms
Cimetidine (and ranitidine) inhibits CYP450 enzymes 1A2, 2C9, 2D6, 3A4 - worry about warfarin

30
Q

H2RA adverse effects

A

generally well tolerated
Headache, somnolence, fatigue, dizziness, constipation and/or diarrhea
Rarely cause thrombocytopenia** (with decreased platelets)
Transient elevations in LFTs
Cimetidine can have rare antiandrogenic effects - Gynecomastia, worsen impotence
CNS effects are rare, mild and reversible* - Confusion*, restlessness, somnolence, agitation, headaches, dizziness; Most commonly seen in elderly and those with reduced renal function

31
Q

general info on PPIs

A 
Most potent acid suppression
Only inhibits “active”
pumps
Usually take ½ hour before breakfast
Takes 3-5 days to reach steady state and maximum benefit - do not use PRN
32
Q

PPI pearls

A

Most effective agents for short and long term management
More effective than H2-RA for erosive disease and those with complications***
Safe for use in pregnancy
Equally efficacious at equivalent dosing

33
Q

OTC PPI dosing

A

esomeprazole: 20 mg QD x 14 days q 4 months
lansoprazole: 15 mg QD x 14 days q4 months
omeprazole: 20 mg QD x 14 days q 4 months
omeprazole + sodium bicarbonate: 20 mg/1100 mg QD x 14 days q4 months

34
Q

erosive GERD PPI dosing

A

dexlansoprazole: 60 mg QD
esomeprazole: 40 mg QD
lansoprazole: 30 mg BID
omeprazole: 20 mg BID
pantoprazole: 40 mg BID
rabeprazole: 20 mg BID
omeprazole + sodium bicarb: 20 mg/1100 mg QD

35
Q

nonerosive GERD and maintenance PPI dosing

A

dexlansoprazole: 30 mg QD
esomeprazole: 20 mg QD
lansoprazole: 15-30 mg QD
omeprazole: 20 mg QD
pantoprazole: 40 mg QD
rabeprazole: 20 mg QD
omeprazole + sodium bicarb: 20 mg/1100 mg QD

36
Q

IV formulated PPIs ***

A

Pantoprazole
Esomeprazole
NOT more efficacious than oral formulations

37
Q

alternative administration routes for PPIs***

A

Open capsules and sprinkle in applesauce OR mix w/ water for NG tube: Omeprazole, Esomeprazole, Lansoprazole, Dexlansoprazole
ODT: Lansoprazole
Do NOT crush: Pantoprazole, Rabeprazole

38
Q

PPI AEs

A

Adverse Effects: Headache, Dizziness, Somnolence, Diarrhea, Constipation, Nausea, Vitamin B12 deficiency
Occur in less than 2% of patients - Generally well tolerated

39
Q

PPIs and CDiff

A

associated diarrhea

  • PPI use can be a risk factor for C. difficile diarrhea development
  • Loss of host defense against ingested spores and bacteria
  • Those with recent abx use are at higher risk
  • Have patients report any diarrhea
  • Up to 65% increase in C. difficile diarrhea among patients on PPI
40
Q

PPIs and pneumonia

A 
Both CAP and HCAP
Believed to be as a result of bacterial overgrowth (reflux gets into lungs) and risk of aspiration
More associated with shortterm use
Long-term risk unclear
Assess vaccine status
41
Q

PPIs and bone fractures

A

Rx PPIs carry FDA advisory for increased fx risk: High-dose PPI for Duration over 1 year
Theorized reduced Ca absorption
Pts with osteoporosis CAN remain on PPIs
Those w/ osteoporosis or risk factors: Ensure adequate Ca/Vit D, BMD studies

42
Q

PPI drug interactions

A

inhibit CYP450 2C19
decreased metabolism of diazepam, phenytoin, R-warfarin
May decrease efficacy of clopidogrel
***AVOID OMEPRAZOLE and ESOMEPRAZOLE
Unnecessary to take risk with other available options
Rabeprazole and pantoprazole have not been shown to interact extensively with CYP450 system
Lansoprazole slightly induces 1A2 - Increased metabolism of theophylline
IV methotrexate: PPIs have been shown to increase mtx toxicity, Thought to be due to reduced excretion of mtx, Switch to H2-RA if on HIGH DOSE IV methotrexate

43
Q

general info on promotility agents

A

Many undesirable side effects
Generally not as effective as acid-suppression
Reduce “backward” flow of acid
***Inferior to H2RAs and PPIs
Need diagnostic evaluation before trying
Cisapride removed from general use due to rare but life threatening arrhythmias

44
Q

metoclopramide MOA

A

promotility agent
**most commonly used in diabetic gastroparesis
Central dopamine antagonist
Enhances response to acetylcholine in upper GI tract
***Increases rate of gastric emptying
Does NOT improve esophageal clearance
Increases LES tone
Dose: 10-15 mg/dose up to 4 times per day Before meals and at bedtime

45
Q

metoclopramide AEs

A

Risk greater in elderly and those with renal impairment
Drowsiness, GI disturbances, increased lactation
Extrapyramidal reactions** in about 1% - Involuntary movements, tremors and rigidity, body restlessness, muscle contractions, Akathisia (“inner” restlessness) is most common, Usually resolves with discontinuation

46
Q

metoclopramide contraindications

A

GI hemorrhage, obstruction or perforation
Pheochromocytoma
Seizure disorders
Parkinson’s disease
MAOIs, TCAs and others that may cause extrapyramidal reactions
Not commonly used or recommended due to adverse effects and contraindications

47
Q

sucralfate overview

A

mucosal protectant - stomach liner, not esophageal liner*
Nonabsorbable aluminum salt
-Limited value in GERD and not recommended
-More useful for peptic ulcer disease

48
Q

surgery for GERD

A

Reserved for those patients who have: Established diagnosis of GERD, Had a responsive to, but are intolerant of acidsuppressive
therapy
Is superior to H2-RA or prokinetic therapies
Is equally effective as PPI therapy - Does have higher incidence of complications
nissen fundoplication
Linx

49
Q

treatment by severity

A

Antacids – PRN or after meals/at bedtime
OTC doses of H2RAs or PPIs
If persistent/recurrent symptoms (at least 2 times/week) then move to “mild symptoms”

50
Q

treating mild symptoms

A

no warning signs
H2RA for 6-12 weeks or PPI for 4-8 weeks
No relief? Change H2RA to PPI
No relief from PPI? Increase PPI dose or refer for endoscopy

51
Q

treating moderate - severe symtoms

A

No warning signs
PPI for 4-16 weeks
No relief? Increase PPI dose or refer for endoscopy

52
Q

treating warning signs/known erosive esophagitis

A

Endoscopy
EE and no complications - PPI for 4-16 weeks (healing dose)
EE and complications - Refer for further evaluation

53
Q

treating refractory GERD

A

No response to optimal PPI dosing
Consider:
-Upper endoscopy
-Specialist visit (ENT, pulmonary, or allergy)
-Ambulatory reflex monitoring
-pH monitoring: Patient should not be on a PPI when this is done
-Anti-reflux surgery: Bariatric surgery should be conducted in obese patients before anti-reflux surgery
-Transient Lower Esophageal Sphincter Relaxation (TLESR)
inhibitors: Baclofen, Arbaclofen

GI and liver (10 decks)

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