This document provides information on gastroesophageal reflux disease (GERD). It discusses the definition, epidemiology, pathophysiology, symptoms, complications, diagnosis, and treatment of GERD. Regarding treatment, it outlines both non-pharmacological options like lifestyle modifications as well as pharmacological treatments including antacids, H2 receptor antagonists, proton pump inhibitors, prokinetic agents, and mucosal protectants. It provides details on the mechanisms of action, examples, and side effects of the different drug classes used to treat GERD.

1. GASTROESOPHAGEAL
REFLUX DISEASE
ANIL DHAKAL

2. INTRODUCTION
 GASTRO ESOPHAGEAL REFLUX
DISEASE IS THE TERM USED TO
DESCRIBE ANY SYMPATOMATIC
CLINICAL CONDITION OR
HISTOPATOLOGICAL ALTERATION
RESULTING FROM EPISODES OF
THE REFLUX OF ACID, PEPSIN
AND OCASIONALLY BILE INTO
THE ESOPHAGUS FROM THE
STOMACH.

3. EPIDEMIOLOGY
 COMMON IN ALL AGES.
 MORTALITY IS RARE.
 RISK FACTORS AND COMORBIDITIES THAT CONTRIBUTE TO THE WORSENING OR
DEVELOPMENT OF GERD SYMPTOMS INCLUDE FAMILY HOSTORY, OBESITY, SMOKING,
ALCOHOL CONSUMPTION, RESPIRATORY DISEASE, AND REFLUX CHEST PAIN SYNDROME.

4. PATHOPHYSIOLOGY
 KEY FACTOR IN THE DEVELOPMENT OF GERD IS THE ABNORMAL REFLUX
OF GASTRIC CONTENTS FROM THE STOMACH INTO THE ESOPHAGUS, ORAL
CAVITY, OR LUNG.
DECREASED GASTROESOPHAGEAL SPHINCTER PRESSURES RELATED TO -:
 SPONTANEOUS TRANSIENT LES RELAXATIONS
 TRANSIENT INCREASES IN INTRA-ABDOMINAL PRESSURE
 AN ATONIC LES, ALL OF WICH MAY LEAD TO THE DEVELOPMENT OF
GATROESOPHAGEAL REFLUX.
 PROBLEMS WITH OTHER NORMAL MUCOSAL DEFENCE MECHANSIMS
ABNORMAL ESOPHAGEAL ANATOMY
 IMPROPER ESOPHAGEAL CLEARANCE
 REDUCED MUCOSAL RESISTANCE TO ACID
 DELAYED OR INEFFECTIVE GASTRIC EMPTYING
 INADEQUATE PRODUCTION OF EPIDERMAL GROWTH FACTORS
 REDUCED SALIVARY BUFFERING OF ACIDS

5. ESOPHAGEAL CLEARANCE
 ESOPHAGEAL ACID CLEARANCE NORMALLY OCCURS AS A TWO-STEP
PROCESS. THE INITIAL STEP OF EMPTYING MOST OF THE FLUID VOLUME
CONTAINED WITHIN THE ESOPHAGUS OCCURS QUICKLY BY GRAVITY OR BY
ONE OR TWO PERISTALTIC SEQUENCES.
MUCOSAL RESISTANCE
 WITHIN THE ESOPHAGEAL MUCOSA AND SUBMUCOSA THERE ARE MUCUS
SECRETING GLANDS. THE MUCUS SECRETED BY THESE GLANDS MAY
CONTRIBUTE TO THE PROTECTION OF THE ESOPHAGUS. BICARBONATE
MOVING FROM BLOOD TO THE LUMEN CAN NEUTRALIZE ACIDIC REFLUXATE IN
THE ESOPHAGUS.
 WHEN THE MUCOSA IS REPEATEDLY EXPOSED TO THE REFLUXATE IN GERD,
OR IF THERE IS ANY DEFECT IN THE NORMAL MUCOSAL DEFENSES,
HYDROGEN IONS DIFFUSES INTO THE MUCOSA, LEADING TO THE CELLULAR
ACIDIFICATION AND NECROSIS THAT ULTIMATELY CAUSE ESOPHAGITIS.

6. GASTRIC EMPTYING
• DELAYED GASTRIC EMPTYING CONTRIBUTES TO
GASTRO ESOPHAGEAL REFLUX. AN INCREASE IN
GASTRIC VOLUME MAY INCREASE BOTH THE
FREQUENCY OF REFLUX AND AMOUNT OF
GASTRIC FLUID AVAILABLE TO BE REFLUXED.
GASTRIC VOLUME IS RELATED TO THE VOLUME OF
MATERIAL INGESTED, RATE OF GASTRIC
SECRETION, RATE OF GASTRIC EMPTYING AND
AMOUNT OF FREQUENCY OF DUODENAL REFLUX
TO STOMACH.
• FATTY FOODS MAY INCREASE THE
POSTPARANDIAL GASTRO ESOPHAGEAL REFLUX
BY INCREASING GASTRIC VOLUME, DELAYING THE
GASTRIC EMPTYING RATE AND DECREASING THE
LOWER ESOPHAGEAL SPHINCTER PRESSURE.

7. SYMPTOMS OF GERD
• HEART BURN USUALLY AFTER EATING, WHICH MIGHT BE WORSE AT NIGHT
• CHEST PAIN
• DIFFICULTY IN SWALLOWING
• SENSATION OF LUMP IN THROAT
• REGURGITATION OF FOOD OR SOUR LIQUID
• EXCESSIVE SALIVATION
• GAS FORMATION
• BLOATING
• TROUBLE SLEEPING
• SENSITIVE TO SOME FOOD AND LIQUIDS
• IF NIGHT TIME ACID REFLUX
• CHRONIC COUGH
• LARYNGITIS
• NEW OR WORSENING ASTHMA
• DISRUPTED SLEEP

8. COMPLICATIONS
 Esophagitis and Barrett’s esophagus
ESOPHAGITIS CAN VARY WIDELY IN SEVERITY WITH SEVERE CASES RESULTING IN EXTENSIVE
EROSIONS, ULCERATIONS AND NARROWING OF THE ESOPHAGUS. ESOPHAGITIS MAY ALSO
LEAD TO GASTROINTESTINAL (GI) BLEEDING. UPPER GI BLEEDING MAY PRESENT AS ANEMIA,
HEMATEMESIS, COFFEE-GROUND EMESIS, MELENA, AND WHEN ESPECIALLY BRISK,
HEMATOCHEZIA. CHRONIC ESOPHAGEAL INFLAMMATION FROM ONGOING ACID EXPOSURE MAY
ALSO LEAD TO SCARRING AND THE DEVELOPMENT OF PEPTIC STRICTURES, USUALLY
PRESENTING WITH THE CHIEF COMPLAINT OF DYSPHAGIA.
 PATIENTS WITH PERSISTENT ACID REFLUX MAY BE AT RISK FOR BARRETT’S ESOPHAGUS,
DEFINED AS INTESTINAL METAPLASIA OF THE ESOPHAGUS

9.  IN BARRETT’S ESOPHAGUS, THE NORMAL SQUAMOUS CELL EPITHELIUM OF THE
ESOPHAGUS IS REPLACED BY COLUMNAR EPITHELIUM WITH GOBLET CELLS, AS A
RESPONSE TO ACID EXPOSURE. CHANGES OF BARRETT’S ESOPHAGUS MAY EXTEND
PROXIMALLY FROM THE GASTROESOPHAGEAL JUNCTION (GEJ) AND HAVE THE POTENTIAL
TO PROGRESS TO ESOPHAGEAL ADENOCARCINOMA, MAKING EARLY DETECTION VERY
IMPORTANT IN THE PREVENTION AND MANAGEMENT OF MALIGNANT TRANSFORMATION

10. DIAGNOSIS

11. DIAGNOSIS
A- ENDOSCOPY AND BARIUM RADIOLOGY
• IT IS THE TECHNIQUE FOR ASSESSING THE MUCOSA FOR
ESOPHAGITIS AND BARRETT’S ESOPHAGUS.
• IT ENABELS THE VISUALIZATION AND BIOPSY OF ESOPHAGEAL
MUCOSA.
 B- PROVACTIVE AND PH TESTING
• CONTINIOUS PH MONITORING CAN BE PERFORMED BY
PASSING A SMALL ELECTRODE PH PROBE INTRANASALLY
AND PLACING IT APPROXIMATELY 5CM ABOVE LOWER
ESOPHAGEAL SPHINCTER.
• THIS TEST IS USED TO ESTABLISH A CASUAL RELATIONSHIP
BETWEEN PATIENT SYMPTOMS AND ABNORMAL ACID
EXPOSURE, ESPECIALLY WHEN ESOPHAGITIS IS NOT
PRESENT.

12.  C- ESOPHAGEAL MANOMETRY
• IT IS TO EVALUATE PERISTALTIC FUNCTION SHOULD BE
PERFORMED IN ANY PATIENT WHO IS A CANDIDATE FOR
ANTIREFLUX SURGERY.
• A MULTILUMEN TUBE IS PASSED INTO THE STOMACH AND THE
PRESSURES ARE MEASURED AS THE TUBE IS PULLED BACK
ACROSS LES, ESOPHAGUS AND PHARYNX.
 D- OMEPRAZOLE TEST
• THE EMPERIC USE OF STANDARD DOSE OR EVEN DOUBLE DOSE,
OMEPRAZOLE AS A THERAPEUTIC TRIAL FOR DIAGNOSING THE
PRESENCE OF GERD.

13. TREATMENT

14. NON PHARMACOLOGICAL TREATMENT

15. SURGICAL TREATMENT
 THE GOAL OF ANTI REFLUX SURGERY IS TO REESTABLISH
THE ANTI REFLUX BARRIER TO POSITION THE LOWER
ESOPHAEGAL SPHINCTER WITHIN THE ABDOMIN WHERE IT
IS UNDER POSITIVE PRESSURE AND TO CLOSE ANY
ASSOCIATED HIATAL EFFECT.
 IT SHOULD BE CONSIDERED IN PATIENTS
A- WHO FAIL TO RESPOND TO PHARMACOLOGIC TREATMENT.
B- WHO OPT FOR SURGERY DESPITE SUCCESSFUL TREATMENT BECAUSE LIFESTYLE
CONSIDERATIONS, INCLUDING AGE, TIME OR THE EXPENSE OF MEDICINES.
C- WHO HAVE COMPLICATION OF GERD.

16. PHARMACOLOGICAL TREATMENT
 1- ANTACIDS WITH ANTACID-ALGINIC PRODUCTS
 2- ACID SUPRESSION WITH H2 RECEPTORS ANTAGONIST
 3- ACID SUPRESSION WITH PROTON PUMP INHIBITORS
 4- PROKINETIC AGENTS
 5- MUCOSAL PROTECTANTS

17. ANTACID WITH ANTACID-ALGINIC PRODUCTS
• AN ANTACID PRODUCT COMBINED WITH ALGINIC ACID FORM A HIGHLY VISCOUS SOLUTIONT THAT
FLOATS ON THE SURFACE OF GASTRIC CONTENTS.
• THIS VISCOUS SOLUTION SERVES AS A PROTECTIVE BARRIER FOR THE ESOPHAGUS AGAINST
REFLUX OF GASTRIC CONTENTS.
• IT ALSO REDUCES THE FREQUENCY OF REFLUX EPISODES.
EXAMPLE: GAVISCON
ADR: DIRRHOEA OR CONSTIPATION AND ALTERATION IN MINERAL
METABOLISM AND ACID-BASE DISTURBANCE.

18. ACID SUPRESSION WITH H2 RECEPTORS ANTAGONIST
 FOR SYMPTOMATIC RELIEF OF MILD GERD, LOW DOSE, NONPRECISION H2-RECEPTOR ANTAGONISTS MAY BE
BENEFICIAL
• CIMETIDINE 800 MG TWICE DAILY
• FAMOTIDINE 40 MG TWICE DAILY
• NIZATIDINE 150 MG FOUR TIMES DAILY
• RANITIDINE 150 MG FOUR TIMES DAILY
ADR: DIARRHOEA, HEADACHE, RASHES,
HEPATOXICITY

19. ACID SUPRESSION WITH PROTON PUMP INHIBITORS
• PROTON PUMP INHIBITORS BLOCK GASTRIC ACID SECRETION BY INHIBITING GASTRIC
H+/K+ ADENOSINE TRIPHOSPHATASE IN GASTRIC PARIETAL CELLS.
• THIS PRODUCES A PROFOUND, LONG-LASTING ANTISECRETORY EFFECT CAPABLE OF
MAINTAINING THE GASTRIC PH.
ADR: DIRRHOEA, HEADACHE, ABDOMINAL PAIN

20. PROKINETIC AGENTS
• THIS IS GIVEN GIVEN TO THE PATIENTS WHO HAVE FAILED HIGH-DOSE PROTON PUMP
INHIBITOR THERAPY.
• PROKINETIC AGENTS HAVE ALSO BEEN USED AS ADJUNCTIVE THERAPY WITH AN H2
RECEPTOR ANTAGONISTS.

21. MUCOSAL PROTECTANTS
• IT IS NONABSORBABLE ALUMINIUM SALT OF SUCROSE OCTASULFATE, HAS VERY
LIMITED VALUE IN THE TREATMENT OF GERD.
• SUCRALFATE HAS SIMILAR HEALING RATES AS H2 RECEPTOR ANTAGONISTS FOR
PATIENTS WITH MILD ESOPHAGITIS.
SUCRALFATE 1G/10ML
ADR: CONSTIPATION, NAUSEA, DRY MOTH,
DIZZINESS

22. NAME: AB
AGE: 60 YRS
SEX: MALE
CHIEF COMPLIANTS : Abdominal
discomfort since 10 days, heartburn
after eating, Regurgitation of sour liquid,
Trouble sleeping "Bloating, epigastric
pain.
Past Medical history: Bronchial asthma
since 3 years.
Past Medication history: Salbutamol
Inhalation loomcg/actuation
SUBJECTIVE

23. OBJECTIVE( LABORATORY PARAMETERS)
ENDOSCOPY: isolated round erosion extending from the junction upwards not
involving entire circumference.
PARAMETER DETECTED VALUES NORMAL RANGE
RBC 4.26 x 10¹²/L ↓ 4.3-5.9 x 1012/L
Hb 10.5 g/dl ↓ 13.8-17.2g/dl
WBC 14.0 x 10⁹/L ↑ 4.5-11.0 x 109/L
ESR 32 mm/hr ↑ <15mm/hr
RBS 205 mg/dl ↑ Less than 200mg/dl
LDL 265 mg/dl ↑ Less than 100mg/dl
HDL 20 mg/dl ↑ 50mg/dl or higher

24. THE PATIENT WAS
DIAGNOSED WITH GERD(
GASTRO ESOPHAEGAL
REFLUX DISEASE)

25. ASSESSMENT(TREATMENT GIVEN)
DAY 1 DAY 2 DAY 3
INJ RANTAC
2ML
INJ RANTAC
2ML
INJ RANTAC
2ML
SYP DIGENE
2TSP BD
SYP DIGENE
2TSP BD
SYP DIGENE
2TSP BD
TAB DOLO 650
PO
TAB DOMSTAL
10MG BD
TAB DOMSTAL
10MG BD
DISCHARGE MEDICATION
TAB RANTAC 150MG BD
TAB DOMSTAL 10MG SOS
SYP DIGENE 2TSP BD

26. INTERVENTION
1-The patient had high cholesterol but no drug was given for that.
2- The perferred treatment option would be PPIs which was not
given to the patient.
3- Dolo was given to the patient without checking the temperature.
4- Since the was anaemic and there was no treatment given for
that.
5- patient RBS is high then the normal, so the patient is found to be
diabetic.

27. MY PLAN
DRUG DOSE FREQUENCY
Cap. Omeprazole 20mg OD
T. Ferrous sulphate 325mg OD
T. Atorvastatin 10 mg h.s
Syrup digene 2 tsp SOS
paracetamol 500mg SOS
metformin 500mg OD

28. PATIENT
COUNSCELING

29. ABOUT DISEASE
•GERD OCCURS DUE TO THE REFLUX OF THE GASTRIC CONTENTS FROM THE STOMACH TO THE
ESOPHAGUS.
• THE SIGN AND SYMPTOMS OF GERD INCLUDE CHEST PAIN, DIFFICULTY SWALLOWING, BLOATING,
SLEEPING TROUBLE.
ABOUT DRUGS
• TAKE TAB OMEPRAZOLE ATLEAST 30 MINUTES BEFORE FOOD.
• ADVISED TO TAKE MEDICATION ON TIME REGULARLY.
• ADVISED NOT TO TAKE DOUBLE DOSE IF THE DOSE IS MISSED.
• TAKE TAB PARACETAMOL WHEN THERE IS PAIN OR FEVER.
ABOUT LIFESTYLE
•PATIENT WAS ADVISED TO EAT 2-3 SMALL MEALS.
• ADVISED TO AVOID IRRITANTS FOODS.
• AVOID EATING IMMIDIATELY PRIOR TO SLEEP.
• AVOID WEARING TIGHT FITTING CLOTHS.

30. REFRENCES
 Clarrett DM, Hachem C. Gastroesophageal Reflux Disease (GERD). Mo Med. 2018 May-Jun;115(3):214-218. PMID:
30228725; PMCID: PMC6140167.
 Poddar U. Gastroesophageal reflux disease (GERD) in children. Paediatr Int Child Health. 2019 Feb;39(1):7-12. doi:
10.1080/20469047.2018.1489649. Epub 2018 Aug 6. PMID: 30080479.
 Chen J, Brady P. Gastroesophageal Reflux Disease: Pathophysiology, Diagnosis, and Treatment. Gastroenterol
Nurs. 2019 Jan/Feb;42(1):20-28. doi: 10.1097/SGA.0000000000000359. PMID: 30688703.
 Sharma P. Barrett Esophagus: A Review. JAMA. 2022;328(7):663–671. doi:10.1001/jama.2022.13298
 JOSHEP T. DIPIRO, EECILY V. DIPIRO PHARMACOTHERAPY HANDBOOK 11TH EDITION 2021.
 . Gastroesophageal Reflux Disease | The University of Kansas Health System. Kansashealthsystem.com. Retrieved
from https://www.kansashealthsystem.com/care/conditions/gastroesophageal-reflux-disease.
 sami, S., & Ragunath, K. (2013). The Los Angeles Classification of Gastroesophageal Reflux Disease. Video Journal
And Encyclopedia Of GI Endoscopy, 1(1), 103-104. https://doi.org/10.1016/s2212-0971(13)70046-3