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Family Medicine Clerkship

Outline for Organization of Brief Written Case Report on a Problem in Family Medicine

Topic selection

During the first week of your clerkship/preceptorship you will see many outpatients who have common medical problems. You should determine your topic when you find a patient with a problem that interests you (a common problem in primary care). The patient you select should be able to provide you with enough information so that you can use his or her case as a basis for your report.

Guidelines

Assume that the audience has a basic understanding of medicine (Year III med student or above). Reports must center around a case discussion.

Be as brief as possible, 3 - 5 pages maximum.

Try to make this as useful as possible for another medical students in your position.

Do not try to discuss anything in depth - reference textbooks will be available in most clinical settings.

Suggested Organization of Written Paper and Evaluation

  • Case Presentation (10 points)
  • Differential Diagnosis (20 points)
  • Diagnostic Evaluation (as appropriate in primary care) (20 points)
  • Management of Problem (20 points)
  • Prevention and Patient Education (20 points)
  • References: which were used and how useful were they? (10points)
  • Total 100 points

Evaluation

Your presentation will be evaluated by faculty on the above scale.

Research

Use a least 2 sources from family practice literature or texts. Do not rely on one text. Reference all material taken from any source, i.e., if you xerox a chart or figure out of the literature, you must include a full citation of sources directly under it. If you have any questions about any aspect of your paper, please ask!

Case Study Example

Simona C. Mirza MS III
Family Medicine
Mar. 12, 1997
CC: Heartburn and stomach pain
S: 33-year-old male with one month history of midepigastric pain and heartburn, which is worse after eating, with occasional regurgitation, and worse at night when lying flat, relieved somewhat by sitting position and over the counter Mylanta and Zantac.
PMIH: Non-contributory.
MEDS: None.
PSH: None.
ALL: NKDA.
FH: Non-contributory.
SOC: Tobacco: None. Alcohol: Socially: 2-3 beer/occasion. Drugs: None.
0:
Vitals: BP 132/78 P80 T99.1 Wgt: 190lbs.
HEENT: Pupils equally round and reactive to light, tympanic membranes clear, canals clear bilaterally, oropharynx pink and moist, no erythema, no tonsillar enlargement, no lesions, no lingual erosion of teeth, no lymphadenopathy, thyroid normal size, no nodulary.
Cor: Regular rate and rhythm, no murmurs, rubs or gallops.
Lungs: Clear to auscultation bilaterally, no wheezing.
Abd: Non-distended, normal active bowel sounds, soft, non-tender.
A/P: Gastroesophageal reflux disease

  1. Start Tagamet 800mg BID for 2 weeks.
  2. Diet modification instruction, including minimal alcohol intake.
  3. Retum for reevaluation in 2 weeks.

FOLLOW-UP VISIT:

Patient states that he is feeling better on the Tagamet. He is advised to continue dietary control and minimal alcohol intake. Follow-up as needed.

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Heartburn is among the most common complaints seen in the Family Medicine office, in otherwise healthy people. Surveys have shown that 4-7% of persons experience daily heartburn and 15-40% monthly. Though few people actually seek medical attention for their symptoms it is at least the primary or secondary reason for 2.5 million office visits nationally over a 1 year period, and in 1985 (as quoted by Weinberg et al. from the Digestive Diseases in the United States: Epidemiology and Impact article from the Department of Health and Human Services, 1994) there was an average of five office visits per patient identified with esophageal disease by the ICD-9 coding. Thus, despite the small percentage of the population requiring medical attention, the burden of this disease is significant.

GERD is any symptomatic clinical condition or histopathologic alteration presumed to result from esophageal exposure to gastric contents. The pathophysiology of GERD is the dysfunction of the following three barriers to reflux of the gastric contents into the esophagus:

  1. High-pressure area near the gastroesophageal junction formed from the intrinsic lower esophageal sphincter (LES) pressure, intraabdominal location of the LES, extrinsic compression by the crural diaphragm and the phrenoesophageal ligament, which creates the acute angle of entry of the esophagus into the stomach (the angle of His).

  2. Esophageal acid clearance via peristalsis and salivation by clearance of the volume and acid neutralization. Esophageal mucosal resistance via the tight junctions (zona occludens), a lipid rich intracellular matrix, the Na+/H+ antiport, and the submucosal bicarbonate secretion.

Defects of these barriers which cause reflux are: transient LES relaxations, hypotensive LES, altered esophageal pressure gradient (i.e. increased adominal pressure, delayed gastric emptying), defects in extrinsic compression: crural diaphragm (hiatal hernia) or phrenoesophageal ligament, esophageal dysmotility (i.e. general and associated with retrograde flow in a hiatal hernia), decreased salivary function (i.e. medication, smoking, sleep). Complications of long-standing GERD is that 10-12% of those patients will develop Barrett's esophagus (a metaplastic change of the esophageal mucosa) and 10% of those patients which will ultimately progress to esophageal cancer. Barrett's esophagus is normally detected in persons between the ages of 40-60, it is more common in men and whites, and more prevalent if associated with prior strictures or ulcerations.

Heartburn is the classic symptom of GERD, but there are associated symptoms of dysphagaia, odynophagia, regurgitation, water brash and belching. Investigating the clinical symptoms and knowing the reasons for those symptoms is the first step in evaluating the patient with GERD.

  1. Heartburn is usually described as a retrosternal burning pain that may also be noted in the epigastrium, neck, throat and occasionally the back. It occurs postprandially, particularly after the consumption of spicy foods, citrus, fats, chocolate, peppermint and alcohol. All of these foods decrease the lower esophageal sphincter pressure, thus allowing the gastric contents into the esophagus. Recumbency and bending over may exacerbate the heartburn.
  2. A slow progressive dysphagia for solids followed by liquids occurs with longstanding heartburn due to a peptic stricture, severe esophageal inflammation or peristaltic dysfunction, all of which can occur with Barrett's esophagus or adenocarcinoma.
  3. Odynophagia occurs when there is ulcerative esophagitis.
  4. Water brash is the slightly sour or salty salivary fluid that appears in the mouth in response to intraesophageal acid exposure.
  5. Excessive belching and burping is initiated by the increase of swallowing of saliva as well as air brought about by the acid reflux. In most patients these symptoms are enough to warrant a trial of therapy without further diagnostic tests. However, according to Dent et al., early investigation should be obtained if the symptoms do not respond to the medical therapy, if the symptoms have been present for an extended period of time, i.e. years, if there is associated dysphagia, if there are a typical symptoms, if there is a suspicion of complications from the reflux disease or if the patient is to undergo antireflux surgery.

There are four diagnostic tests available and they are used in accordance with the patient's symptoms. They are endoscopy, barium esophagram, esophageal manometry and esophageal pH monitoring.

  1. Endoscopy is used in patients with persistent reflux symptoms or frequent relapses after H2 blocker therapy to assess the possible presence of esophagitis or other complications of GERD, and 2-3 months after aggressive medical therapy for esophagitis to ensure proper healing. Endoscopy is the most sensitive test for direct visualization of esophageal mucosal damage and should be used periodically as a screening test for cancer in high risk patients with Barrett's esophagus.
  2. Barium esophagrams should be the first diagnostic tests in patients with dysphagia. It is a more sensitive test, than endoscopy for the detection of esophageal strictures and rings, for evaluating esophageal function or the presence of hiatal hernia.
  3. Esophageal manometry evaluates esophageal motility and LES pressure, but it is not a useful diagnostic test, since only 25-50% of the patients with GERD have a low resting LES pressure. This test is mainly used for the diagnosis of achalasia, for monitoring the proper placement of the pH electrode and as a mandatory test prior to antireflux surgery to determine the motility function of the esophagus.
  4. Esophageal pH monitoring is the most reliable method of diagnosing GERD. It measures the times pH is less than 4 in upright, supine or combined positions, the number of reflux episodes lasting longer than 5 minutes and the longest reflux episode, while the patient is having ad lib activities, including eating foods known to provoke their symptoms, therefore it helps correlate the symptoms with the actual reflux. Although the typical symptoms of GERD make the disease an easy one to diagnose, according to Weinberg et at.

In this article, there are a variety of atypical presentations that are being described in the literature which lengthen the differential diagnosis list:

1. Respiratory symptoms:

  • Nonseasonal asthma
  • Chronic cough
  • Sleep apnea
  • Recurrent pneumoniaa
  • Pulmonary fibrosis

2. Otolatyngologic symptoms:Globus sensation

  • Hoarseness
  • Posterior laryngitis (including ulceration and granuloma formation)
  • Pharyngitis
  • Excessive salivation
  • Laryngospasm

3. Chest pain

4. Dental erosions

Management of GERD is based on selective diagnostic testing. In patients without esophagitis, relief of acid related symptoms is the therapeutic goal. When esophagitis is present, the healing of the mucosa and prevention of relapse and complications is indicated. Richter advised the following approach to the management of GERD in his article:

Symptoms without esophagitis Mild esophagitis  Severe esophagitis or intractable symptoms
Acute Lifestyle changes
Medications as needed
Antacids, Alginic acid,
H2 Antagonists,
Prokinetics 
  Lifestyle changes
Daily medications
H2 Antagonists
Cisapride
  Lifestyle changes
Daily medications
Proton pump inhibitor
Maintenance Medications as needed
As above lifestyle changes
  H2 Antagonists
Cisapride
  Proton pump inhibitor
Antireflux surgery 

Educating the patient about the following lifestyle changes is helpful in preventing reflux:

  1. Avoidance of large meals, which increase gastric volume.
  2. Losing weight, if patient is obese.
  3. Taking the evening meal at least 3 hours before bedtime.
  4. Not lying down after meals to prevent supine reflux.
  5. Elevation of the head of the bed by 6-inch blocks to improve nocturnal clearance of refluxed acid.
  6. Dietary changes include: avoiding agents that are direct esophageal irritants, such as citric juices, tomato-based products, alcohol, cigarette smoking, soda and coffee, and those foods which adversely affect LES pressure such as fatty foods, chocolates, coffee, or carminatives.

Medical therapeutic agents recommended in the treatment of GERD symptoms and esophagitis are:

  1. Antacids and alginic acids are useful against mild esophagitis brought on by lifestyle indiscretions, but are not effective in healing esophagitis. They serve as quick and short acting acid neutralizers and mucosal coating substances.
  2. Prokinetic drugs such as bethanechol and metoclopramide relieve heartburn symptoms, but their use in treating esophagitis is equivocal. Cisapride, a new prokinetic drug is more effective in treating mild esophagitis and increasing LES pressure, improving peristalsis and accelerating gastric emptying by promoting the release of acetycholine at the myenteric plexus.
  3. H2 blockers is the backbone of treating GERD and mild to moderate esophagitis. Richter mentions some clinical trials in his article that demonstrated a 75-90% healing rate in mild esophagitis, 40-50% in moderate esophagitis and up to 60% relief of heartburn in patients after up to 12 weeks of treatment. All H2 blockers are equally effective, however the over the counter doses of cimetidine and famotidine have been shown to prolong the relief of heartburn over the antacids, but their onset of action is still more delayed than the antacids.
  4. Proton pump inhibitors (PPI), omeprazole and lansoprazole are potent, long-acting inhibitors of both basal and stimulated acid secretions, by noncompetitively inhibiting the H+/K+ ATPase pump in the parietal pump.

Clinical studies have shown that complete healing of esophagitis occurs after 8 weeks in 80% of patients and healing occurs in nearly 100% of patients if the dose is increased or used for longer period of time, and that they are superior to H2 blockers in the treatmentof severe esophagitis. However, long-term use of these agents have been shown to cause hypoacidity which stimulates gastrin release, promoting the proliferation of enterochromafin-like cells in the gastric fundus and in the rat model only, it causes gastric carcinoids.

According to Weinberg et al. the increasing use PPIs has reduced the need for effective antireflux surgery. Any of the commonly performed procedures (Nissen fundoplication, Betsey Mark IV repair and Hill posterior gastropexy) can produce good results, but side effects like ineffective reflux prevention, gas-bloat syndrome, inability to belch or vomit and postoperative breakdown are not uncommon. New surgical techniques are being investigated, including video-assisted thoracoscopy and laparoscopic antireflux surgery. Current indications for surgery remain:

  1. Severe refractory esophagitis.
  2. Esophagitis with intolerable symptoms.
  3. Recurrent aspirations.
  4. Recurrent stricture.
  5. Recurrent laryngeal inflammation.
  6. Severe disease in a young person to avoid lifelong medical therapy.

In summary, GERD is a common clinical problem encountered in the family medicine practice. Its clinical presentation and management are generally straightforward, however, by being aware that atypical symptoms are not infrequent, physicians can appropriately recognize and treat this disease early to avoid complications. Patient education for lifestyle changes is enough to prevent symptoms in some patients. Most of those patients in which lifestyle changes is not enough, medical therapy for shorter or longer durations will suffice, few of which will need definitive surgical therapy for their relief. A small, but significant proportion of patients will present with or develop significant complications of GERD, most importantly Barrett's esophagus. There is no set protocol for follow-up or cancer screening in those patients, but because esophageal cancer has such a poor prognosis, a customized plan should exist for those individual patients, with upper esophageal endoscopy, with or without periodic biopsy, being the most accurate diagnostic test available today.

References

  1. The Diagnosis and Management of Gastroesophageal Reflux Disease; Weinberg-D-S., Kadish-S-L.: MEDICAL CLINICS OF NORTH AMERICA (1996 Mar) vol. 80(2) 411-29.
  2. Esophageal Motility and Reflux Testing. State of the Art and Clinical Role in the Twenty-First Century; Dent-J. Holloway-R-H.: GASTROENTEROLOGY CLINICS OF NORTH AMERICA -- MANAGED CARE AND OFFICE PRACTICE ISSUE, (1996 Mar) vol. 25(l): 51-73.
  3. Typical and Atypical Presentations of Gastroesophageal Reflux Disease. The Role of Esophageal Testing in Diaonosis and Management; Richter-J-E.: GASTROENTEROLOGY CLINICS OF NORTH AMERICA -- MANAGED CARE AND OFFICE PRACTICE ISSUE, (1996 Mar) vol. 25(l): 75-102.
  4. Laparoscopic Antireflux Surgery: The Merits and Problems; Myrvold-H-E.: ANNALS OF MEDICINE, (1995 Feb) vol. 27(l): 29-33.
  5. The Role of Videothoracoscopy in the Diagnosis and Treatment of Chest Diseases; Salo-J-A.: ANNALS OF MEDICINE, (1994 Dec) vol. 26(6): 401-4.

The most useful references were the first three articles, especially the first and second. There were no useful articles in any of family medicine journals listed in our handout, even though this is a common problem in the family medicine practice. The only text I had available was the Essentials of Family Medicine by Sloane, Start and Curtis, and GERD or any of the associated diseases were not even mentioned. Most of these patients can be directly and straightforwardly managed by a primary care physician without involving the GI specialist, yet I cannot believe the lack of information of this disease in the primary care texts and journals. In the 4 weeks at my preceptor's office, we have evaluated and treated at least 7-8 patients with symptoms of GERD without involving the specialist or ordering any intensive diagnostic tests. Thus, I hope you will take that into consideration when you look at my sources of reference.

 

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