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153 Cards in this Set
- Front
- Back
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GERD definition
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symptoms or mucosal damage**
resulting from abnormal reflux of the stomach contents into the esophagus |
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Erosive esophagitis
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erosion of the squamous epithelium of the esophagus
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Nonerosive reflux disease
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symptomatic GERD patients who do not have evidence of erosive disease- no one ever uses this term (this is the majority of patients)
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dyspepsia
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painful, difficult or disturbed digestion; often referred to as indigestion- != GERD
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% in western countries that have GERD sx on weekly basis
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10-20%
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reasons why it's hard to detemermine incidence of GERD (3)
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incidence hard to establish as everyone will have reflux of some sort
sx do not always relate to severity of disease difficulty in establishing a gold std for definition of GERD |
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barret's esophagus results from...
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repeated exposure to gastric reflux
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histo properties of barrett's esophagus (2)
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normal squamous epithelium
is replaced with columnar epithelium cells change in color in esophagus due to being replaced by intestinal cells |
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incidence and progression of barrett's esophagus
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very low incidence
associated with adenocarcinoma of the lower esophagus if left untreated |
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what is a stricture?
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narrowing of esophagus-->hard to swallow
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strictures- results from what? how do they form?
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Results from inflammation in the lower part of the esophagus due to reflux
repeated inflammation/healing = scarring = stricture development |
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if they get too small, how can you fix strictures?
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stent
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Complications of GERD (3)
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barrett's esophagus
strictures adenocarcinoma of the esophagus (from barrett's) |
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normal physiology of the esophagus/sphincter (when you eat) (2)
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lower esophageal sphincter at distal (far end) is usually contracted to prevent reflux of gastric stuff from stomach
swallowing causes this sphincter to relax and allow food into the stomach |
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3 possible pathophysiologies of GERD that relate to LES
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1) spontaneous transiet relaxation of LES
2) transient increases in intraabdominal pressure 3) atonic LES (no tone) |
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spontaneous relaxation of LES (2) occurs normally when?
association with GERD |
a. Occurs normally after meals
b. Associated with more than half the reflux episodes in those with GERD although rarely the sole reason for development |
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transient increases in intraabdominal pressure (2) when might this occur, when might this lead to GERD
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a. May occur during straining, coughing, bending over
b. These events may lead to reflux in the situation of a weakened LES |
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why is there often more heartburn at night (related to LES pressure)
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there is less LES pressure at night so food can seep in from stomach
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LES pressure can be decreased be...(3)
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fatty foods, gastric distension,
smoking has to do with hormones...? |
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medications that can cause lowered LES pressure- CNS type drugs (3)
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anticholinergics
dopamine nicotine (smoking) |
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substances that can cause lower LES pressure (not drugs, but they are chemicals) (2)
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ethanol
caffeine |
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2 hormones that can lower LES pressure
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progesterone
estrogen |
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5 drugs (can't really classify) that lower LES
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tetracycline
nitrates theophyilline babiturates dihydropyridine CCBs (amlodipine, etc) |
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direct food irritants to esophagus (4) mucosa
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• Spicy foods
• Orange juice- acidic • Tomato juice • Coffee |
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drugs that irritate esophagus (5) mucosa
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• Alendronate (bisphosphonates)- can cause esophageal erosion if it sits there
• Aspirin • NSAIDs • Iron • Potassium |
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incidence of pregnancy reflux
2 things that cause pregnancy reflux |
pretty common
Hormonal effects from estrogen and progesterone as well as a growing fetus placing pressure on the stomach are factors involved |
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general causes of GERD (6)
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LES issues
pregnancy esophageal clearance rate mucosal resistance decreased gastric emptying composition of gastric acid |
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what is a major determinant of causing GERD in ppl with low esophageal CL rates
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the amount of time the reflux is in contact with the esophagus is the underlying issue is more of issue than overproduction of acid
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how does swallowing help with esophageal CL
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Swallowing helps with esophageal clearance in part by increasing the
flow of saliva which contains bicarbonate which acts as a buffer to acid |
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swallowing and nocturnal GERD sx
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swallowing is decrease at night which helps facilitate nocturnal
GERD symptoms |
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types of issues that cause lower espohageal CL that may cause GERD (2)
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lower saliva production
difficulty swallowing (elderly, anticholinergic meds, etc) |
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mucosal resistance- 2 things secreted that protect mucosal lining
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Mucus secretion from the esophagus and stomach help to provide protection to the esophagus
Bicarbonate is also secreted to provide neutralizing effects on the gastric contents |
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2 main things that cause delayed gastric emptying (anything that causes delayed GE will cause gerd though)
how does this cause GERD |
i assume it causes GERD because it increases abdominal pressure
• Delayed gastric emptying (i.e. – diabetic gastroparesis)- slows down forward motion- more pressure against esoph. sphincter • High fat meals which lead to delayed gastric emptying |
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Duodenogastric reflux esophagitis properties (2)
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alkaline (note that reflux contents can be acid or alkaline)
induced by the reflux of biliary and pancreatic fluids |
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bile acid reflux effect on mucosa (2)
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may have a direct irritating effect
may help to increase hydrogen ion permeability into the mucosa |
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typical sx of GERD (4)
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• Heartburn
• Regurgitation • Belching • Hypersalivation |
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atypical sx of GERD (5)
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• Nonallergic asthma
• Chronic cough • Hoarsemess • Chest pain • Dental erosions |
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2f typical sx of GERD that are highly specific
when do these typically occur relieved by what? |
Presence of heartburn, regurgitation or both are highly specific for GERD; typically occur after meals and are aggravated by bending over; often relieved with antacids
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atypical sx of GERD: characteristics and how most people go about treating these sx
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Less specific for GERD especially in the presence of a normal EGD; many will rule out other causes and end up treating empirically
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alarm sx of GERD (5)
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• Dysphagia (difficulty swallowing)
• Odynophagia (painful swallowing) • Bleeding • Weight loss (unintentional) • Anemia |
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what do alarm sx of GERD indicate?
action to take |
Presence of these symptoms indicate complicated disease including strictures, Barrett’s, and esophageal cancer
refer to doc |
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methods/labs to go about "diagnosing" GERD (4)
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1) empirical treatment
2) ambulatory pH monitoring (meh) 3) barium swallow 4) Esophagogastroduodenoscopy (EGD) |
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tests to confirm GERD- when are they done (2)
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Tests to confirm GERD are available but not done unless alarm symptoms are present or they fail to respond to empiric treatment
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how ambulatory pH monitoring works (2)
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1. pH tube placed transnasally to just above the LES
2. Patients will record s/s of GERD and the pH probe will record the time the pH of the esophagus is below 4 |
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Esophagogastroduodenoscopy/EGDs- when used? (2)
properties of the test itself (2) allows you to see what? |
usually only if warning sx or if need PA for insurance
highly specific (95%) but not highly senstitive (~50%) Allows visualization of the esophagus, stomach, and duodenum |
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GERD treatment goals (4)
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1. Eliminate symptoms or reduce severity
2. Decrease frequency of symptoms 3. Facilitate healing of injured mucosa 4. Prevent development of complications |
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8 lifestyle/nonpharm changes that can improve GERD ( maybe)
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Avoidance of fatty meals
cessation of smoking avoid laying down for 3 hours after meals eat smaller meals reduce/discontinue alcohol consumption weight reduction if obese and having symptomatic episodes avoid tight clothes elevate head when sleeping |
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lifestyle modification level of evidence
how would you make recs? |
lacking evidence but encouraged
therefore in order to not interfere too much with life make recs that are specific to their type of GERD (e.g. nighttime? daytime? after eating?) |
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"patient directed therapy" (basically self treating, OTC) limited to whom? (2)
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limited to two weeks (because pharma companies don’t want to say take this indefinitely in case something bad going on with pt)
and for those with intermittent symptoms which are mild |
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who should not use OTC treatment? (2)
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symptoms lasting longer than two weeks or those with alarm symptoms
should be referred to physician |
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% of pt that will respond to OTC meds
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60-70% of patients will respond to OTC meds
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Esophageal clearance meds (2)
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bethanecol
cisapride (limited use) |
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Esophageal mucosal resistance (2)
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sucralfate- decreases acidity
alginic acid |
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LES pressure meds (3)
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bethanecol- muscarinic agonist?
metolopramide cisapride (limited use) |
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gastric acid meds (3)
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antacids
H2R blockers PPI |
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area of stomach where most commonly used GERD meds tend to work
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gastric acid
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gastric emptying meds (2)
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metoclopramide
cisapride (limited use) (prokinetic) |
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5 targets of GERD therapy in stomach
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Esophageal clearance meds
Esophageal mucosal resistance LES pressure gastric acid gastric emptying |
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overall goal of acid suppressing drugs
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Overall goal is to maintain the pH above 4 during times of reflux symptoms
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Coral calcium as a source for supplementation (antacid)
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marketing ploy
as the body doesn’t know the difference |
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antacids- more useful for what type of GERD (2), dosing (general disadvantage)
onset and what this entails for when it is considered most useful |
More useful for occasional dyspepsia/heartburn rather than full-blown GERD
Most require multiple times per day dosing quick relief and most useful when symptoms are present- |
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antacids level of evidence
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studies (of poor quality) did not show reductions in severity or frequency of heartburn
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Key point of early antacid trials:
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they had small numbers thus were
likely underpowered to show differences in efficacy compared to placebo |
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alginic acid- derived from where
frequency of use |
1. Derived from seaweed the concept is to provide a gelatinous barrier to help reduce reflux
2. Hardly ever used |
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H2R blockers (4) perception of efficacy, dosing adjustments?, dose dependency?
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considered "less effective" than PPIs
dosage reductions required in renal function decline efficacy is dose dependent- need higher doses for GERD than simple dyspepsia |
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how to go about starting someone on H2R blockers
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give 6 week trial and if inadequate response, probably isn't going to get any better (can try something else)
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rate of heartburn relief occurs at what rate per week
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occurs at 6.5% per week
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usage of H2R blockers (indications)- best for treating what? (4)
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best at treating episodic heartburn and postprandial heartburn that occurs more frequently – due to second quickest onset
Better choice for mild/moderate symptoms; do not work as well for more severe symptoms nighttime GERD due to suppression of basal acid |
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H2R blockers- MoA vs. PPI
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suppress meal-stimulated and basal acid secretion- huge difference vs. PPI which are better at suppressive meal stimulated acid secretion
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H2R blockers are ineffective at treating what (2)
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ineffective for severe esophagitis and severe GERD
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most studies done on H2R blockers were done using what duration of therapy?
what does this imply for usage in maintenance therapy? |
Most studies in GERD were of short duration (~4 weeks)
these agents are not considered to be great for maintenance therapy but may be used |
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ADRs of H2R blockers (5)
mostly a problem in what population |
well tolerated
but potential for CNS adverse effects (HA, lethargy, confusion, depression, insomnia) more of a problem in older individuals and may occur with any of the H2RAs |
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cimetidine properties (3)
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First one on the market
lots of DDIs originally QID but now BID |
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OTC cimetidine primarily indicated for what
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intermittent heartburn
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cimetidine dosing: non erosive GERD and erosive GERD
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Non-erosive GERD: 400 mg BID
Erosive GERD: 400 mg q 6 hours |
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4 H2R blockers
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cimetidine
famotidine ranitidine nizatidine |
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ranitidine (zantac) dosing- non erosive and erosive GERD
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Non-erosive GERD: 150 mg BID
Erosive GERD: 150 mg q 6 hours |
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ranitidine vs cimetidine: advantage
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less drug interactions but still be careful
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famotidine dosing: non erosive and erosive GERD
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Non-erosive GERD: 20 mg BID
Erosive GERD: 40 mg q 12 hours |
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famotidine properties (2)
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longer half-life thus true BID dosing is an option
preferred drug by most clinicians |
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brand names: pepcid, tagamet, zantac, axid
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pepcid- famotidine
tagamet- cimetidine zantac- ranitidine nazitidine - axid |
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what is pepcid complete
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Pepcid Complete is taking advantage of the quick onset of the antacid with the prolonged effect of the H2RA
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nizatidine dosing: erosive and non-erosive GERD
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Non-erosive GERD: 150 mg BID
Erosive GERD: 150 mg q 6 hours |
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most potent inhibitors of gastric acid secretion
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PPI
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PPI vs. H2 blockers- rate of heartburn relief per week
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Complete relief of heartburn occurs at a quicker rate than H2 blockers, at 11.5% per week
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MoA of PPIs (2) which cells affected
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a. These agents inhibit the Na/K ATPase pump located on the surface of the parietal cells
inactivated enzymes are recruited and become activated with subsequent meals; this process repeats itself over several days |
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why are PPIs often suboptimal after first dose
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b. They only inhibit activated Na/K ATPase thus the initial reduction in gastric acid after the first dose is often suboptimal
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why these agents are not good choices for intermittent symptoms
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they are not expected to provide adequate acid inhibition when used on a PRN basis (due to the recruitment of inactivated enzymes-->become activated-->then block more)- idk look into this more
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for intermittent symptoms of GERD use what?
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H2R blockers
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PPI time to steady state
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• Steady state is not achieved for several days
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one way to make PPI work faster
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load the patient by BID-TID
dosing for the first couple of days |
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best time to take PPI
why? |
in morning because that’s when ATPase is most active (after fasting)
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most common AE for PPIs (4)
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headache, diarrhea, constipation, and abdominal pain
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long term safety issues for PPIs (8)
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prolonged hypergastrinemia
gastric atrophy vitamin B12 deficiency Risk of developing enteric infections hypersecretion following discontinuation increased risk of hip/wrist/spine fractures (age > 50)- often add calcium carbonate to it allergic interstitial nephritis hypomagnesemia |
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PPI hip fracture issue- not related to what?
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not tied into calcium absorption- don't have to supplement calcium
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prolonged hypergastermia- initially caused concern due to what info found in studies? was this true in humans (2)?
do you need to do anything about this? |
• Concern was linked to gastric carcinoid tumors in rats- only at 4x normal dose- i guess too much gastrin caused tumors
• There have been no neoplastic changes in humans based on > 15years of omeprazole use • Association was thought to be species related • No need to perform serum gastrin measurements although a link is present for H. pylori infection |
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gastric atrophy- linked to what?
concern primarily in what patient group do you have to take action? |
loss of ability to secrete acid
chronically theoretically linked to increased incidence of gastric cancer concern mainly for those receiving maintenance therapy with H. pylori infection do not recommend that you check and treat for H. pylori --> they feel the risk for atrophic gastritis is low and the clinical consequences are uncertain |
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gastric atrophy is also a problem with which drug
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may occur from H2RA’s
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PPI induced B12 deficiency- mechanism, more likely to occur when (2), how to handle
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reduced bio availability of B12
may occur with long-term use and more likely to occur in those with atrophic gastritis (gastric acid used to release B12 from food) Suggested to assess B12 levels periodically |
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3 types of enteric infections that can be caused by PPI
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issue mostly camphylobacter gastroenteritis- data not robust
risk for aspiration pneumonia if on mechanical ventilation c. diff risk (FDA) |
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hypersecretion following d/c of PPI- mechanism, effect peaks how long after cessation, when would you use a taper, and over how long?
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tied into negative feedback cycle (you inhibit acid, which turns down negative feedback)
peaks 1-2 weeks after cessation of PPI if taking PPI more than 2 weeks, should taper off over 4-6 weeks |
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increased hip/wrist/spine fractures with PPI- found in what population (age)
how would is this dealt with in hospitals |
over 50
not really related to calcium absorption but many give calcium carbonate anyways |
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theoretical mechanism of fractures with PPI
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inhibition of osteoclast proton pumps although other mechanisms are theorized as possibilities
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allergic interstitial nephritis definition
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• Allergic reaction which occurs within the interstitium leading to acute rises in serum creatinine
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allergic interstitial nephritis- more frequently associated with what drug
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• Associated more with NSAID’s however proton pump inhibitors also may cause this event
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profound hypomagnesemia (idk mechanism) caused by PPIs can lead to what? (4)
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arrhythmias, EKG changes, nausea/vomiting/diarrhea, and paresthesias
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key points of PPIs- best time to take
work when? |
The amount of K/Na ATPase is highest after a prolonged fast thus the best time
to dose these is 30-60 min before the morning meal work when the parietal cells are stimulated which, occurs with the presence of food |
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Decision to double the dose or give twice daily of PPIs- when would you do each?
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• If adequate acid suppression during the day and return of symptoms at night = give second dose
• If inadequate acid suppression during the day and worsening at night = double the dose |
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all efficacy data for PPIs is based on what frequency of dosing
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all efficacy data for PPI’s is from once-daily dosing
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when is someone considered a treatment failure for PPIs
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• If someone fails BID dosing, they are considered treatment failures
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different classes of PPIs- is there a difference clinically?
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no clinical differences among the class; most of the data is related to dosing issues
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omeprazole dosing
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Erosive/non-erosive GERD:
20 mg QD-BID |
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lansoprazole dosing
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Erosive/non-erosive GERD:
30 mg QD-BID |
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pantoprazole dosing
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Erosive/non-erosive GERD:
40 mg QD-BID |
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rabeprazole dosing
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Erosive/non-erosive GERD:
20 mg QD-BID |
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esomeprazole dosing
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Erosive/non-erosive GERD:
20-40 mg QD-BID (mostly given as 40mg) |
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dexlansoprazole dosing (2 types of dosing plans depending on type of GERD
distinguish between healing and maintenance dosing |
Erosive esophagitis:
60 mg QD for up to 8 weeks (healing) 30 mg QD for up to 6 months (maintenance) Non-erosive GERD: 30 mg QD |
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6 PPIs
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omeprazole (prilosec)
lansoprazole (prevacid) pantoprazole (protonix) rabeprazole (aciphex) esomeprazole (nexium) dexlansoprazole (dexilant) |
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issues with omeprazole
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Potential for drug interactions through CYP2C19 (clopidogrel)
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OTC version of omeprazole vs rx
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OTC version is actually omeprazole magnesium 20.6 mg (to make a tablet)
equal to 20 mg of the original omeprazole |
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pantoprazole properties (3)
routes indication cost |
first IV formulation
indication: erosive esophagitis ( i guess can also do non-erosive) slightly lower cost than rest of PPIs |
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rabeprazole- differentiating factor from other PPIs
is this significant? |
higher BA so food doesn't interfere with (take with or without food) but all PPIs have delayed onset and best used chronically (at steady state) so absorption doesn't really matter
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esomeprazole (nexium)- properties (2)
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most potent
isomer of omeprazole |
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dexlansoprazole property
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isomer of lansoprazole
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Erosive esophagitis maintenance therapy (3) evidence and recurrence rates
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with PPIs
strongest evidence for this aspect of GERD (for maintenance therapy) those not maintained have high recurrence, those who are have decreased recurrence majority of GERD pt will be on chronic therapy |
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non erosive GERD maintenance therapy (4) evidence, primary focus of therapy, how to treat (2)
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evidence less clear
primary focus of treatment is symptomatic relief with PPIs if sx resolve after 2-3 mo, give a trial off can also use on demand in those who have sx of GERD but no erosive disease- but not a great tactic |
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indications that require maintenance PPI therapy (3)
which 2 are lifelong? |
esophageal strictures*
Barrett’s esophagus * erosive esophagitis |
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rec'd dosing for PPI maintenance
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whatever dosing controls the symptoms
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chronic PPI therapy- insurance issue
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insurance usually authorizes a 90 day supply initially then require a prior authorization for ongoing use o fproton pump inhibitors
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promotility agent usage
evidence |
Only used as adjunctive therapy to acid suppression in selected patient
data is not convincing that these agents help |
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promotility agent options (2)
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bethanecol
metoclopramide |
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bethanecol mechanism (3)
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cholinergic agent that stimulates parasympathetic nervous system
causes contractions of the GI tract and bladder noted to increase LES tone; |
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bethanecol AE (3)
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sedation, irritability, extrapyramidal adverse effects limit use
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metoclopramide MoA (3)
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has both cholinergic and dopamine antagonistic properties;
increases resting LES tone improves peristalsis |
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metoclopramide AE (3)
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sedation, irritability, extrapyramidal adverse effects limit use
(same as bethanecol) |
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cisapride MoA
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similar prokinetic drug to metoclopramide but lacks the dopamine blocking properties (and many of the CNS adverse effects)
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cisapride AE (3)
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lacks CNS AE but causes heart issues like torsades, QT prolongation and Vtach/fib --> FDA removed it from market and limited its use to specalist approval only
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surgery for GERD (3) when to use, evidence,
most common technique |
1. Reserved for those refractory to medications
2. Somewhat controversial as many who undergo surgical intervention will end up back on acid suppressive therapy and surgery is not without complications 3. Most common technique is the Nissen fundoplication |
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endoscopic therapy options (3)
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1. Radiofrequency to the LES to help increase the reflux barrier of the LES
2. Various sewing techniques have also been used 3. For those with strictures, use of stents is another option |
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GERD mgmt in pregnancy (3)
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antacids + lifestyle change- first line
cimetidine/ranitidine preferred also PPI probably safe but no info available |
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reflux in kids/babies- when does concern arise? why?
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reflux is common
concern araises in infants only if frequent regurgitation or failure to thrive systemic/neurologic diseases may be involved |
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reflux in babies may lead to...(3)
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irritability, refusing to feed, and apnea
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things that can help with reflux in babies (3)
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may be intolerance to protein in cow’s milk; try milk free formula trial for a couple weeks, or hypoallergenic
Thickened feedings and positional changes may also be helpful |
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reflux treatment in peds- pharmacotherapy- what to give (2)? meds are reserved only for whom? what not to give?
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similar to adults but are reserved for those who are having
problems with the reflux (not the infants who are thriving and not irritated) Limited trials of acid suppressive therapy are recommended proton pump inhibitors are preferred options prokinetic agents have minimal role |
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step up therapy plan (3 steps)
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start with lifestyle and dietary modifications-->transition into
pharmacotherapy mainly with H2RA’s, then move on to proton pump inhibitors as needed |
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step up therapy intended for what type of patients (3)
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intended for patients without erosive changes, those with
mild/moderate symptoms, and those with intermittent symptoms |
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step down therapy plan
main issue |
to start with potent meds followed by incremental reductions in
intervention until breakthrough symptoms, then base treatment on minimum treatment that can control those main issue: people don't step down listen again |
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step down or up therapy?
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majority of patients you encounter will have the non-erosive form of GERD so if you start with a proton pump inihibitor,
please try to taper them down to at least H2RA’s remember to use an adequate dose and that you can always go back up if needed |
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Mild, intermittent heartburn treatment options (3)
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antacids and/or
OTC H2RA or OTC omeprazole |
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calcium carbonate dose?
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--
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mild/moderate GERD treatment options (2) indicate duration of therapy
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rx strength H2RA for 6-12 wks (keep in mind most are generic)
OR PPI qd 4-8 weeks (preferred if moderate to severe) |
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Severe symptoms or erosive esophagitis treatment options (2)
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PPI BID 4-16 weeks (more preferred)- there is evidence for maintenance therapy though...? so i guess they'd stay on it longer (but not lifelong like if you had complications)
OR high dose H2RA for 8-12 weeks |
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barrett's or strictures- treatment
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PPI initially and then used as maintenance therapy
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