Week 3 Discussion Advance Practice

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South University College of Nursing and Public Health Graduate Online

Nursing Program

Aquifer Family Medicine

Family Medicine 19: 39- year-old man with epigastric pain

Author:Author: Joel Heidelbaugh, MD

INTRODUCTION HISTORY DIAGNOSES

 

Today, you are working at a family medicine clinic with Dr. Medel. Together, you review her clinic schedule for the day and she suggests that you see Mr. Cesar Rodriguez, a 39-year-old uninsured man who recently moved to the U.S. from the Dominican Republic. This is Mr. Rodriguez’s first visit to the clinic.

Molly, Dr. Medel’s medical assistant, has already escorted Mr. Rodriguez to the examination room and has arranged for a Spanish-speaking interpreter to be present for the visit, since he speaks and comprehends very little English. Molly tells you that Mr. Rodriguez has been having “worsening abdominal pain over the past several months,” and is “worried that something is wrong.”

Dr. Medel says to you, “How would you begin to think about what might be going on with Mr. Rodriguez?”

You reply, “Abdominal pain can be caused by a wide variety of conditions. I’ll need to get more information about his symptoms to form an appropriate differential diagnosis. At this point I’d have to consider several organ systems as potential etiologies of the pain.”

“Very good,” Dr. Medel responds. “Why don’t you go ahead and talk with Mr.

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Rodriguez and come find me afterward. Lola, our Spanish-speaking interpreter can help.”

Systems Approach to Abdominal Pain

Gastrointestinal

Appendicitis, cholecystitis/cholelithiasis, diverticulitis/diverticulosis, dyspepsia, gastroesophageal reflux disease, gastritis, acute or chronic hepatic failure with resultant complications (e.g., ascites), acute hepatitis (e.g., viral, autoimmune, alcoholic, drug-induced), inflammatory bowel disease, intestinal ischemia, intestinal obstruction, irritable bowel syndrome, pancreatitis, peptic ulcer, perforation/peritonitis (e.g., gastric, colonic, intestinal), gastric outlet obstruction, tumor (e.g., gastric, hepatic, pancreatic, intestinal, colonic).

Cardiac Myocardial infarction, angina pectoris, abdominal aortic aneurysm dissection or rupture.

Psychogenic Anxiety, panic disorder, somatiform disorder, post- traumatic stress disorder.

Pulmonary Pleurisy, pneumonia, pulmonary infarction, tumor.

Renal Nephrolithiasis, pyelonephritis, cystitis, tumor.

Musculoskeletal Abdominal wall muscle strain, hernia (e.g., ventral, inguinal, incarcerated), abscess (e.g., psoas, subphrenic), trauma (e.g., contusion, hematoma).

Metabolic Drug overdose, ketoacidosis, iron or lead poisoning, uremia.

Also consider:Also consider:

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medication, vitamin, and herbal supplement side effects foods issues (dietary intolerances, such as lactose, gluten, fructose, or

artificial sweeteners (e.g., sorbitol, xylitol, sucralose)

ELICITING THE HISTORY HISTORY

You and Lola greet Mr. Rodriguez.You and Lola greet Mr. Rodriguez.

!

How to Interview a Patient Via an Interpreter

Talk as you would normally, directly to the patient and not to the interpreter.

The translator should interpret in the first person, without editing it in any way.

Often, the interpreter will sit just behind the patient and in their ear, or off to the side where the interpreter won’t obstruct your ability to face the patient, make direct eye contact, and feel like you’re talking with the patient directly.

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Ideally, it should feel like the translator is just a conduit for the conversation between you and the patient.

As you walk down the hall, Lola, the Spanish-speaking interpreter, gives you some tips on how to interview a patient with an interpreter.

Then, you and Lola enter the room. You sit directly across from Mr. Rodriguez, with Lola sitting just off to your left and facing him. You sense that Mr. Rodriguez seems anxious about coming to the physician today. You introduce yourself and ask,

“What brings you in today?”

“Well, I’ve been having this abdominal pain, and it just seems like it won’t go away. It started probably a year ago. It used to happen a few times a week, now it hurts every day. It usually burns right here.” (He points to the epigastric area of his abdomen).

“Is there anything that makes the pain better or worse?”

“It’s hard to say. Sometimes eating or drinking makes it better, or sometimes worse. Sometimes eating spicy foods makes it worse.”

“What worries you the most about your symptoms?”

“I don’t know,” he says nervously. “I just want to make sure nothing is wrong.”

Thinking about some of the common causes of abdominal pain, you conduct a focused review of systems:

General:General: Denies weight loss, fevers, chills, or night sweats. He has had no recent illnesses. Aside from a recent move to the US from the Dominican Republic, he has not travelled recently.

GI:GI: Denies any dysphagia, regurgitation, nausea, vomiting, anorexia, early

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satiety, hematemesis, hematochezia, melena, diarrhea or constipation. GU:GU: Denies dysuria, hematuria, or change in frequency. CVS/Respiratory:CVS/Respiratory: No chest pain or shortness of breath.

References

American Association of Medical Colleges. Guidelines for use of medical interpreter services. https://www.aamc.org/download/70338/data/interpreter-guidelines.pdf. Accessed April 21, 2017.

MEDICAL AND FAMILY HISTORY HISTORY You now direct your attention to Mr. Rodriguez’s medical history.

“Do you have any chronic medical problems?”

“I don’t really have medical problems, just the stomach pain.”

“Have you ever been hospitalized or had any surgeries?”

“I’ve never been hospitalized. Never been operated on.”

“Do you take any medicines or supplements?”

He tells you, “Just ibuprofen if I’m tired and sore after work, probably most days of the week. I drink some tea that’s good for the stomach, ‘Yerba Buena,’ but it doesn’t really help.”

“Does anyone in your family have any medical conditions?”

“My father had high blood pressure, my mother had diabetes.”

“Does anyone have pain similar to yours?”

“I don’t know if anyone has these stomach problems like me.”

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You ask Mr. Rodriguez a few more questions and discover that he works as a farm laborer. He has no known drug allergies. He smoked a few cigarettes daily, but quit six months ago. He drinks three to four beers per week. He denies other drug use.

You congratulate Mr. Rodriguez on quitting smoking and you thank him for answering all of your questions. You review in your mind what you’ve learned from Mr. Rodriguez so far, and find yourself still wondering about why he seems a little anxious. Before you go to get Dr. Medel, you inquire,

“It seems like this has really been bothering you. Is there anything else we haven’t talked about that seems important?”

“Well, I guess I would have come sooner, but I don’t have any health insurance and haven’t had the money to come to the doctor. I want to feel better, but I hope it’s not something serious.”

ACCESS TO CARE TEACHING You reply, “Well, I’m glad you came in today, and I’ll be sure and share your concern with Dr. Medel. Thanks for telling me.”

You ask him to change into a gown, taking off all of his clothes except his underwear. You reassure him that you will return with Dr. Medel momentarily, and you and Lola leave the exam room while Mr. Rodriguez changes.

In the hallway, you comment to Lola that you are concerned about why Mr. Rodriguez waited to come see a doctor.

Question Which factors, in addition to finances, may have contributed to Mr. Rodriguez not seeking medical care in the recent months? Select all that apply.

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The best options are indicated below. Your selections are indicated by the shaded boxes.

A. He may be an undocumented immigrant.

B. Undocumented immigrants in the US are at a higher

risk of exploitation than legal residents.

C. Lack of concern about his overall health.

D. His impression that allopathic care is not considered

holistic.

E. He may view the U.S. healthcare system as unfriendly

and intimidating.

SUBMITSUBMIT

Answer Comment The correct answers are A, B, D, E.The correct answers are A, B, D, E.

Potential Cultural Barriers to Seeking Medical Attention

There may be a variety of reasons for an individual’s reluctance to seek medical care, making it imperative that the physician explore and address these issues with each patient individually and not rely on assumptions about his or her reasons.

While all patients should be directly asked the reason for their reluctance to seek medical care, the patient’s occupation (farm worker) should raise a flag. Undocumented immigrants may fear that if they seek medical attention, the healthcare system may report them to the government, placing them at risk of deportation. This fear is not unfounded, and providers should be sensitive about disclosing patients’ undocumented status.

Also, patients may view health from a holistic standpoint, where

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physical problems cannot be separated from non-physical problems; those with this viewpoint may be less likely to visit a physician’s office or access preventive services, including vaccinations. This approach has been shown to improve health outcomes in some studies, and should not be dismissed.

Recent immigrants who are unfamiliar with the U.S. healthcare system can view it as confusing, intimidating, and unfriendly. (Even native residents of the U.S. may feel this way!) Latino patients may also be wary of receiving lower quality of a medical care and lower treatment standards because of discrimination and racism. Providers should actively check their biases to ensure they are providing an equal standard of care.

References

DeNavas-Walt C, Proctor B, Smith J. Income, Poverty, and Health Insurance Coverage in the United States: 2007. http://www.census.gov/prod/2008pubs/p60-235.pdf. Published August 2008. Accessed April 29, 2017.

Diaz VA. Hispanic male health disparities. In: Haines CA, Wender RC (eds.) Primary Care: Clinics in Office Practice. Philadelphia, PA: Saunders/Elsevier, 2006;33(1).

Hispanic population of the United States, US Census Bureau. http://www.census.gov/population/hispanic/. Accessed October 19, 2016.

MacNaughton NS. Health disparities and health-seeking behavior among Latino men: a review of the literature. Journal of Transcultural Nursing. 2008;19(1):83-91.

U.S. Census Bureau, 2010 Census Briefs: The Hispanic Population 2010. Issued May 2010. http://www.census.gov/prod/cen2010/briefs/c2010br-04.pdf

Wallace SP, Villa VM. Equitable health systems: cultural and structural issues for Hispanic elders. American Journal of Law and Medicine. 2003;29:247-267.

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SUMMARY STATEMENT CLINICAL REASONING

Dr. Medel asks you what you have learned about Mr. Rodriquez’s historyDr. Medel asks you what you have learned about Mr. Rodriquez’s history so far.so far.

!

You find Dr. Medel in the clinic precepting room, and she asks you, “Well, what have you learned so far?”

You summarize Mr. Rodriguez’s story for Dr. Medel.

Question Based on what you know about the patient so far, write a one- to three-sentence summary statement to communicate your understanding of the patient to other providers.

Guidelines for summary statements.

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A summary statement should:

1. Include accurate information and not include misleading information. 2. Facilitate understanding of the primary problem and appropriately narrow the differential diagnosis through the inclusion of pertinent key features. (The aim is to frame understanding of the primary problem rather than to report all information indiscriminately.) 3. Express key findings in qualified medical terminology (e.g., heart rate of 180 beats/minute is tachycardia); synthesize details into unifying medical concepts (e.g., retractions + hypoxia + wheezing = respiratory distress). 4. Use qualitative terms that are more abstract than patient’s signs; these are often binary in nature (e.g., acute vs. chronic; constant vs. intermittent).

Ultimately, a good summary statement should provide an understanding of the patient presentation while being concise, complete, and accurate.

Your response is recorded in your student case report.

Letter Count: 0/1000

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SUBMITSUBMIT

Answer Comment Mr. Rodriguez is a previously well 39-year-old Latino immigrant who presents with chronic progressively worsening pain in his upper abdomen. He denies any vomiting, hematemesis, hematochezia, melena or association with meals. He recently quit smoking and consumes alcohol occasionally and takes NSAIDs and traditional herbal teas.

The ideal summary statement concisely highlights the most pertinent features without omitting any significant points. The summary statement above includes:

Epidemiology and risk factors: 39-year-old previously well latino immigrant.

Key clinical findings about the present illness using qualifying adjectives and transformative language:

chronic progressively worsening no vomiting, hematemesis, hematochezia, melena, or association

with meals quit smoking occasional alcohol consumption uses NSAIDs uses traditional herbal teas.

DIFFERENTIAL DIAGNOSIS CLINICAL REASONING Dr. Medel praises your summary and then asks you to commit to a provisional differential diagnosis for Mr. Rodriguez’s abdominal pain, based on your findings from his history.

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The best options are indicated below. Your selections are indicated by the shaded boxes.

Question From the following, select the top three diagnoses on your differential.

A. Anxiety

B. Pneumonia

C. Gastroesophageal reflux disease (GERD)

D. Abdominal wall muscle strain

E. Acute Pancreatitis

F. Peptic ulcer disease (PUD)

G. Diverticulitis

H. Angina pectoris

I. Gastritis

SUBMITSUBMIT

Answer Comment The correct answers are C, F, I.The correct answers are C, F, I.

DiXerential for Chronic Progressively Worsening Upper Abdominal Pain

Most Likely / Most Important DiagnosesMost Likely / Most Important Diagnoses

May present with mild epigastric pain, and symptoms commonly worsen aftersymptoms commonly worsen after mealsmeals, although the pain is classicallyclassically

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GERDGERD

described as “burning”described as “burning” and may be located in the substernalsubsternal rather than epigastric area. Hematemesis in the setting of GERD-like symptoms is unusual and represents an alarm symptom indicative of an upper GI bleed or tumor and warrants prompt GI referral for evaluation and upper endoscopy. Hematochezia and melena are not typically associated with GERD.

PepticPeptic ulcerulcer diseasedisease (PUD)(PUD)

Epigastric abdominal pain thatEpigastric abdominal pain that improves with mealsimproves with meals is the hallmark of PUD. However, in some cases, symptoms of PUD may worsen with meals. NSAIDNSAID use is associated with the development of PUD. Hematemesis, if present, suggests more complicated disease including bleeding ulcer and warrants urgent GI referral and endoscopy. Melena commonly occurs in the setting of an upper GI bleed secondary to PUD or hemorrhagic gastritis (e.g. NSAID-gastritits). Hematochezia only occurs in the setting of an upper GI bleed when massive (e.g. variceal rupture).

GastritisGastritis

Inflammation or irritation of the stomach lining often causing sharp epigastricsharp epigastric painpain. This pain may be variably worsenedworsened or improved with eating foodor improved with eating food. Inflammatory forms of gastritis may be caused by chronic infections such as H.H. pyloripylori or acute infections such as viruses.viruses. Non-inflammatory forms of ‘gastritis’ are more properly histologically termed

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gastropathy. These may be caused by chemical irritants to the stomach, including alcoholalcohol and NSAIDNSAIDs.

Less Likely DiagnosesLess Likely Diagnoses

Anxiety

A possible etiology for abdominal pain, but other diagnoses should be considered first. Can be associated with different types of body pain and patients who have anxiety disorders may self-medicate (i.e. with alcohol), which may warrant further careful exploration by the physician.

Pneumonia Unlikely in the absence of pulmonary symptoms.

Abdominal wall muscle strain

Can cause upper abdominal pain. This diagnosis is unlikely in the absence of a positional component to the pain.

Diverticulitis

Commonly presents with acute leftacute left lower quadrant abdominal pain,lower quadrant abdominal pain, change in bowel movements, andchange in bowel movements, and feverfever. Most common in patients over 50over 50 yearsyears of age.

Angina pectoris

Classically presents with substernalClassically presents with substernal chest painchest pain, but may present with epigastric abdominal pain andepigastric abdominal pain and nausea or vomitingnausea or vomiting. Interestingly, GERD is the most common cause of non-cardiac chest pain.

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Acute pancreatitis

Causes severe abdominal pain,severe abdominal pain, associated nausea and vomiting, illassociated nausea and vomiting, ill appearance on exam, and clinicalappearance on exam, and clinical signs of dehydration such assigns of dehydration such as tachycardia.tachycardia. Pain is typically located in the epigastricepigastric area with radiation to the backarea with radiation to the back and worsens with eatingworsens with eating. Symptoms often last for many hours without relief. Acute and chronic pancreatitis may be caused by alcohol usealcohol use. Remember that some patients may not be forthcoming about their actual alcohol use, especially if they perceive they are being judged or if they are in denial about problem use/abuse.

The absence of hematemesis, hematochezia, or melena is reassuring that significant GI bleeding is unlikely to be present, but does not help to distinguish between these three diagnoses, all of which can present without GI bleeding.

DYSPEPSIA DEFINED TEACHING

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You and Dr. Medel discuss dyspepsia.You and Dr. Medel discuss dyspepsia.

!

After careful consideration, you tell Dr. Medel that you are concerned that Mr. Rodriguez has either gastritis, gastroesophageal reflux disease (GERD), or peptic ulcer disease (PUD). You and Dr. Medel discuss the various causes of dyspepsia.

You tell Dr. Medel you are confused how to differentiate these etiologies of dyspepsia. Dr. Medel replies, “That is understandable, as this is like piecing together a puzzle. There is no one right answer for every patient. Instead, you have to consider the clinical picture as a whole. We’ll need to consider each possible etiology for dyspepsia for Mr. Rodriguez.”

Dyspepsia – DeYnition, Symptoms, Epidemiology & Etiology

DefinitionDefinition

Dyspepsia is literally “bad digestion.”

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SymptomsSymptoms

Patients with this condition experience upper abdominal pain or discomfort that is episodic or persistent. It is often associated with belching, bloating, heartburn, nausea, or vomiting.

EpidemiologyEpidemiology

About a quarter of adults are affected by it, but many people self-diagnose and self-treat it. Even though most people don’t seek medical care for it, dyspepsia accounts for approximately 5% of all visits to family physicians and is the most common symptom leading to GI referral in the US.

EtiologyEtiology

ConditionCondition % of Dyspepsia Cases% of Dyspepsia Cases

Functional or non-ulcer dyspepsia (specific etiology for dyspepsia can’t be identified)

~ 50%

Peptic ulcer disease (PUD) 20%

GERD 20%

Gastritis / duodenitis 15%

Medication side effects Common

Pancreatitis Less common

Gastric, pancreatic, and esophageal cancer

Important though uncommon (< 2%)

Non-GI causes (such as angina and dissecting aortic aneurysm)

Rare, but should always be included in ddx

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The best options are indicated below. Your selections are indicated by the shaded boxes.

Question Which of the following agents have been proven to cause or contribute to the development of peptic ulcer disease? Select all that apply.

A. Aspirin

B. Acetaminophen

C. Ibuprofen

D. Psychosocial stress

E. Moderate physiologic stress

F. Caffeine

G. Cigarette smoking

H. Helicobacter pylori

SUBMITSUBMIT

Answer Comment The correct answers are A, C, E, G, H.The correct answers are A, C, E, G, H.

Agents that Cause or Contribute to Peptic Ulcer Disease

Aspirin and other non-steroidal anti-inflammatory drugsAspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are the predominant pharmacologic agents that(NSAIDs) are the predominant pharmacologic agents that contribute to the development of PUDcontribute to the development of PUD. Classically, the elderly are at the highest attributable risk of ulceration and perforation

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due to chronic NSAID use. Chronic NSAID use is a leading cause of morbidity in the elderly.

Moderate to severe physiologic stress may lead toModerate to severe physiologic stress may lead to stress ulcerationstress ulceration, predominantly in patients in the intensive care unit (ICU).

Colonization of the stomach byColonization of the stomach by H. pyloriH. pylori renders the underlying mucosa more vulnerable to peptic acid damage by disrupting the mucous layer, liberating enzymes and toxins, and adhering to the gastric epithelium. In addition, the body’s immune response to H. pylori incites an inflammatory reaction that contributes to tissue injury and leads to chronic gastritis. In most individuals the chronic gastritis is asymptomatic and does not progress. In some cases, however, altered gastric secretion coupled with tissue injury leads to peptic ulcer disease. In other cases, gastritis progresses to mucosal atrophy, intestinal metaplasia, and eventually gastric carcinoma. Rarely, persistent immune stimulation of gastric lymphoid tissue can lead to gastric lymphoma.

There is no evidence to support a cause-and-effect association between cigarette smoking and PUD. However, cigarettecigarette smokingsmoking does decrease vascularity to gastric mucosal cells, resulting in decreased rates of mucosal healing after insult, and in combination with NSAID use or H. pylori infection, increases the risk of ulceration.

There is no evidence to support a cause-and-effect association between acetaminophen (B), psychosocial stress (D), or caffeine intake (F) and PUD.

References

Ford A., Moayyedi P. Current guidelines for dyspepsia management. digestive diseases: Clinical Reviews. Vol. 26, No. 3, 2008.

Fisher RS, Parkman HP. Management of nonulcer dyspepsia. N Engl J Med. 1998;339:1376-81.

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The best options are indicated below. Your selections are indicated by the shaded boxes.

Heidelbaugh JJ, Inadomi JM. Magnitude and economic impact of inappropriate use of stress ulcer prophylaxis in non-intensive care unit hospitalized patients. Am J Gastroenterol. 2006;101(10):2200-5.

Spirt M, Stanley S. Update on Stress Ulcer Prophylaxis in Critically Ill Patients. Critical Care Nurse. Vol. 26 (1): February, 2006. http://ccn.aacnjournals.org/content/26/1/18.full. Accessed April 29, 2017.

Wight N, Hawkey C. Nonsteroidal anti-inflammatory drug-related peptic ulcer disease. In: Irvine E, Hunt R (eds). Evidence-based gastroenterology. Hamilton, Ontario: BC Decker; 2002:102-118.

CAUSES OF DYSPEPSIA TEACHING You tell Dr. Medel that you are still unsure how to differentiate between dyspepsia due to gastroesophageal reflux disease (GERD) and dyspepsia due to peptic ulcer disease (PUD).

Question Which of the following are TRUE regarding dyspepsia due to GERD or PUD? Select all that apply.

A. GERD can be distinguished from other gastrointestinal

disorders with reasonable accuracy on the basis of symptoms.

B. Eating and drinking make GERD symptoms improve

and PUD symptoms worse.

C. Peptic ulcers may be associated with nausea and

vomiting that can occur anytime shortly after eating up to several

hours later.

D. Non-erosive reflux disease (NERD) is the most common

form of GERD.

E. Patients with GERD report lower health-related quality

of life than patients with heart failure.

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SUBMITSUBMIT

Answer Comment The correct answers are A, C, D, E.The correct answers are A, C, D, E.

The symptoms that patients describe often overlap and can make it tricky to determine the etiology of dyspepsia. However, some symptoms can help distinguish GERD from other gastrointestinal disorders with reasonable accuracy.

Peptic Ulcer Disease vs. Gastroesophageal Re\ux Disease Symptoms

Some symptoms of PUD directly contrast those of GERD.

PUDPUD GERDGERD

U sually characterized by episodic or recurrent epigastric ‘aching’, ‘gnawing’, or ‘hunger-like’ pain or discomfort

Classic symptoms of heartburn and regurgitation

Symptoms occur on an empty stomach and are commonly relieved by meals

likely to occur when gastric volume is increased (after large meals)

However, this is not always true, and there can be some differences in symptoms based on the location of an ulcer.

For example, gastric ulcer pain may occur 5 to 15 minutes after eating and remain until the stomach empties, which may be up to several hours in duration, and the pain may otherwise be absent during times of fasting. Pain from duodenal ulcers is often relieved by eating, drinking milk, or taking antacids but may

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return anywhere from 90 minutes to 4 hours after eating a meal. Both gastric and duodenal ulcers may be associated with nausea and vomiting occurring anytime shortly after eating to several hours later.

Gastroesophageal Re\ux Disease – Pathophysiology, Symptoms, Complications, and Quality of Life

PathophysiologyPathophysiology

GERD is a chronic relapsing condition in which gastric contents reflux through the lower esophageal sphincter (LES) into the esophagus or oropharynx. Transient LES relaxations are believed to be the primary etiologic factor. Ineffective esophageal clearance (as seen with scleroderma, for example) and delayed gastric emptying (as seen with gastroparesis, for example) may also be contributing factors in some patients.

SymptomsSymptoms

1. Gastroesophageal reflux1. Gastroesophageal reflux – epigastric burning that sometimes radiates to the throat and tends to worsen when:

gastric volume is increased (after large meals) gastric contents are located near the gastroesophageal junction

(reclining or bending) intra-abdominal pressure is increased (such as with obesity,

pregnancy, tight binders or girdles).

2. Esophageal spasm2. Esophageal spasm – sharp, stabbing, substernal pain and can be triggered by temperature extremes (e.g. hot coffee, ice water).

Heartburn and esophageal reflux and spasm commonly occur at night or after the consumption of a large meal.

Symptoms of GERD may also be precipitated by:

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spicy and fatty foods chocolate mint smoking alcohol and caffeinated beverages eating large portions lying flat after a meal wearing tight clothing around the waist some medications (calcium channel blockers, beta-agonists,

alpha-adrenergic agonists, theophylline, nitrates, and some sedatives)

When severe reflux reaches the pharynx and mouth or is aspirated, it can cause atypical signs and symptoms of GERD or laryngopharyngeal reflux (LPR). Atypical symptoms may point to (but don’t sufficiently support by themselves) a diagnosis of GERD.

Atypical signs and symptoms of GERD:

asthma chronic cough dental enamel loss globus sensation hoarseness noncardiac chest pain recurrent laryngitis recurrent pharyngitis subglottic stenosis

ComplicationsComplications

About 60% of cases of GERD can be classified as non-erosive reflux disease (NERD). Unfortunately, symptom frequency, duration, and severity do not help to differentiate the grade of esophagitis and cannot be used to reliably diagnose complications of GERD.

Quality of lifeQuality of life

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Patients who have GERD generally report decreased quality of life, reduced productivity, and decreased well-being. In many patients, reported health-related quality of life is lower than age-matched patients who have untreated angina pectoris, diabetes mellitus or chronic heart failure.

References

National Guideline Clearinghouse (NGC). Guideline summary: Guidelines for the diagnosis and management of gastroesophageal reflux disease. Agency for Healthcare Research and Quality (AHRQ). https://www.guidelines.gov/summaries/summary/43847/guidelines-for-the-diagnosis- and-management-of-gastroesophageal-reflux-disease?q=GERD. Accessed August 24, 2017.

COMPLICATIONS AND ALARM SIGNS TEACHING You and Dr. Medel discuss complications of GERD and PUD.

Dr. Medel tells you about alarm symptoms, concluding, “Mr. Rodriguez does not demonstrate any of these right now, but we should remember them, because any of these symptoms would warrant timely referral to a gastroenterologist for endoscopy.”

Complications of GERD and PUD

GERDGERD

EsophagitisEsophagitis develops when the mucosal defenses that normally counteract the effect of injurious agents are overwhelmed by refluxed acid, pepsin, or bile.

Peptic stricturesPeptic strictures from fibrosis and constriction occur in about 10 percent of patients with reflux esophagitis.

Replacement of the squamous epithelium of the esophagus by columnar epithelium (Barrett’s esophagusBarrett’s esophagus) may result from reflux esophagitis. Two to five percent of cases of Barrett’s esophagus may be further complicated

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by adenocarcinomaadenocarcinoma.

PUDPUD

HemorrhageHemorrhage oror perforationperforation into the peritoneal cavity or adjacent organs (causing severe, persistent abdominal pain).

Ulcer scar healing or inflammation can impair gastric emptying leading to gastric outlet obstruction syndromegastric outlet obstruction syndrome.

Alarm Symptoms Warranting Referral to Gastroenterology for Endoscopy

Dysphagia

Difficulty in swallowing. Dysphagia to solids suggests possible development of peptic stricture. Rapidly progressive dysphagia potentially indicates adenocarcinoma. Dysphagia to liquids suggests development of a motility disorder.

Initial onset of upper GI symptoms after age 50

Increased chance of cancer.

Early satiety May be associated with gastroparesis or gastric outlet obstruction (stricture or cancer).

Hematemesis

Vomiting blood, which suggests bleeding ulcer, mucosal erosions (erosive gastritis/esophagitis), esophageal tear (Mallory-Weiss), or esophageal varices.

Hematochezia Passing red blood with stool, which may indicate a rapidly bleeding ulcer or mucosal erosions.

Iron The presence of hematemesis, hematochezia, and/or

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deficiency anemia

iron deficiency anemia may indicate possible bleeding from a peptic ulcer, mucosal erosions, or cancer.

Odynophagia Painful swallowing, which is associated with infections (e.g. candida), erosions, or cancer.

Recurrent vomiting

Suggestive of gastric outlet obstruction.

Weight loss Associated with malignancy.

References

Ross C.L. Integral Healthcare: The Benefits and Challenges of Integrating Complementary and Alternative Medicine with a Conventional Healthcare Practice. Integr Med Insights. 2009;4:13–20.

PREPARING FOR THE PHYSICAL EXAM TEACHING Now Dr. Medel says, “Let’s think about how the physical exam might help us narrow our differential. What do you think?”

“That’s a trick question!” you exclaim. “In most of cases of patients presenting with symptoms related to GERD and PUD, the physical examination will be normal. But, we will want to look for signs of complications.”

Dr. Medel replies, “You’re right. We will want to look for signs of complications, as well as signs of other diseases that could be associated with dyspepsia.”

GERD/PUD Physical Exam: Signs of Complications or Other Associated Diseases

Hemodynamic status

Hypotension or tachycardia may indicate significant blood loss from a gastrointestinal bleed.

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Signs of anemia

Brittle nails and cheilosis (cracks and sores on the lips) are signs of anemia. Pallor of palpebral (eyelid) mucosa or nail beds may also be present with anemia.

Signs of malignancy

Weight loss, palpable mass, presence of signal lymph nodes (Virchow’s nodes) and acanthosis nigricans (velvety, hyperpigmented skin, usually on the neck, under the arms or in the groin) are signs of possible malignancy.

Signs of gall bladder disease

Jaundice or a positive Murphy’s sign. (A test for Murphy’s sign is performed by asking the patient to breathe out and then gently placing the hand in the approximate location of the gallbladder. The patient is then instructed to inspire. If the patient stops inhaling (as the tender gallbladder comes in contact with the examiner’s fingers) the test is considered positive.)

Signs of hypo or hyperthyroidism

Constipation, cool or pale skin, coarse hair, or non- pitting edema (myxedema) or delayed relaxation phase of deep tendon reflexes (DTRs) may be present in hypothyroidism. Diarrhea, warm skin, thinning hair, eyelid lag, brisk DTRs, or tachycardia may be present in hyperthyroidism. Though a very rare cause of dyspepsia, thyroid disease should be considered.

References

Ross C.L. Integral Healthcare: The Benefits and Challenges of Integrating Complementary and Alternative Medicine with a Conventional Healthcare Practice. Integr Med Insights. 2009;4:13–20.

PHYSICAL EXAM PHYSICAL EXAM

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You perform a physical exam on Mr. Rodriguez while Dr. Medel observes.You perform a physical exam on Mr. Rodriguez while Dr. Medel observes.

!

You knock on the door and ask Mr. Rodriguez if he is ready for you, Lola, and Dr. Medel to re-enter the exam room. Mr. Rodriguez says “Yes,” and you proceed with your exam, which reveals:

Vital signs:Vital signs:

Temperature:Temperature: 98.5 Fahrenheit Heart rate:Heart rate: 78 beats/minute, regular Respiratory rate:Respiratory rate: 16 breaths/minute Blood pressure:Blood pressure: 123/72 mmHg Body Mass Index:Body Mass Index: 24.8 kg/m2

General:General: Well-appearing, middle-aged man.

Head, eyes, ears, nose and throat (HEENT):Head, eyes, ears, nose and throat (HEENT): Sclera anicteric, no conjunctival pallor, oropharynx without lesion or significant dental abnormality.

Neck:Neck: Supple, no mass, lymphadenopathy or thyromegaly.

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Cardiovascular:Cardiovascular: Regular heart rate and rhythm, S1, S2, no murmurs, rubs, or gallops.

Respiratory:Respiratory: Bilaterally clear lungs to auscultation without wheezes, rales or rhonchi.

Abdominal:Abdominal: Flat appearance without scars. Normoactive bowel sounds heard in four quadrants. Soft, non-distended, with minimal epigastric tenderness on deep palpation without rebound tenderness or guarding, no hepatosplenomegaly, and no herniae or masses.

Skin:Skin: Tanned; no jaundice, several tattoos on his upper extremities, no suspicious lesions..

Extremities:Extremities: Warm and well-perfused, no cyanosis, clubbing or edema.

You inform Mr. Rodriguez that his symptoms and physical examination so far do not seem to indicate a serious medical problem and tell him that you are going to step out to give him a chance to dress. Seeing Mr. Rodriguez relax a bit in his chair, you feel that he seems somewhat reassured.

DIAGNOSIS AND TREATMENT PLAN MANAGEMENT You and Dr. Medel discuss your findings and consider a diagnosis and treatment plan. She agrees with your assessment that it is challenging to accurately diagnose Mr. Rodriguez with either non-ulcer dyspepsia, GERD or PUD, or gastritis given the history and exam findings alone.

Dr. Medel asks

“Is there anything about Mr. Rodriguez today that seems to be an urgent concern?”

Question Next, she asks: “Which two of the following options are the most

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The best options are indicated below. Your selections are indicated by the shaded boxes.

appropriate first steps in diagnostic testing and therapeutic planning for this patient?” Choose the twotwo best answers.

A. Using an empiric treatment strategy with a proton

pump inhibitor (PPI)

B. Referring the patient for an upper endoscopy

(esophagogastroduodenoscopy / EGD)

C. Ordering an upper GI series (barium swallow

radiograph)

D. Focusing on lifestyle modifications to promote

symptomatic improvement

E. Referring the patient for a 24-hour pH probe

SUBMITSUBMIT

Answer Comment The correct answers are A, D.The correct answers are A, D.

Empiric Treatment for GERD, Gastritis & PUD

An empiric treatment strategy for GERD, gastritis, andAn empiric treatment strategy for GERD, gastritis, and PUD is the most widely accepted initial therapeuticPUD is the most widely accepted initial therapeutic intervention in patients without red flag symptoms.intervention in patients without red flag symptoms.

The empiric treatment strategy for a patient who exhibits the classic symptomatology of GERD with heartburn and regurgitation begins with a self-directed trial of over-the-counter anti-secretory therapy, either a histamine-2 receptor antagonist or a proton- pump inhibitor (PPI). Many patients consult their primary care physicians because their symptoms have persisted, or because they would like a prescription, which may reduce their out-of-

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pocket cost for anti-secretory therapy.

Several randomized trials have demonstrated that the “PPI test”, defined as a short-term trial of prescription-strength PPI, is both sensitive and specific for diagnosing GERD in patients with classic symptoms and can significantly reduce the need for upper endoscopy/EGD and 24-hour pH monitoring. This test has been shown to save over $350 per patient evaluated, reduce upper endoscopies by 64%, and reduce the number of esophageal monitoring tests by 53%.

The natural history of both GERD and non-ulcer dyspepsia are variable, and anti-secretory therapy should be stopped after a successful four- to eight-week course, or used in a pulse dose manner (daily for short periods of time when symptoms recur) to determine the need for chronic daily use.

Addressing lifestyle modifications with patients who complain of symptoms of GERD and dyspepsia is a reasonable approach to therapy. There is reported benefit in some patients and expert opinion suggests that dietary/lifestyle changes be encouraged in patients with GERD, although there is little evidence to support improvement in symptomatic outcomes in the absence of pharmacotherapy.

Patients should be referred for upper endoscopy/EGD in the setting of alarm or extraesophageal symptoms to rule out significant disease, or in cases that do not respond to the empiric treatment strategy after eight weeks.

The upper GI series can be useful in determining complications of GERD (e.g. esophageal stricture), but has poor utility in diagnosing GERD and should not be used for this purpose. In some cases, the upper GI series may reveal a gastric or duodenal ulcer, but it is not considered to be the gold standard test to make this diagnosis.

The 24-hour pH probe is most appropriately utilized when the diagnosis of GERD cannot easily be determined, when patients

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desire referral for surgical treatment of their GERD/hiatal hernia (Nissen fundoplication) or when patients with classic symptoms of GERD (heartburn, regurgitation) do not improve after appropriate trials of several different PPIs.

References

Kalyanakrishnan R, Salinas RC. Peptic Ulcer Disease. Am Fam Physician. 2007;76(7):1005-1012. http://www.aafp.org/afp/2007/1001/p1005.html. Accessed April 29, 2017.

SHARING TREATMENT PLAN MANAGEMENT

You give Mr. Rodriguez a patient handout in Spanish.You give Mr. Rodriguez a patient handout in Spanish.

!

Together, you, Dr. Medel and Lola re-enter Mr. Rodriguez’s room. You tell him, “At this point, it seems most likely that you may either have some acid from your stomach that is irritating your esophagus, the tube that connects your

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mouth and stomach, or that you might have irritation from acid in your stomach, ibuprofen, or infection in your stomach, which may have caused an ulcer.” Mr. Rodriguez appears startled at the word “ulcer”, and he becomes visibly more worried as you finish your sentence.

You take a moment to ask him,

“It seems like something I’ve said made you nervous. Did it?”

“I heard you saying it could be some acid in my stomach, but then when you said “ulcer,” I remembered a friend who had to have an operation for a stomach ulcer.”

You reply, “I’m sorry, I didn’t mean to upset you. While we want to carefully consider possible causes, we don’t think your symptoms today represent a serious condition.”

You add, “Sometimes people may experience other symptoms that might indicate more serious disease.” You review the alarm symptoms of potential complications warranting referral to a gastroenterologist with him, asking him to let you know right away if he experiences any of these symptoms. You also give him a patient handout in Spanish.

You tell Mr. Rodriguez that a medication called omeprazole may help reduce or take away his pain and heal a possible ulcer. You instruct him to take 20 mg every day for four weeks, on an empty stomach, 30 minutes prior to the first meal of the day. You also suggest that he cut back on alcohol, caffeine, spicy foods, and ibuprofen, substituting acetaminophen instead. Mr. Rodriguez repeats the instructions back to you correctly after you ask him to do so.

Mr. Rodriguez thanks you adding, “I feel a little better about things, but I’m not sure I can pay for the medication. Do you have any samples in your office?”

You tell him, “Unfortunately, we do not have any samples to give you, but I can direct you to Marcia, one of our nurses, who can help get this medication for you through a patient assistance program.”

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Mr. Rodriguez thanks you for your help, and you recommend a follow-up visit in one month to check on his progress.

References

Heidelbaugh JJ, Goldberg K, Inadomi JM. Overutilization of proton pump inhibitors: a review of cost-effectiveness and risk. Am J Gastroenterol. 2009;104:S27-S32.

MODIFYING TREATMENT PLAN MANAGEMENT

You see Mr. Rodriguez on his one-month follow-up visit.You see Mr. Rodriguez on his one-month follow-up visit.

!

Mr. Rodriguez returns to the clinic four weeks later. You greet him and Lola, who has returned to serve as his interpreter.

You ask,

“How have you been feeling since the last visit?”

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The best option is indicated below. Your selections are indicated by the shaded boxes.

“The medication you gave me didn’t work. I took it every day just like you said, but I still have burning stomach pain right here (points to epigastrium) every day.”

You remember that Mr. Rodriguez’s symptoms were fairly ambiguous and that classic symptoms of GERD are more specific, so you try to clarify,

“Do you have any burning in your chest or stomach after meals or feel like your food is coming back up after you eat it?”

“Not really, not every day.”

“Have your original symptoms changed? Did you develop any alarm signs or symptoms from the list I gave you?”

“No, not really. I haven’t vomited at all, and I haven’t noticed any black or tarry stools.”

On more detailed questioning and review of his vital signs including weight, you do not elicit any worrisome alarm signs or symptoms from Mr. Rodriguez, but you are concerned that overall his condition has not improved. You excuse yourself for a moment while you go find Dr. Medel.

Question Should you refer Mr. Rodriguez to a gastroenterologist at this point?

A. Yes

B. No

SUBMITSUBMIT

Answer Comment

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Answer Comment The correct answer is B.The correct answer is B.

Since there are no alarm signs or symptoms suggesting GI bleeding of cancer, a referral to a gastroenterologist is not warranted. Further workup can continue in the office setting.

FOLLOW-UP TREATMENT PLAN MANAGEMENT

You tell Dr. Medel about Mr. Rodriguez’s You tell Dr. Medel about Mr. Rodriguez’s continuing symptoms.continuing symptoms.

!

You find Dr. Medel in the hallway and tell her Mr. Rodriguez’s symptoms have not improved. You relate that the lack of improvement and the absence of classic symptoms of GERD are making you think GERD is a less likely diagnosis. His past NSAID use makes you wonder if he more likely has PUD, with or without H. pylori infection, although he could still have functional/non-

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The best options are indicated below. Your selections are indicated by the shaded boxes.

ulcer dyspepsia (NUD) as well.

Dr. Medel agrees with your assessment and asks, “Given that PUD is our next most likely diagnosis at this point, but we are still considering functional dyspepsia, what do you think we should do next?”

Question Which of the following are appropriate next steps in diagnostic and therapeutic planning? Select all that apply.

A. Ask about current NSAID and/or aspirin use

B. Perform a digital rectal examination and guaiac-based

fecal occult blood test (FOBT)

C. Start tricyclic antidepressants to modulate visceral

sensation and minimize pain

D. Order H. pylori IgG serology

E. Order an H. pylori fecal antigen test

F. Obtain a complete blood count (CBC)

G. Refer for a urease breath test

SUBMITSUBMIT

Answer Comment The correct answers are A, B, D, F.The correct answers are A, B, D, F.

Management of Dyspepsia Unresponsive to Short- Term PPI Trial

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Check for contributing agentsCheck for contributing agents

Inquire about NSAID and/or aspirin useNSAID and/or aspirin use, as this may play a role in the symptoms. Additionally, healthcare providers should reconcile medications at each encounter, to determine which medications and doses a patient is currently taking.

Antisecretory therapyAntisecretory therapy

There are several therapies for functional dyspepsia that are similar to those for PUD.

PPI therapy has been shown to be superior to placebo treatment with regard to relative risk reduction of functional dyspepsia (Number needed to treat (NNT) = 9).

Evidence exists to support an empiric trial of histamine-2 receptor antagonists, although some data suggests these medications are no more beneficial than prokinetics (e.g. metoclopramide) or antacids.

A subset of patients with functional dyspepsia will not respond favorably to any form of anti-secretory therapy and will continue to experience symptoms. Studies have observed an approximately 10% reduction in dyspepsia symptoms 12 months after H. pylori eradication therapy in patients with functional dyspepsia (NNT = 17).

Test for Test for H. pyloriH. pylori

Testing for H. pylori is not indicated in patients with classic GERD and should be performed only in patients with dyspepsia or other upper GI concern (e.g. nausea, epigastric pain) if the clinician plans to offer treatment for positive results. Deciding which test to use in which situation relies upon an understanding of the benefits, limitations, and costs of the individual tests, as well as the suspected prevalence of H. pylori infection in the patient population.

The H. pylori IgG serologic test only confirms evidence of past infection and an immunologic response to H. pylori . In a

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population with a high prevalence of active H. pylori infection, it is a useful first-time test. However, if the prevalence of active infection is low, then the test may yield a high number of false- positive results. It should not be used to confirm eradication of H. pylori after treatment as it can remain positive for years.

The urea breath test accurately detects active infection but is more expensive than serologic testing. It is less accurate during PPI therapy, and patients would need to stop the PPI for at least two weeks before a urea breath test (bismuth and antibiotics should also be stopped for at least two weeks before a urea breath test.). However, urea breath testing may be appropriate depending on the characteristics of the population being tested.

The stool antigen test for H. pylori is also accurate and widely available, but it is more expensive and less convenient than serologic testing. The stool antigen and urease breath tests may also be used as confirmatory tests after a positive serologic test.

If an endoscopy is indicated (i.e. due to the presence of alarm symptoms), or in patients who have been taking a PPI, antibiotics, or bismuth, endoscopic testing for H. pylori, (which consists of tissue biopsies from the gastric body and antrum for rapid tissue urease testing or histology) should be performed in lieu of other H. pylori tests.

After H. pylori infection is ruled out, the following therapies have been proposed for functional dyspepsia:

Tricyclic antidepressants have been found to improve symptoms in patients with functional dyspepsia without affecting the sensation of gastric distention.

A systematic review determined that there is insufficient evidence to support the efficacy of psychological therapies, including cognitive behavioral therapy, hypnotherapy, relaxation training and interpersonal therapy, for the treatment of functional dyspepsia. However, individual trials have reported some modest clinical benefits in symptomatic improvement.

Alternative therapies are gaining popularity in patients with gastrointestinal conditions, and studies of varying quality suggest that slippery elm, capsaicin, peppermint oil, caraway oil and

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artichoke leaf may improve symptoms in some patients; however, there is as yet no compelling evidence on which to base a recommendation for these alternative therapies. Note:Note: Peppermint oil decreases lower esophageal sphincter pressure and may worsen GERD symptoms. Patients should be educated that herbal remedies are not regulated by the US Food and Drug Administration (FDA), may not have been studied for safety, and can have adverse side effects, which very often include GI side effects.

Rule out GI bleedingRule out GI bleeding

If symptoms have not improved, it is reasonable to consider fecal occult blood testing (FOBT) to rule out occult bleeding. Fecal immunochemical testing (FIT) is more sensitive and specific than FOBT for detecting occult lower GI bleeding; however, it is not suitable for detecting gastric bleeding, and it should not be used if the suspected source of bleeding is proximal to the ligament of Treitz. The guaiac-based fecal occult blood tests (FOBT), such as Hemoccult II SENSA, are best used to check for occult upper GI bleeding. Multiple negative FOBTs or FITs do not exclude the presence of either upper or lower GI blood loss. Diets high in red meat, iron, and vitamin C may cause false positive results with guaiac-based tests.

A complete blood count is a useful test to evaluate for anemia, but the CBC is neither sensitive nor specific for upper GI bleeding. In patients who with a positive FOBT, it is important to obtain a CBC to assess the degree of blood loss and to determine the urgency of GI referral.

EndoscopyEndoscopy

It might seem reasonable to refer the patient at this point to gastroenterology for endoscopy to determine if the patient has endoscopically-confirmed PUD vs. functional dyspepsia (in which case an upper endoscopy would appear unremarkable). But, in the absence of alarm symptoms, the cost and risk of endoscopy

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does not outweigh the benefits of testing and treating at this point.

References

Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808-1825.

Malfertheiner P, Megraud F, O’Morain C, et al. Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report. Gut. 2007;56:772-781.

Saad R, Chey WD. Current and emerging therapies for functional dyspepsia. Aliment Pharmacol Ther. 2006;24:475-92.

van Rossum LG, van Rijn AF, Laheij RJ, et al. Random comparison of guaiac and immunochemical fecal occult blood tests for colorectal cancer in a screening population. Gastroenterology. 2008;135:82-90

H. PYLORI TEACHING

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H. pyloriH. pylori biopsy of gastric antrum, 400x biopsy of gastric antrum, 400x

!

You and Dr. Medel return to see Mr. Rodriguez and find:

Mr. Rodriguez denies taking NSAIDs or aspirin since the last visit.

Vital signs:Vital signs:

Heart rate:Heart rate: 80 beats/minute and regular Blood pressure:Blood pressure: 126/75 mmHg

Abdominal exam:Abdominal exam: He has minimal epigastric tenderness without rebound or guarding, which is unchanged compared to his previous exam four weeks ago.

Rectal exam:Rectal exam: Reveals a negative FOBT test, without any evidence of gross blood or anatomic abnormality.

You excuse yourselves from Mr. Rodriguez’s room, reassuring him that you will return shortly.

You tell Dr. Medel, “It’s possible that Mr. Rodriguez may have a peptic ulcer,

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The best options are indicated below. Your selections are indicated by the shaded boxes.

but I don’t feel that he needs to be emergently evaluated. He hasn’t taken any NSAIDs in over a month, and he doesn’t have a history of excessive use. I am concerned that he could have an ulcer or gastritis due to H. pylori infection. His history of immigrating from the Dominican Republic places him at a higher risk of having this condition.”

Question Which of the following are true regarding the natural history of H. pylori infection? Select all that apply.

A. H. pylori is spread through human saliva and feces and

via food and water sources.

B. Ninety percent of patients worldwide with duodenal

ulcers are infected with H. pylori.

C. The incidence of H. pylori is declining worldwide.

D. The gastric mucosa offers H. pylori protection from

host immune mechanisms.

E. The strongest evidence to support the role of H. pylori

as an etiology of PUD is the elimination of ulcer recurrence after

eradication.

SUBMITSUBMIT

Answer Comment The correct answers are A, B, C, D, E.The correct answers are A, B, C, D, E.

Epidemiology of H. pylori Infection

An estimated 30% to 40% of the US population is infected with

TEACHING POINTTEACHING POINT

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H. pylori. The prevalence of H. pylori infection varies across different

geographic regions, ethnic groups, and household conditions. H. pylori infection is thought to occur via fecal-oral transmission

during childhood in underdeveloped nations. Ninety percent of patients worldwide with duodenal ulcers are

infected with H. pylori. It is rare in developed countries, and the worldwide prevalence

is decreasing. H. pylori is uniquely adapted to life in the stomach. Its location

in the gastric mucosa, where it does not invade the gastric epithelium, which provides the organism with protection from the host immune mechanisms and results in challenges in the delivery of antimicrobial agents to eradicate infection.

The strongest evidence to support the role of H. pylori as an etiology of PUD is the elimination of ulcer recurrence after eradication.

Serological studies in developing nations, including Latin and Central America, have demonstrated prevalence rates of 80 to 90% for H. pylori infection in all adults, regardless of age. A population-based study examining the prevalence of H. pylori infection across several generations of Latinos in the San Francisco Bay Area found prevalence rates in immigrants, first, and second-generation US-born Latinos to be 31%, 9% and 3%, respectively. Compared with second-generation US-born Latinos, the age-adjusted odds ratios for H. pylori were 9.70 for immigrants and 4.32 for first-generation US-born Latinos (95% CI). Both household and birth-country environment have probably contributed to declining H. pylori prevalence among successive generations of Latinos.

References

” DEEP DIVEDEEP DIVE

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Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994:772.

Tsai CJ, Perry S, Sanchez L, et al. Helicobacter pylori infection in different generations of Hispanics in the San Francisco bay area. Am J Epi. 2005;162(4):351-357.

Vakil N, Megraud F. Eradication therapy for Helicobacter pylori. Gastroenterology. 2007;133(3):985-1001.

TREATING H. PYLORI TESTING

You and Dr. Medel discuss You and Dr. Medel discuss H. PyloriH. Pylori with Mr. Rodriguez. with Mr. Rodriguez.

!

Together, you and Dr. Medel decide that you suspect that Mr. Rodriguez may have gastritis or peptic ulcer due to gastritis or peptic ulcer due to H. pyloriH. pylori.. Dr. Medel tells you since there is a high prevalence of H. pylori in the patients seen at the clinic, she generally makes treatment decisions based on the serologic test for H. pylori.

You discuss this with Mr. Rodriguez, highlighting that he could have contracted H. pylori as a child and remained asymptomatic for years, how it is common in developing countries like the Dominican Republic, and how it is a treatable condition. You ask him if he has ever heard of H. pylori, and whether

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The best options are indicated below. Your selections are indicated by the shaded boxes.

or not he has ever been treated for it. He replies that he hasn’t. You tell him that you plan to order a lab test to evaluate his exposure to H. pylori.

You order an H. pylori IgG serology and let him know you’ll call him when the results are ready.

The next day, you and Dr. Medel are reviewing laboratory results. You notice that Mr. Rodriguez’s complete blood count is unremarkable for anemia, but his H. pylori IgG assay is positive:

HELICOBACTER PYLORI IgG ANTIBODY BY EIA – QUALITATIVE

Result: POSITIVE

——————INTERPRETATION——————–

NEGATIVE….. No H. pylori IgG antibody detected

POSITIVE….. H. pylori IgG antibody detected

You have the nurse call Mr. Rodriguez to ask him come in and discuss the results.

Question Which of the following are approved initial treatment regimens for the eradication of H. pylori? Select all that apply.

A. PPI therapy for an additional 4 weeks for 8 weeks of

total therapy

B. Addition of an H2 receptor antagonist to the PPI

regimen for 8 weeks of total therapy

C. Standard dose PPI + amoxicillin 1 gram +

clarithromycin 500mg all twice daily for 10-14 days

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D. Standard dose PPI + trimethoprim/sulfamethoxazole

double strength + erythromycin 500mg all twice daily for 10-14

days

E. Standard dose PPI + amoxicillin 1 gram + levofloxacin

500mg all twice daily for 10 days

F. Standard dose PPI once or twice daily + metronidazole

250 mg, tetracycline 500 mg, + bismuth subsalicylate 525 mg each

four times daily for 10-14 days

SUBMITSUBMIT

Answer Comment The correct answers are C, F.The correct answers are C, F.

First-line Treatment for H. pylori

“Triple therapy” for 10 to 14 days (70% to 85% eradication”Triple therapy” for 10 to 14 days (70% to 85% eradication rate)rate):

PPI standard dose twice daily (esomeprazole is dosed once daily)

Amoxicillin 1 g twice daily Clarithromycin 500 mg twice daily

“Quadruple therapy” for 10 to 14 days (75% to 90%”Quadruple therapy” for 10 to 14 days (75% to 90% eradication rate):eradication rate):

PPI standard dose once or twice daily (OR ranitidine 150 mg twice daily)

Metronidazole 250 mg four times daily Tetracycline 500 mg four times daily Bismuth subsalicylate 525 mg four times daily

An alternative 10- to 14-day triple regimen to consider in patients who are allergic to penicillin (70% to 85% eradication rate):

TEACHING POINTTEACHING POINT

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PPI standard dose twice daily Clarithromycin 500 mg twice daily Metronidazole 500 mg twice daily

References

Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808-1825.

Duck WM, Sobel J, Pruckler JM, et al. Antimicrobial resistance incidence and risk factors among Helicobacter pylori-infected persons in the United States. Emerg Infect Dis. 2004;10(6):1088- 1094.

Jafri NS, Hormung CA, Howden CW. Meta-analysis: sequential therapy appears superior to standard therapy for Helicobacter pylori infection in patients naïve to treatment. Ann Intern Med. 2008;148:923-931.

Malfertheiner P, Megraud F, O’Morain C, et al. Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report. Gut. 2007;56:772-781.

INITIATING PPI TRIPLE THERAPY MANAGEMENT You and Dr. Medel confirm that the patient has no known drug allergies and decide to treat Mr. Rodriguez with standard PPI triple therapy, which the clinic is able to obtain for him through a voucher program.

You give him written instructions in Spanish highlighting how to take the medications and again review alarm signs and symptoms of complicated upper GI disease with Lola’s help. You explain that if he experiences any of these symptoms, he should notify the practice immediately, otherwise he should return in four weeks to re-evaluate his condition.

You also educate him regarding possible temporary side effects of the medications, such as nausea, abdominal pain, diarrhea, and altered taste.

Finally, you explain the possibility of an allergic reaction, as with any medication, and instruct him to call if he experiences any problems such as rash or swelling.

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