Peptic Ulcer Disease Case Study (60 min)

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Mrs. Baker is a 54 year old female who presented to the ED complaining of nausea and severe epigastric pain x 3 days. She reports a history of osteoarthritis and reports taking ibuprofen 400 mg 3-4 times a day regularly for the last few months since her “arthritis has gotten really bad”.

What initial nursing assessments should be performed?

  • Put the patient on a monitor to assess EKG. A 12-lead EKG should be done to rule out cardiac involvement, request order for cardiac enzymes from provider
  • Auscultate heart and lung sounds
  • Full abdominal assessment – inspect, auscultate, palpate and percuss. Assess for tenderness over specific areas, feel for masses, and look for guarding.
  • Get more detailed history questions – vomiting? Bloody stools? Has this happened before?

Patient demonstrates guarding when palpating epigastric region, no tenderness to palpation over RLQ, LLQ, or LUQ. Some tenderness over RUQ.  Bowel sounds are hyperactive, lungs are clear to auscultation, S1 and S2 heard clearly with no murmurs. As you finish your assessment, Mrs. Baker reports she is going to be sick and vomits approximately 300 mL of coffee-ground emesis.

Explain the significance of coffee-ground emesis.

  • Coffee-ground emesis is vomit that looks like it has coffee-grounds in it.
  • These black specs are actually hemolyzed blood cells/clots.
  • Coffee-ground emesis is indicative of a slow source of bleeding within the stomach or refluxing from the duodenum.

You notify the provider of the coffee-ground emesis, administer Ondansetron 4 mg IV per provider orders, and assist Mrs. Baker with oral care.

What further diagnostic testing do you expect to be performed for this patient?

  • Complete Blood Count
  • Occult blood testing of stool and emesis
  • Patient may need an EGD (esophagogastroduodenoscopy) to check for bleeding ulcers

Mrs. Baker is now weak and drowsy. Her fecal occult test is positive and her CBC shows a Hemoglobin of 10 g/dL and a Hematocrit of 31%.  Per provider orders, you insert an NG tube to evaluate stomach contents and decompress the stomach. You connect the NG tube to intermittent low wall suction.

What is likely going on with Mrs. Baker physiologically?

  • Mrs. Bakers chronic heavy use of NSAID’s may have caused ulcers to form in the lining of her stomach and/or duodenum
  • It is possible that these ulcers are now bleeding

What is the benefit to decompressing the stomach via NG tube?

  • Decompressing the stomach removes the majority of stomach acid, thereby decreasing the irritation on the stomach lining
  • The hope is to prevent further irritation to any bleeding ulcers

The UAP notifies you that Mrs. Baker’s blood pressure has dropped to 96/60. You enter the room and see that the suction canister is over halfway full of bright red blood.

What is your priority assessment at this time?

  • Assess Mrs. Baker – LOC, heart and lung sounds, confirm the accuracy of vital signs
  • Protect airway – suction if needed, minimize risk for aspiration

What may be happening to Mrs. Baker?

  • She may have an ulcer that is bleeding more actively than before. With that amount of blood, it could possibly be an arterial bleed.

Mrs. Baker is pale, diaphoretic, and drowsy. Her heart rate is up to 122. You notify the provider who orders to transfuse 2 units of PRBC’s and calls the Gastroenterology team for a STAT EGD. Within 30 minutes the patient is taken to the GI lab for an EGD, where they find two slow-bleeding gastric ulcers, which they cauterize, and 1 arterial bleed which they repair as well.  Mrs. Baker returns to the unit post-procedure for observation.

What are nursing priorities for Mrs. Baker after this procedure?

  • Keep NPO until gag reflex returns
  • Assess and monitor output from NG tube
  • Monitor vital signs closely
  • Monitor LOC as she awakens from sedatives used during the procedure
  • Ensure the full 2 units of PRBC’s were administered. If not, continue transfusion.

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Jon Haws

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  • Published: 15 June 2020

Pattern and outcome of perforated peptic ulcer disease patient in four teaching hospitals in Addis Ababa, Ethiopia: a prospective cohort multicenter study

  • Jatani Arero Bupicha 1 ,
  • Hailu Wondimu Gebresellassie   ORCID: orcid.org/0000-0002-6720-4193 1 &
  • Abebe Alemayehu 1  

BMC Surgery volume  20 , Article number:  135 ( 2020 ) Cite this article

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Perforated peptic ulcer disease is a surgical emergency with a high morbidity and mortality. The socio-demographic characteristic and the factors associated with morbidity and mortality seems to differ between the developed and developing world. This is the first a prospective cohort study in Ethiopia designed to analyze pattern and outcome of patients with perforated peptic ulcer disease in four teaching hospitals affiliated with SOM, CHS of Addis Ababa University.

This is a prospective cohort study of patients operated for perforated peptic ulcer disease from June 1, 2018 to May 31, 2019 in four teaching hospital affiliated to department of surgery of SOM, CHS of Addis Ababa university.

A total of 97 patients were operated in a year. 86.6% were males with a male to female ratio of 6.5:1. The age group 21–30 were most affected constituting 42.3% of all patients. Mean age is 31.9, Median of 27, age ranges from 16 to 76. Alcohol use (45.4%) and previous history of ulcer disease (75.3%) were the most prevalent risk factors.33% were smokers. Abdominal was present in all and most presented within 48 h (79.4%). 85.6% had pneumo = peritoneum in an x-ray at presentation. Size of the perforation is 10 mm or less in 81.3%. 91(93.8%) had anterior first part duodenum perforation. Repair with pedicled omental patch was done in 65 (67.1%) patients. Age, duration of presentation, hypotension at presentation, size of perforation, degree of peritoneal contamination were found to be the significant factors for morbidity and mortality. Major morbidities were observed in 16 (16.5%) and mortality occurred in 3 (3.1%) patients.

Perforation of peptic ulcer disease here occurs in the young. Age, duration of presentation, hypotension at presentation, size of perforation, degree of peritoneal contamination were found to be the significant factors for morbidity and mortality. Morbidity and mortality rate of 16.5 and 3.1% observed here are quite acceptable.

Peer Review reports

The natural history of peptic ulcer disease ranges from spontaneous resolution without intervention to development of life threatening complication such as bleeding and perforations. Perforated peptic ulcer is the 2nd most common ulcer related emergency following bleeding [ 1 ].

Perforated peptic ulcer is a surgical emergency and is associated with short-term mortality in up to 30% of patients and morbidity in up to 50% [ 1 ]. Worldwide variations in demography, socioeconomic status, Helicobacter pylori prevalence, and prescription drugs make investigation into risk factors for perforated peptic ulcer difficult [ 2 ].

Peptic ulcer related morbidity and mortality decreased in the western world since the mid-twentieth century especially in the young but ulcer mortality in senior citizens has, none the less, remained essentially unchanged or even increased [ 3 ].

The situation is different in the developing part of the world like Ethiopia where perforated PUD remains to be one of the top causes of acute abdomen and emergency surgery. Recent publication from Ethiopia put perforated peptic ulcer disease to be 3rd most common cause of acute abdomen following appendicitis and intestinal obstruction. More over our patients are younger, males are affected much more than females and the vast majority of perforations are duodenal [ 4 , 5 ].

Most of the risk factors associated with perforation such as alcohol, smoking are well known but some may be related to local habits such as use of khat ( Catha edulis ), a stimulant leaf widely used in east Africa and Arabian peninsula and known for many gastrointestinal adverse effects [ 6 ].

Various techniques of closure (and their modifications) of the perforation were described such as simple closure, closure with vascularized omental pedicle (Cellon-Jones) and free omental plug (Graham’s). Putting a sub-hepatic drain after closure is being practiced in some centers like ours although its value is not substantiated [ 7 ].

The situation of the patient at presentation, delay at presentation and surgical intervention are now well known to be related to outcome of the patient [ 8 ].

Ethics approval and consent to participate

Ethical approval were gained from research and publication committee of department and approved by school of medicine in May 2018 reference number Dept. of surgery/SOM/61. Patients were counselled and written agreement obtained.

Patient selection

All consecutive patients operated for perforated peptic ulcer disease in the four teaching hospitals (Minilik hospital, Yekatit-12 hospital, Zewditu Memorial Hospital, Tikur Anbessa specialized hospital) affiliated to department of surgery of school of medicine from June 1, 2018 to May 31, 2019 are included in the study.

Patient management

All patients were initially resuscitated with crystalloids, nasogastric tube inserted, urinary bladder catheterized and metronidazole and 3rd generation cephalosporin often ceftriaxone started. Informed consent for emergency surgery obtained. Laparotomy done and the intra-abdominal situation assessed. The intra-peritoneal sucked out and a thorough lavage with warm saline done. Then the perforation were dealt with either free omental patch or a vascularized pedicled omental patch depending on the preference of operating surgeon.

Statistical analysis

Patient demography, possible risk factors, status at presentation, intra-operative findings, post-operative complications and final outcome were collected and filled in to a pre-prepared format. Patients were followed from admission to discharge or death. The data were collected by surgical residents and interns and checked by the authors.

Statistical analysis was performed using IBM-SPSS-version-25 statistical package. The mean standard deviation (SD), median and ranges were calculated for continuous variables whereas proportions and frequency tables were used to summarize categorical variables. Chi-square test was used to test for the significance of association between the independent (predictor) and dependent (outcome) variables in the categorical variables. The level of significance was considered as P < 0.05.

Patients’ background

During the study period 97 patients were operated. 84 (86.6%) were males and 13 (13.4%) were females with a male to female ratio of 6.5 to 1. Patients’ age ranged from 16 to 76, Mean age of 31.9, Median of 27. Only 15 (15.5%) came outside the city. 77.3% were orthodox Christians and 16.5% were Muslims. Regular alcohol use were reported by 44 (45.4%) and smoking in the third (33%) of all patients. Use of the local addictive stimulant khat ( Catha edulis ) were found in 17 (17.5%) of patients. Although 73 (75.3%) patients gave history of PUD the Helicobacter Pylori status of 90 (92.8%) were known at the time of presentation. Perforation occurred while fasting 13(13.4%) patients (Table  1 ).

Forty four (45.4%) presented within 24 h, 33 patients presented between 24 and 48 h after onset of abdominal pain. Abdominal pain were the presenting complaint in all patients and physical examination revealed generalized peritonitis in 85 (87.6%) patients. 17 (17.5%) had hypotension and raised WBC count were observed in 45 (46.4%). X-ray evidence of free peritoneal air were found in 83 of the 97 (85.6%) patients (Table  2 ).

Intraoperative finding and procedure done

The location of the perforation were in the first part of duodenum anteriorly in 91 (93.8%) and the size of the perforation was less than 10 mm in diameter in 79 (81.3%). Less than a liter of peritoneal GI content were found in 72 (74.2%) patients.

Repair with vascularized omental patch were performed in 65 (67.1%) and free omental patch in 28 (28.8%) patients (Table 2 and Table  3 ).

Postoperative outcome

Major complications such as surgical site infection, pneumonia, post-operative collection and patch failure were observed in 16 (16.5%) of the patients. 94 (96.6%) were discharged improved and 3 (3.1%) died. The majority (53 patients or 54.6%) were discharged within 7 days (Table  4 ).

Analysis in terms of morbidity and mortality of the possible risk factors showed higher age (> 40 years), longer duration at presentation (> 48 h), hypotension at presentation, higher degree of peritoneal contamination were significant risk factors (P < 0.05) (Table  5 ).

This study showed that male to female ratio of patients with perforated peptic ulcer disease is 6.5 to 1.0. This is similar the two studies done in hospitals here in Addis Ababa by Assefa Z and Ersemo T where the male to female ratio was reported to be 6.6: 1and 5.6:1.0 respectively. A study by Phillipo L Chalya et al. from Tanzania showed the male to female ratio of only 1.3 to 1 [ 9 , 10 ]. This difference in incidence do not seem to be the case in developed countries as a study by Thorsen K et al. on epidemiology of perforated peptic ulcer disease in Norway showed that females are affected more than males (that 89 of 172 of their patients were females) [ 11 ].

The mean age of patients in this study is just 31.9 and 42.3% of our patients were aged between 21 and 30 suggesting that our patients here in Ethiopia are much younger than most other reports. Two studies from Nigeria (one on Five-Year Review of Perforated Peptic Ulcer Disease in Irrua, Nigeria by A. E. Dongo et al. and another on Audit of Perforated Peptic Ulcer Disease in a Tropical Teaching Hospital) showed the pick age of their patients to be on 5th decade [ 12 , 13 ] and patients with PUD perforation in developed countries are even more older as seen by the study in Norway by Thorsen K et al. (68% of their patients were aged 60 years or older).

Similar to a previous study by Abebe B in Minilik II hospital, most of our patients (84.5%) came from the capital city Addis Ababa [ 14 ].

A regular use of alcohol and smoking were found in 45.4 and 33% of our patients respectively. A study in a tertiary hospital in Tanzania 85.7% use alcohol and 64.3% were smokers. A study from eastern India by Nishith M Paul Ekka and Shital Malua also reported 65.73% were known smokers while 42.86% patients were admittedly alcoholics [ 15 , 16 ].

Consumption of the stimulant leaf Khat (Catha edulis) which is wide spread in eastern Africa and Arabian Peninsula were found in nearly one in five of our patients (17.5%) with PUD perforation. This is much lower than the finding in a study on pattern and seasonal variation of PUD perforation in this city by Abebe B and his colleagues where 50.5% were found to be a regular consumer. Another study from Zewditu Memorial hospital by Assefa Z and G/eyesus A. showed 75% of their patients’ with PUD perforation use Khat. The use of this substance is associated with a number of gastrointestinal problems [ 9 , 14 ].

75.3% of our patients gave history of PUD and this is similar to reports from Tanzania where 69% had PUD history but the study in Irrua, Nigeria 59.6% had no history of peptic ulcer disease [ 17 ]

Unlike the studies in developed countries like Norway comorbidities and use of NSAID were found in only in 3.1 and 2.1% respectively in this study but a study in Ghana by J. C. B. Dakubo and his colleagues revealed a regular ingestion of NSAIDS in 47.7% patients and 18.2% had associated co-morbid conditions [ 18 ].

Among the seasons of the year perforation occurred more in the spring (March 1 to May 31) which happens to be the fasting months for both Orthodox Christian and Muslims in Ethiopia but only 13.4% were fasting when the perforation occurred. This has been reported to be the case in some studies [ 19 ].

Abdominal pain were the presenting complaint in all of our patients followed by vomiting and abdominal distension similar to finding Nigerian study by A. E. Dongo et al. Nearly half (45.4%) our patients came within 24 h of onset this is similar to the study in in Accra, Ghana but a study on presentation and management of Perforated Peptic Ulcer Disease in a Tertiary Centre In South Nigeria by Dodiyi-Manuel A et al. only 11.1% patients presented within 24 h of the onset of symptoms [ 17 , 20 ].

Generalized peritonitis were present on 85 of 97 patients (87.6%) in this study and this is similar to the study in eastern India where 97.8% of their patients had abdominal rigidity or guarding. The study from Tanzania also showed that abdominal tenderness and classical signs of peritonitis were demonstrable in 88.1 and 66.7% patients respectively [ 18 ].

In this study hypotension at presentation were observed in only 17 of 97(17.5%) patients but the Tanzanian study reported shock occurred in 33.3% of their patients. Leukocytosis were found in 45/97 our patients (46.4%) but 91.2% had leukocytosis in the Indian study [ 16 ].

Air under diaphragm was found in 83 of the 97(85.6%) patients in this study similar a clinical study of peptic ulcer perforation in eastern India where 82.41% patients showed radiological sign of gas under diaphragm [ 13 , 16 ].

The location of the perforation is first part of duodenum in 93.8% of our patients. This is similar to the study in Northwestern Tanzania where most perforations were located on the duodenum {92.9%), whereas in the remaining 7.1% patients had their ulcers located on the stomach. Reports from Norway, The Netherlands and Iceland showed gastric ulcer perforation predominate over duodenal perforations in that part world [ 21 ].

The size of the perforation is < 10 mm in diameter in 81.3% of our patients but this was not the finding in a study on Clinical profile and outcome of surgical treatment of perforated peptic ulcers in Northwestern Tanzania where thirteen (15.5%) of the perforations were of minimal size (≤5 mm) and sixty-four (76.2%) were massive (> 10 mm). Another study from in Irrua, Nigeria showed 49% of perforations had a diameter of < 10 mm [ 22 ].

Repair with pedicle omental patch was done in 67.1%, free Grahams omental patch in 28.8% and 4 (4.1%) were found to have a sealed perforation in this study. Graham’s Omentopexy was procedure of choice in Nigerian study accounting for 69.2%. Ibadan Nigeria Simple closure was performed in 25%, pedicled omental plug done in 60% and primary closure with an onlay omentum in 15% of the patients [ 18 , 20 ].

In this study significant morbidities (such as patch failure, pneumonia, SSI) occurred in 16 of 97 patients (16.5%) and this is acceptable and lower than most reports from Africa. We have three postoperative deaths making mortality rate 3.1% similar to SeungJin et al. where an overall 30-day mortality rate to be 3.17%.(The statistically significant factors associated with increased morbidity and mortality in this study with a P-value less than 0.05 were older age, hypotension at presentation, delay at presentation and perforation greater than 10 mm in diameter. In a paper that summarize the evidence for perforated peptic ulcer management and identify directions for future clinical research in the Lancet all of the above were described to significant factors for postoperative morbidity and mortality in patients with PUD perforation [ 8 , 23 ].

Perforation of peptic ulcer disease here occurs in the very young. Age, duration of presentation, hypotension at presentation, size of perforation, degree of peritoneal contamination were found to be the significant factors for morbidity and mortality. Morbidity and mortality rate of 16.5 and 3.1% observed here quite acceptable.

Availability of data and materials

The original data collected and compiled SPSS file is available with corresponding author.

Abbreviations

School of medicine

College of health sciences

Addis Ababa university

Gastrointestinal

  • Peptic ulcer disease

Addis Ababa

Vakil NB. In: Feldman M, editor. Epidemiology and etiology of peptic ulcer disease; 2018. Available from: Epidemiology and etiology of peptic ulcer disease - UpToDate.

Google Scholar  

Søreide K, Thorsen K, Harrison EM, Bingener J, Møller MH, Ohene-yeboah M, et al. Perforated peptic ulcer. Lancet. 2015;386:1288–98.

Article   Google Scholar  

Kang JY, Elders A, Majee AD, Ll JDM, Bardhan KD. Recent trends in hospital admissions and mortality rates for peptic ulcer in Scotland 1982–2002. Aliment Pharmacol Ther Recent trends Hosp admissions Mortal rates peptic ulcer Scotl 1982–2002 J Y KANG*, A ELDERS ,AMAJEEDà,J DMAXWELL* &K DBARDHAN§ *Department. 2006;24(1):65–79.

Gebresellassie HW, Tamerat G. Audit of surgical services in a teaching hospital in Addis Ababa , Ethiopia. BMC Res Notes. 20191–5. Available from. https://doi.org/10.1186/s13104-019-4709-y .

Tamrat G, Osman M, Deyessa N, Taye M, Lett R, Bekele A. Delay of emergency surgical interventions in Ethiopia : patient and health system factors. East Cent Afr J Surg. 2018;23(2):59–65.

Abdelwahab SI, Alsanosy RM, Rahim BE, et al. Khat (Catha edulis Forsk.) Dependence potential and pattern of use in Saudi Arabia. Biomed Res Int. 2015;2015:604526. https://doi.org/10.1155/2015/604526 .

Odula PO. Omentoplasty in perforated peptic ulcer surgery : is it still the gold standard ? Ann Afr Surg. 2017;14(2):57–60.

Bae S, Shim K, Kim N, Kang JM, Kim D, Kim K, et al. Incidence and short-term mortality from perforated peptic ulcer in Korea : a population-based study. J Epidemiol. 2012;22(6):508–16.

Assefa Zelalem GA. Perforated peptic ulcer disease in Zewditu hospital. EMJ. 2012;50(2):145–51.

Ersumo T, Ali A, Kotiso B. Complicated peptic ulcer disease in Tikur Anbessa Hospital, Addis Ababa. Ethiop Med J. 2004;42(2):87–95.

Thorsen K, Søreide JA, Kvaløy JT, Glomsaker T, Søreide K, Thorsen K, et al. Epidemiology of perforated peptic ulcer : age- and gender- adjusted analysis of incidence and mortality. World J Gastroenterol. 2013;19(3):347–54.

Dongo AE, Uhunmwagho O, Kesieme EB, Eluehike SU, Alufohai EF. A five-year review of perforated peptic ulcer disease in Irrua, Nigeria. Int Sch Res Not F 18% M. 2017;2017Available from. https://doi.org/10.1155/2017/8375398 .

Afuwape O, Irabor DO, Ayandipo O. An audit of perforated peptic ulcer disease in a tropical teaching hospital. East Cent Afr J surg An. 2013;18(December):40–4.

Bekele A, Zemenfes D, Kassa S, Deneke A, Taye M, Wondimu S. Patterns and seasonal variations of perforated peptic ulcer disease : experience from Ethiopia. Ann AFRICAN Surg. 2017;14(2).

Chalya PL, Mabula JB, Koy M, Mchembe MD, Jaka HM, Kabangila R, et al. Clinical profile and outcome of surgical treatment of perforated peptic ulcers in northwestern Tanzania : a tertiary hospital experience. World J Emerg Surg [Internet]. 2011;6(31):1–10 Available from: http://www.wjes.org/content/6/1/31 .

Ekka NMP, Malua S. Clinical study of peptic ulcer perforation in eastern India : an tertiary institution-based study. Int J Med Sci Public Heal. 2016;5(12):2540–4.

Pn W, Vc E. Presentation and management of perforated peptic ulcer disease in a tertiary Centre in south South Nigeria presentation et gestion des ulcère gastroduodénal dans un Centre supérieur au Sud du Sud Nigeria. J West African Coll Surg. 2015;5(3).

Wegdam HHJ, Hillah AA. Modified open omental plugging of peptic ulcer perforation in a municipal Hospital in Ghana. Postgrad Med J Ghan. 2013;2(1):20–3.

Agbonrofo PII rowa Ooo AL. Clinics in surgery seasonal variation of gastro - duodenal perforation in. Clin Surg. 2018;3:10–3.

Ugochukwu AI, Amu OC, Nzegwu MA, Dilibe UC. Acute perforated peptic ulcer : on clinical experience in an urban tertiary hospital in south East Nigeria acute perforated peptic ulcer : on clinical experience in an urban tertiary hospital in south East Nigeria. IJSU. 2013;11(3):223–7Available from:. https://doi.org/10.1016/j.ijsu.2013.01.015 .

Article   CAS   Google Scholar  

Thorsen K, Søreide JA, Søreide K. What is the best predictor of mortality in perforated peptic ulcer disease ? A population-based , multivariable regression analysis including three clinical scoring systems. J Gastrointest Surg. 2014;18:1261–8.

Gona. SKKA. Postoperative morbidity and mortality of perforated peptic ulcer: retrospective cohort. Gastroenterol Res Pract. 2016;2016Available from. https://doi.org/10.1155/2016/2640730 .

Rickard J. Surgery for peptic ulcer disease in sub- Saharan Africa : systematic review of. J Gastrointest Surg. 2016;20(4):840–50.

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Acknowledgements

We would like to thank residents, interns, nurses of the four hospitals for helping out in collecting data. We are also grateful to staff and head of surgery department for the support they provided in preparation and undertaking of the research.

It was partially funded by school of medicine, college of health sciences, Addis Ababa University.

The school of medicine, college of health sciences of AAU covered the cost of collecting data and stationers required. Approved the design of the study but did not take part in analysis, interpretation and writing the manuscript.

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Jatani Arero Bupicha, Hailu Wondimu Gebresellassie & Abebe Alemayehu

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All authors have approved the final version of the manuscript. HWG took part in research proposal preparation, collection, analysis and writing of manuscript of data. JAB wrote the proposal, collected data, participate in analysis as well as writing the manuscript. AA took part in data analysis and in writing of the manuscript.

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Correspondence to Hailu Wondimu Gebresellassie .

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Ethical approval were obtained from the department of surgery’s research and publication committee as well as the school of medicine of CHS of AAU in a letter dated April 12, 2018. Written consent to participate were obtained from each patient.

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Bupicha, J.A., Gebresellassie, H.W. & Alemayehu, A. Pattern and outcome of perforated peptic ulcer disease patient in four teaching hospitals in Addis Ababa, Ethiopia: a prospective cohort multicenter study. BMC Surg 20 , 135 (2020). https://doi.org/10.1186/s12893-020-00796-7

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Case Studies (January 2016)

  • Craig I. Coleman, PharmD

What should these pharmacists do?

A young mother comes to your pharmacy with her 3-yearold son, DT, who has been rubbing and tugging at his right ear and appears to be in discomfort. His physician gave him a diagnosis of acute otitis media. DT’s mother presents you with a prescription for amoxicillin 600 mg oral suspension twice daily for 7 days. While viewing DT’s patient profile, you notice that he has an allergy to penicillin. When you question the nature of his allergy, the mother describes a severe case of hives that resulted in an emergency department visit. DT is otherwise healthy, with no other known drug allergies.

As the pharmacist, would you fill DT’s prescription for amoxicillin? What else could you recommend?

KM, a 40-year-old man, comes to your pharmacy having been given a diagnosis of Helicobacter pylori -induced peptic ulcer disease. He hands you prescriptions for azithromycin 250 mg twice daily, amoxicillin 1000 mg twice daily, and omeprazole 20 mg twice daily, each to be taken for 10 days, followed by an additional 18 days of omeprazole 20 mg. He has no comorbid conditions or known drug allergies.

As the pharmacist, is this an appropriate drug regimen? If not, what changes would you recommend?

Case 1: Acute otitis media (AOM) is a very common infection of the middle ear, especially in young children. According to guidelines from the American Academy of Pediatrics (AAP), first-line antibiotic treatment for AOM is high-dose amoxicillin (80-90 mg/kg/d in 2 divided doses; a 7-day course for children aged 2 to 5 years). However, in the case of a hypersensitivity reaction to penicillin, the preferred alternative therapeutic options are certain second- and third-generation oral cephalosporins, which have been identified as highly unlikely to be associated with cross-reactivity with penicillin allergy. The 3 oral medications designated for this purpose by the AAP guidelines are cefdinir (14 mg/kg/day in 1 or 2 doses), cefuroxime (30 mg/kg/day in 2 divided doses), and cefpodoxime (10 mg/kg/day in 2 divided doses); the usual course of therapy is 7 to 10 days for medications. The pharmacist should call DT’s pediatrician and recommend a change of antibiotic to one of the 3 noted above. DT’s mother should also be reminded to shake the bottle well before measuring.

Case 2: Peptic ulcer disease (PUD) has 3 main etiologies: the use of nonsteroidal antiinflammatory drugs, the presence of H pylori, and stress. Each has its own distinct set of pharmacologic and nonpharmacologic therapies. In the case of KM’s H pylorirelated PUD, the guidelines established by the American College of Gastroenterology recommend a proton pump inhibitor (PPI)-based triple drug regimen. This regimen includes a standard dose of a PPI twice daily (esomeprazole is the exception and should only be dosed once daily), clarithromycin 500 mg twice daily, and amoxicillin 1000 mg twice daily—all for 10 to 14 days. If an active ulcer exists at the initiation of therapy, an additional 18 days of once-daily PPI use is recommended. In the case of KM, the prescriber substituted azithromycin, a different macrolide antibiotic, for clarithromycin. The guidelines clearly state that azithromycin and erythromycin should not be substituted for clarithromycin, as evidence shows that clarithromycin is the most effective antibiotic in the treatment of PUD. KM’s prescriber should be contacted to change the azithromycin to clarithromycin. If KM had a penicillin allergy on file, metronidazole 500 mg twice daily would be substituted for amoxicillin. Recommend to KM that he take the omeprazole 1 hour before meals to improve efficacy and to take both antibiotics with meals to prevent nausea and dyspepsia.

Read the answers

Mr. McGrath is a PharmD candidate from the University of Saint Joseph School of Pharmacy, Hartford, Connecticut. Dr. Kohn is an assistant professor at the University of Saint Joseph School of Pharmacy. Dr. Coleman is professor of pharmacy practice, as well as codirector and methods chief, at Hartford Hospital Evidence-Based Practice Center at the University of Connecticut School of Pharmacy.

function showAnswer() {document.getElementById("answer").style.display = 'block';document.getElementById("link").style.display = 'none';}

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case study for peptic ulcer

Describe the functions of the following components of gastric juice.

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PEPTIC ULCER DISEASE PATHOPHYSIOLOGY-A Case Study

Profile image of Jazelle  Rivera

Peptic Ulcer Disease (PUD) is a term used to describe a group of ulcerative disorders that occurs in areas of the gastrointestinal tract that are exposed to acid-pepsin secretion. It is also described as a break, or ulceration, in the protective mucosal lining of the lower esophagus, stomach, or duodenum. PUD develops when there is an imbalance between mucosal protective factors and the erosive factors.

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Ulcerations (sores) in the lining of upper part of the digestive tract are known as Peptic Ulcers. The ulcers may exist in the lower part of food pipe (esophagus), in the stomach or in the initial part of the intestine (duodenum). About 10% of all adults are affected with Peptic ulcers at some time in their life. The incidence of Peptic ulcers is more common in males as compared to females.

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The term peptic ulcer distinguishes this condition from other ulcerative diseases that affect other parts of the body. Peptic ulcer refers to erosions of the stomach and duodenum. The disease is characterized by damage to the mucous membrane of the stomach, sometimes to the stomach muscle itself or to the duodenum, which causes open wounds. Mucous membranes are usually swollen and irritated. Peptic ulcer occurs when the wall of these organs is eroded by the aggressive action of gastric juice. Decomposition of one's own mucosa occurs as a result of a disturbed balance of aggressive factors that normally exist in the stomach and are used for food digestion and mucosal defense factors.

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Peptic ulcer is erosion in lining of digestive tract, typically occurs in lower esophagus, stomach and proximal duodenum. Major forms are gastric ulcer and duodenal ulcer, caused by digestive action of stomach acid and pepsin. Causative agents mainly are infection caused by Helicobacter pylori (H. pylori) or an excessive use of non-steroidal anti-inflammatory agents (NSAIDs). Symptoms include epigastric pain that often cause awakening of patient at night, heartburn, loss of an appetite, w

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SAHAR M HAKAMI

ABSRACT A peptic ulcer is a sore on the lining of the stomach or duodenum. The two most common types of peptic ulcer are called " gastric ulcers " and " duodenal ulcers ". Peptic ulcers are found to be due to an imbalance between aggressive factors such as hydrochloric acid (HCL), pepsin, refluxed bile, leukotrienes (LTs), reactive oxygen species (ROS) and defensive factors, which include the function of the mucus-bicarbonate barrier, prostaglandins (PGs), mucosal blood flow, cell renewal and migration, no enzymatic and enzymatic antioxidants and some growth factors. H. pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the predominant causes of peptic ulcer disease. Also, a numbers of factors are implicated in the pathogenesis of gastric ulcer, among which major factors involved are bacterial infection (Helicobacter pylori), certain medications (NSAID), chemicals (Hcl/ethanol) ,gastric cancer and minor factors are stress, smoking, spicy food and nutritional deficiencies. The idea behind treating ulcers is to lower the amount of acid that your stomach makes, to neutralize the acid that is made and to protect the injured area so it can have time to heal. The main aim of this review article has to summarize the ulcerogenic mechanisms of various mediators involved in Peptic ulcer disease.

PEPTIC ULCER OF THE STOMACH AND DUODENU

HAMED ELYAMANY

It is necessary to distinguish between peptic ulcer and symptomatic ulcers. The latter include ulcerations of the gastroduodenal mucosa, which occur in various diseases and conditions. These are ulcers in endocrine pathology (adenoma of the parathyroid glands, Zollinger-Ellison syndrome), stress, acute or chronic circulatory disorders, allergies, and taking non-steroidal anti-inflammatory drugs.

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  • v.4(7); 2012 Jul 16

A study of the changes in the cause of peptic ulcer bleeding

Correspondence to: Haruka Fujinami, MD, Assistant Professor of Medicine, Department of Gastroenterology, University of Toyama, 2630 Sugitani, Toyama 9300194, Japan. pj.ca.amayot-u.dem@25akurah

Telephone: +81-76-4347301 Fax: +81-76-4345027

AIM: To clarify the frequency of and changes in the cause of peptic ulcer bleeding.

METHODS: This study retrospectively evaluated the out- and inpatients who underwent endoscopy between 2002 to 2008. The subjects were patients presenting with peptic ulcer bleeding. The details of these patients were obtained from their endoscopic reports and medical records.

RESULTS: The rates of Helicobacter pylori (H. pylori) infection were significantly low ( P = 0.039), while the proportion of nonsteroidal antiinflammatory drugs (NSAIDs) users and vascular disease significantly increased over the period studied ( P = 0.034 and P = 0.04, respectively). However, there was no significant difference in the proportion of low-dose aspirin users ( P = 0.832).

CONCLUSION: It’s found that the primary cause of peptic ulcer bleeding changed from H. pylori infection to use of NSAIDs over the 7-year period of study. It seems that the number of low-dose aspirin users has increased with the increase in the proportion of vascular disease. It is necessary to take measures to prevent peptic ulcer bleeding among NSAIDs and low dose aspirin users.

INTRODUCTION

Helicobacter pylori ( H. pylori ) infection and the use of nonsteroidal antiinflammatory drugs (NSAIDs) are two of the major risk factors for peptic ulcers and ulcer complications[ 1 ]. H. pylori infection has been recognized in more than 87% of patients with gastric ulcers and about 96% of patients with duodenal ulcers[ 2 ]. The incidence of peptic ulcers has steadily decreased in Western countries, and this decrease is thought to result from both the widespread eradication of H. pylori and the decreasing prevalence of H. pylori infection in the population as a result of the improvement in hygienic conditions[ 3 , 4 ]. On the other hand, the use of NSAIDs is associated with an increased risk of major upper gastrointestinal complications, including bleeding and perforation[ 5 - 7 ]. With the increase in the elderly population, which has led to an increase in musculoskeletal and joint disorders, it seems that the consumption of NSAIDs has increased. In addition, antiplatelet therapy with low-dose aspirin (75-325 mg) reduces the risk of vascular events in patients with cardiovascular and cerebrovascular diseases[ 8 - 10 ]. Although low-dose aspirin has the advantages of being both highly effective and inexpensive, they pose a significant risk for developing peptic ulcer bleeding[ 11 - 13 ]. The aim of this study is to clarify the frequency and trends of peptic ulcer bleeding over the past seven years.

MATERIALS AND METHODS

This study retrospectively evaluated the 199 994 of out- and inpatients who underwent endoscopy at ToyamaUniversityHospital between January 2002 and December 2008. We collected the following details of patients with peptic ulcer bleeding from their endoscopic reports and medical records: age, gender, symptoms, H. pylori infection, NSAIDs intake, low-dose aspirin intake, previous ulcer history, cardiovascular and cerebrovascular diseases, endoscopic findings, and interventions. The rate of gastroduodenal ulcer (GDU) and peptic ulcer bleeding, average age, body proportions, hematemesis, melena, and previous ulcer histories, rate of H. pylori infection, rate of cardiovascular and cerebrovascular diseases and proportion of NSAIDs and low-dose aspirin users were calculated and compared from 2002 to 2008 based on this information. The subjects were checked for H. pylori infection using the 13 C-urea breath test (UBT) and/or rapid urease test (RUT). H. pylori status was defined as H. pylori -negative when UBT was negative and H. pylori -positive when either UBT or RUT were positive. Peptic ulcer bleeding was defined as a clinical presentation of hematemesis and/or melena, and endoscopic examination showed a peptic gastric and/or duodenal ulcer. However, we also anticipated the presence of upper gastrointestinal tract neoplasm, erosive gastritis, erosive duodenitis, Mallory-Weiss syndrome, and esophagogastricvarices.

Statistical analysis

The following details of peptic ulcer bleeding patients were obtained from their endoscopic reports and medical records: age, gender, symptoms, H. pylori status, NSAIDs intake, low-dose aspirin intake, previous ulcer history, endoscopic findings, and interventions. The rate of peptic ulcer and/or peptic ulcer bleeding, average age, body proportions, hematemesis, melena, previous ulcer histories, rate of H. pylori infection, rate of cardiovascular and cerebrovascular diseases and rate of NSAIDs, low-dose aspirin users were calculated and compared from 2002 to 2008 based on this information.

Changes in each parameter over the period studied were analyzed using the chi-square test. Differences were considered to be statistically significant when P < 0.05.

The details of subjects were showed in Table ​ Table1. 1 . The rate of GDU decreased from 16.9% to 11.3% over the period studied, and there were significant changes ( P < 0.001). The rate of peptic ulcer bleeding significantly increased from 4.87% to 9.03% during the first three years ( P < 0.001) and significantly decreased from 9.03% to 5.95% during the last three years ( P < 0.05). The clinical details of those patients who presented withpeptic ulcer bleeding are shown in Table ​ Table2. 2 . Age and gender did not change significantly over the period studied. The rate of GDU decreased. Cardiovascular and cerebrovascular diseases significantly increased from 29.2% to 61.9% over the period studied ( P = 0.04). The risk factors of peptic ulcer bleeding are shown in Table ​ Table3. 3 . H. pylori infection rate was 84.2% in 2002, 72.6% in 2005, and 71.4% in 2008, which demonstrates a significant decrease ( P = 0.048). The greatest cause of peptic ulcer bleeding was the use of gastrointestinal injury drugs, such as NSAIDs and low-dose aspirin. The proportion of NSAIDs users significantly increased ( P = 0.034), but the there were no significant changes in the proportion of low-dose aspirin users ( P = 0.832). The proportion of NSAIDs (including low-dose aspirin) users significantly increased over the period studied ( P = 0.021).

The incidence of peptic ulcer bleeding

The rate of GDU significantly decreased during the period studied ( P < 0.001). The rate of peptic ulcer bleeding significantly increased during the first three years and significantly decreased during the last three years.GDU: Gastroduodenal ulcer.

Clinical characteristics of patients with peptic ulcer bleeding

Clinical characteristics of patients with peptic ulcer bleeding. There was significantly increased in vascular disease over the period studied.

Risk factors of peptic ulcer bleeding

The H. pylori infection rate significantly decreased. On the other hand, the proportion of NSAIDs users was significantly increased. The proportion of low-dose aspirin users demonstrated no significant changes. NSAIDs:Non-steroidal anti-inflammatory drugs.

In this study, it was found that the number of peptic ulcer bleeding cases significantly increased during the first three years. One explanation for this is that while the H. pylori infection rate decreased over this period, the main cause of peptic ulcer bleeding changed from H. pylori infection to use of NSAIDs, including low-dose aspirin. NSAIDs were associated with approximately 30% of the bleeding peptic ulcers diagnosed in Japan, which shows a significant increase from the figures of previous reports. One reason of the increased number of NSAIDs users is that it is used in treating back and joint pain, which has shown an increased incidence among the increasing elderly population[ 14 , 15 ]. In the Unitd States, hospitalization and death due to NSAID-related gastrointestinal events have been estimated at 103 000 and 16 500 patients per year, respectively[ 16 ]. In a population-based retrospective case-control study, the adjusted relative risk (RR) of upper gastrointestinal bleeding (UGIB) associated with NSAIDs use was 5.3 [95% confidence interval (CI): 4.5-6.2][ 17 ]. In our study, NSAIDs use was significantly associated with an increased risk of bleeding ulcer, and the rate of H. pylori infection was significantly lower throughout the observed period. Nonetheless, the number of peptic ulcer bleeding was decreased during the last three years. As one of the possibilities, a study of the Swedish population from 1974-2002 was reported that the increasing the amount of proton pomp inhibiter (PPI) has reduced the incidence of peptic ulcer complications[ 18 ]. In fact that gastroesophageal reflux disease is increasing and the usage of PPI is actually increasing in Japan[ 19 ].

Low-dose aspirin is also one of the causes of drug-induced peptic ulcer bleeding. It is widely used because it reduces the risk of cardiovascular events and death in patients with coronary and cerebrovascular diseases. It seems likely that the number of low-dose aspirin users will increase in the future because coronary and cerebrovascular diseases have increased in recent years. However, the use of aspirin, even at a low dose for secondary prevention of cardiovascular events, remains a risk factor for developing UGIB. In addition, more than a few epidemiological studies have suggested that H. pylori infection increases the risk of UGIB in patients taking low-dose aspirin[ 20 , 21 ]. Taha et al. reported that the increase in UGIB associated with the use of gastrointestinal toxic drugs increased in subjects treated with low-dose aspirin between 1996 and 2002[ 22 ]. A recent study indicates that the relative risk of UGIB after exposure to low-dose aspirin is 3.7 (95% CI: 3.0-4.5)[ 17 ]. In our study, we found that the proportion of low-dose aspirin users also increased from 8.3% in 2002 to 14.3% in 2008. In addition, our data showed the significant increasing of cardiovascular and cerebrovascular diseases. Therefore, the proportion of low-dose aspirin users will be increased in future. Recently it was suggested that the damaging effect of aspirin alone on the gastric mucosa might be less potent than the effect of NSAIDs[ 23 ]. In a case-control study by Hallas et al., the age- and sex-adjusted odds ratios associating drug use with UGIB were 1.8 (1.5-2.1) for low-dose aspirin, 1.1 (0.6-2.1) for clopidogrel, 1.9 (1.3-2.8) for dipyridamole, 1.8 (1.3-2.4) for vitamin K antagonists, 7.4 (3.5-15) for clopidogrel and aspirin, 5.3 (2.9-9.5) for vitamin K antagonists and aspirin, and 2.3 (1.7-3.3) for dipyridamole and aspirin. These results suggest that combined antithrombotic therapy with low-dose aspirin is associated with an increased risk of UGIB[ 24 ]. We also found that the proportion of NSAIDs and low-dose aspirin users was significantly increasing over the period studied. The odds ratio of a combination of NSAIDs and low-dose aspirin was reported as 12.7 (95% CI: 7.0-23.0). Furthermore, the concurrent use of non-aspirin antiplatelet agents with traditional NSAIDs also potentiated the risk of UGIB[ 17 ]. In a meta-analysis of randomized, placebo-controlled trials of low-dose aspirin, prior gastrointestinal events, older age, and the use of other injurious medications, such as NSAIDs, anticoagulants, and corticosteroids seemed to be factors associated with an increased risk for UGIB[ 25 ].

In the future, it will be necessary to prevent the association between UGIB and the use of NSAIDs and low-dose aspirin because it is expected that the more the proportion of the elderly population increases, the more coexisting diseases, such as cardiovascular disease, cerebrovascular disease, and musculoskeletal disorders will increase. The use of both NSAIDs for the treatment of musculoskeletal pain and low-dose aspirin as an antithrombotic therapy has increased recently. This tendency has been deduced from our data, which reveals that cardiovascular and cerebrovascular diseases have increased from 2002 to 2008. In addition, it is useful to note that few patients complained of epigastric symptoms in our study. In fact, most NSAIDs-associated GDU are asymptomatic[ 26 , 27 ]. In low-dose aspirin users, there were no significant differences between the ulcer and non-ulcer groups in the frequency and severity of symptoms, such as nausea, acid regurgitation, and heartburn[ 28 ]. Moreover, there were more patients without symptoms than with abdominal pain among NSAIDs users, since NSAIDs have an analgesic effect. On the contrary, peptic ulcers treated with NSAIDs and low-dose aspirin develop suddenly by hematemesis and melena. In fact, those patients taking NSAIDs and low-dose aspirin became serious cases because they had a coexisting disease, such as cardiovascular or cerebrovascular disease.

The prevention of peptic ulcers related to the use of NSAIDs and/or low-dose aspirin will become an important issue in the future. It is suggested that those patients who need NSAIDs treatment use the prostaglandin analogue misoprostol[ 29 ] or acid-suppressive agents, such as high-dose H 2 receptor antagonists[ 30 ] and PPI[ 31 ]. Switching from non-selective NSAIDs to cyclooxygenase-2 inhibitors[ 32 ] is also a choice. In the prevention of ulcers caused by NSAIDs and/or low-dose aspirin, the effectiveness of H. pylori eradication therapy has been reported[ 33 ]. In naive NSAIDs users, it has been suggested to receive H. pylori eradication therapy before NSAIDs use. A similar strategy has also been suggested for naive aspirin users[ 34 ]. In chronic NSAIDs/aspirin users, the recommendations may depend on the risk for peptic ulcer complications. Those who continue taking NSAIDs/aspirin, being at high-risk for peptic ulcer complication, should be tested for the presence of H. pylori infection and, if positive, receive H. pylori eradication therapy, as well as long-term therapy with a PPI[ 35 - 37 ].

Where the elderly population is increasing, it seems likely that the consumption of NSAIDs and low-dose aspirin will also increase in the future. Therefore, it is necessary to make guidelines for the use of NSAIDs and low-dose aspirin with the cooperation of gastroenterologists, neurologists, cardiologists, and orthopedic surgeons.

Helicobacter pylori ( H. pylori ) infection and non-steroidal anti-inflammatory drugs (NSAIDs) including low dose aspirin are two of the major risk factors for peptic ulcers. With the increase in the elderly population, which has led to an increase in musculoskeletal and joint disorders, ischemic heart disease and cerebrovascular disease, it seems that the incidence of NSAID-related peptic ulcer has increased. The aim of this study is to clarify the frequency and trends of peptic ulcer bleeding over the studied period.

Research frontiers

In Western countries, H. pylori infection rate is low and the cause of peptic ulcer was NSAIDs. Since the same tendency was recognized in Japan, it is necessary to investigate about changes in the cause of peptic ulcer.

Innovations and breakthroughs

In this study, it was found that the number of peptic ulcer bleeding case was increased and H. pylori infection rate was decreased over the studied period, the main cause of peptic ulcer bleeding changed from H. pylori infection to use of NSAIDs, including low-dose aspirin.

Applications

In fact that gastroesophageal reflux disease is increasing and the usage of proton pump inhibitors (PPI) is actually increasing in Japan. The results suggest that peptic ulcer will be decreased in the future.

Terminology

Peptic ulcer bleeding: Defined as a clinical presentation of hematemesis and/or melena, and endoscopic examination showed a peptic gastric and/or duodenal ulcer bleeding.

Peer review

This paper describes the rate of peptic ulcer bleeding and the change in the causes of that. Although H. pylori infection and the use of NSAIDs were adopted as a risk factor, it was indicated that other factors (i.e., corticosteroid, warfarin and clopidogrel) should also have been examined. Though we find that frequency on gastrointestinal bleeding has been subsequently decreasing recent years, it was reported that the increase in the usage of PPI is related. To investigate the cause by which the peptic ulcer bleeding is decreased will be desired from now on.

Peer reviewers: José Luiz Sebba Souza, MD, Clinics Hospital, University of São Paulo, 255 Eneas de Carvalho Ave. 9 th Floor, Room 9159, São Paulo, Brazil; Michal Procke, MD, Department of Internal Medicine-Gastroenterology and Endoscopy, Charles University, 2nd Medical School, Motol University Hospital, Prague, Czech Republic

S- Editor Yang XC L- Editor A E- Editor Yang XC

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Pathophysiology and clinical presentation – correct diagnosis

Normal physiology of the peptic tissues and mechanisms

The peptic tissue includes two major layers (mucous barrier & surface mucous cells) and utilizes numerous gastric mucosal mechanisms to safely contain the digestive gastric acid.

  • secrete a protective, gel-like mucus layer to protects gastric mucosa against autodigestion from pepsin and erosion by acids and other caustic materials from ingestion.
  • secrete bicarbonate ions to neutralize acids from the lumen
  • form tight junctions to repel harsh fluid that may injure the stomach lining
  • retrieves excess hydrogen ions back-diffused into the mucosa from the lumen and transport bicarbonate to mucosa
  • sustains high cellular metabolic and regenerative activity
  • promotes secretion of bicarbonate
  • promote production of gel mucous barrier
  • maintain mucosal blood flow (vasodilator)

case study for peptic ulcer

Figure 1. Cross section of peptic tissue (Glyn, 2018)

Pathophysiology

Breakage or ulceration of the protective mucosal lining in the lower esophagus, stomach (i.e., gastric ulcers), and duodenum (i.e., duodenal ulcers; most common).

case study for peptic ulcer

Figure 2. (A) Endoscopic and (B) histologic cross section views of peptic ulcer (Pathology for health Professionals 4th. edition, 2013)

Underlying causes

  • Inhibition of prostaglandin synthesis by aspirin and NSAIDs — decrease in protective mucus production, decrease in bicarbonate secretion (decrease in buffering capacity).

case study for peptic ulcer

  • Stress-Related factors secondary to serious illness or ischemic conditions, such as multiple system organ failure, head trauma, and severe burn, resulting in multiple ulceration or ischemia in the stomach and/or duodenum.

Risk factors

H. pylori , habitual use of aspirin and/or NSAIDs, alcohol, smoking, chronic obstructive pulmonary disease, and acute pancreatitis.

Key criteria for diagnosis

  • Epigastric pain – burning sensation occurs after meals (gastric ulcers), 2-3 hours after meal or in the middle of night (duodenal ulcers) due to sensorineural stimulation by acid or muscle spasm. Duodenal pain could be immediately relieved by ingestion of food or NSAIDs.
  • Habitual use of aspirin and/or NSAIDs.
  • Presence of  pylori.
  • Bleeding — more often seen in stress-related mucosal diseases with coagulopathy or mechanical ventilation.

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  1. Patient Case Presentation

    Height: 167 cm Weight: 58.2 kg Past medical history Gastritis with Helicobacter pylori (H. pylori) infection, diagnosed 5 years ago. Resolved with pharmacotherapy, frequent recurrence. Heart attack 3 months ago, has started taking aspirin since then. Osteoarthritis, diagnosed 3 years ago.

  2. Evidence-based clinical practice guidelines for peptic ulcer disease

    Therapeutic algorithms for the treatment of peptic ulcers differ based on ulcer complications. In patients with NSAID-induced ulcers, NSAIDs are discontinued and anti-ulcer therapy is administered. If NSAIDs cannot be discontinued, the ulcer is treated with proton pump inhibitors (PPIs).

  3. Case Study: Peptic Ulcer

    A peptic ulcer is a sore that occurs in the lining of a part of the gastrointestinal tract that is exposed to pepsin and acid secretions. Most peptic ulcers occur in the lining of the stomach or duodenum. 90% of all duodenal ulcers and 80% of all gastric ulcers are caused by H. pylori infection.

  4. Peptic Ulcer Disease Case Study (60 min)

    Start Free Trial Outline Mrs. Baker is a 54 year old female who presented to the ED complaining of nausea and severe epigastric pain x 3 days. She reports a history of osteoarthritis and reports taking ibuprofen 400 mg 3-4 times a day regularly for the last few months since her "arthritis has gotten really bad". Critical Thinking Check

  5. Peptic Ulcer Case Study

    Stephine Burrows Yichun Lin Our rationale for choosing this condition We chose Peptic Ulcer disease due to the fact that it's commonly seen among the patients taking NSAIDs and Aspirin; therefore, we anticipate seeing this condition frequently.

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    Case report. June 23, 2022. Current concepts in clinical therapeutics: peptic ulcer disease. Etiopathogenetic principles and peptic ulcer disease classification. Diagnosis and treatment of gastrinoma in the era of proton pump inhibitors. 8600 Rockville Pike HHS Vulnerability Disclosure

  7. Nutritional care in peptic ulcer

    Prospective and retrospective studies show higher mortality from peptic ulcer in smokers when compared to nonsmokers. Researches show that, among other tobacco constituents, nicotine accounts for most of the peptic ulcer development, because it has a harmful effect on the protective mucus of the gastric epithelium, altering bicarbonate 30 .

  8. Management of Acute Bleeding from a Peptic Ulcer

    Paimela H, Oksala NK, Kivilaakso E. Surgery for peptic ulcer today: a study on the incidence, methods and mortality in surgery for peptic ulcer in Finland between 1987 and 1999. Dig Surg 2004 ;21: ...

  9. Pattern and outcome of perforated peptic ulcer disease patient in four

    Perforated peptic ulcer disease is a surgical emergency with a high morbidity and mortality. The socio-demographic characteristic and the factors associated with morbidity and mortality seems to differ between the developed and developing world. This is the first a prospective cohort study in Ethiopia designed to analyze pattern and outcome of patients with perforated peptic ulcer disease in ...

  10. Case Report: Atypical presentation of perforated peptic ulcer disease

    In a recent multicentre European study, the prevalence of peptic ulceration was 8.1% in children presenting with abdominal pain, the majority of patients being males in the second decade of life. 1 Helicobacter pylori infection and non-steroidal anti-inflammatory drug ingestion are the main aetiological risk factors in the paediatric age. 2 The ...

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    Peptic ulcer disease can involve the stomach or duodenum. Gastric and duodenal ulcers usually cannot be differentiated based on history alone, although some findings may be suggestive (see DDx).Epigastric pain is the most common symptom of both gastric and duodenal ulcers, characterized by a gnawing or burning sensation and that occurs after meals—classically, shortly after meals with ...

  12. A Case of Peptic Ulcer Disease: Healing the Digestive Tract with

    Rosenstock S, Jorgensen T, Bonnevie O, Andersen L. Risk factors for peptic ulcer disease: a population based prospective cohort study comprising 2416 Danish adults. Gut. 2003;52(2):186-193. Kurata JH, Nogawa AN. Meta-analysis of risk factors for peptic ulcer. Non steroidal anti inflammatory drugs, Helicobacter pylori, and smoking.

  13. Case Studies (January 2016)

    CASE 2 . KM, a 40-year-old man, comes to your pharmacy having been given a diagnosis of Helicobacter pylori-induced peptic ulcer disease. He hands you prescriptions for azithromycin 250 mg twice daily, amoxicillin 1000 mg twice daily, and omeprazole 20 mg twice daily, each to be taken for 10 days, followed by an additional 18 days of omeprazole ...

  14. Essentials of Anatomy & Physiology

    Case Background. A peptic ulcer is a sore that occurs in the lining of a part of the gastrointestinal tract that is exposed to pepsin and acid secretions. Most peptic ulcers occur in the lining of the stomach or duodenum. 90% of all duodenal ulcers and 80% of all gastric ulcers are caused by H. pylori infection.

  15. PEPTIC ULCER DISEASE PATHOPHYSIOLOGY-A Case Study

    PEPTIC ULCER DISEASE PATHOPHYSIOLOGY-A Case Study. Jazelle Rivera. Peptic Ulcer Disease (PUD) is a term used to describe a group of ulcerative disorders that occurs in areas of the gastrointestinal tract that are exposed to acid-pepsin secretion. It is also described as a break, or ulceration, in the protective mucosal lining of the lower ...

  16. CASE STUDY IN GASTROENTEROLOGY & HEPATOLOGY: An Uncommon Complication

    CASE STUDY IN GASTROENTEROLOGY & HEPATOLOGY: An Uncommon Complication of Peptic Ulcer Disease - PMC Journal List Gastroenterol Hepatol (N Y) v.10 (5); 2014 May PMC4076883 As a library, NLM provides access to scientific literature.

  17. GI Case Study Questions: Peptic Ulcer H. pylori Gastritis and Endoscopy

    9 30 hypertensive socrative. Looking for ulcerations, foregin bodies, bleeding, cancers. Therapeutic - to stop bleeding. Know quadrants and organs in each. Antacids- OTC- neutralize acid in the stomach. 1. Paul is a 56 year old male who was recently diagnosed with a peptic ulcer based. on a recent endoscopy.

  18. Peptic Ulcer Disease: A Brief Review of Conventional Therapy and Herbal

    1. Introduction. Peptic ulcer is an acid-induced lesion of the digestive tract that is usually located in the stomach or proximal duodenum, and is characterized by denuded mucosa with the defect extending into the submucosa or muscularis propria [].The estimated prevalence of peptic ulcer disease in the general population is 5-10% [], but recent epidemiological studies have shown a decrease ...

  19. A Case Presentation on Peptic ulcer

    10 likes • 10,156 views DR. METI.BHARATH KUMAR STUDYING DOCTOR OF PHARMACY (Contact me: [email protected]) Healthcare A CASE PRESENTATION ON PEPTIC ULCER 1 of 23 What's hot (20) Similar to A Case Presentation on Peptic ulcer (20) CASE PRESENTATION ON ACUTE INFECTIOUS HEPATITIS

  20. A study of the changes in the cause of peptic ulcer bleeding

    In this study, it was found that the number of peptic ulcer bleeding case was increased and H. pylori infection rate was decreased over the studied period, the main cause of peptic ulcer bleeding changed from H. pylori infection to use of NSAIDs, including low-dose aspirin.

  21. Pathophysiology and clinical presentation

    Pathophysiology. Breakage or ulceration of the protective mucosal lining in the lower esophagus, stomach (i.e., gastric ulcers), and duodenum (i.e., duodenal ulcers; most common). Figure 2. (A) Endoscopic and (B) histologic cross section views of peptic ulcer (Pathology for health Professionals 4th. edition, 2013) Underlying causes.