MINISTRY OF HEALTH

KOTA KINABALU ALLIED HEALTH SCIENCE COLLEGE

CASE STUDY

TOPIC:DUODENAL ULCER FORREST 2a

THAMAYANTHY A/P RAMAN

PB (S) 1/2016 - 0179

MENTOR

MDM RUSINAH SOLIGI

GASTROINTESTINAL ENDOSCOPY COURSE

MAC 2016 INTAKE

CONTENTS

TITLES PAGE
GIA Details 3
Acknowledgment 4
Objective 5
Anatomy and Physiology stomach

6-17
Introduction of disease 18-23
Pathophysiology duodenal ulcer 24- 25
Risk factor of duodenal ulcer 26- 29
Treatment duodenal ulcer 30-31
Classification ulcer 32
Patient particular 33
Reason for admission 34-36
Patient assessment 37-38
Indication for OGDS 39-45
Preparation OGDS for Miss K 46-47
Pathophysiology Miss K 48-49

Management of patient: 50-56

Pre - procedure

Intra - procedure
Therapeutic treatment
 57-61
Post - procedure

62-63
Ward progress:

Day 1(8 / 4 / 2016)

Day 2 (9/ 4 / 2016) 64-72

Day 3 (10 / 4 / 2016)

Bay 4 (11 / 4 /2016)

Health education discharge 73-74
Blood result investigation 75-76
summary 77
Conclusion 78-79
bibliography 80
NAME : THAMAYNTHY A/P RAMAN

DATE OF BIRTH : 22 OCTOBER 1981

I/C N0 : 811022 – 08 - 6554

MATRIKS N0 : PB ( S ) 1/2016 – 0179

COURSE DURATION :1 MARCH 2016 – 31 AUGEST 2016

INSTITUITION : KOLEJ SAINS KESIHATAN BERSEKUTU KOTA

KINABALU

WORKING PLACE :HOSPITAL FATIMAH IPOH PERAK DARUL

RIDZUAN.
ACKNOWLEGMENT

I would like to give a special thank you to Madam Rosaline Sulit , Madam

Rusinah Soligi and Madam Haslinda for the guidance and lectured, I willing to

complete my case study. Not forgotten, big thank full to Datuk Dr. Jayaram and

Mr. Philip, All the gastroenterologist and surgeon of Queen Elizabeth Hospital for

helping me and support me a lot and giving me the opportunity to work with them

during this 6 month of my post basic. Not forgotten to all the Endoscopy staff of

QEH who really care, concern and team work with us, thank you so much. They

willing to teach, help and share their knowledge with us.

Last but not least, special thank you to Miss K and her daughter for the

permission and allow me to be the patient for my case study. Thank you for the full

cooperation during the interview. Lastly, thanks to all my colleague for the support

and the team works.

------------ THANK YOU -------------

OBJECTIVE

Describe the anatomy and physiology of the gastrointestinal tract and how

this is altered by illness and disease especially stomach and duodenum.

Demonstrate and understanding of the application of specialist knowledge

related to safety , competent endoscopic care during OGDS.

Explain the pathologies and outline the various diagnostic , therapeutic ,

treatment and management associated in the peptic ulcer disease.

Understand and perform the pre – procedural , intra – procedural and post –

procedural care of patient undergoing endoscopic procedure.

Learn about the indication , contraindication & complications for endoscopic

treatment.
What is the stomach?
Stomach is a muscular organ are located on the left side of upper abdomen.

Stomach can receive food from the esophagus. It enters the stomach

through a muscular valve called the Lower esophageal Sphincter.

Stomach secretes acid and enzymes that digest food. Ridges of muscle

tissue called Rugae line in the stomach.

The stomach muscles contract periodically, churning food to enhance

digestion.

The pyloric sphincter is a muscular valve that opens to allow food to pass

from stomach to the small intestine.

 .

What is function of the stomach?

The stomach is J- shaped and it can expand to temporarily store

food.

Partial digestion of the food takes place here. The churning action of

the stomach muscles physically breaks down the food.

The stomach releases acids and enzymes for the chemical breakdown

of food. The enzyme pepsin is responsible for protein breakdown.

The stomach releases food into the small intestine in a controlled and

regulated manner.

A network of blood vessels and nerves surrounds the stomach; this is

responsible for the regulation of the secretion and the motion of stomach

muscles that churns food.

What are the layer of the stomach?
The stomach consist of four layers, similar to other parts of the
gastrointestinal tract. These layers, starting with :-
 Serosa - the outer serous layer of visceral peritoneum that covers the

exterior of the stomach includes both the greater omentum, which hangs in a
1. .
double layer from the greater curvature over the anterior side of the

abdominal viscera, and the lesser omentum, which connect the lesser

curvature to the underside the liver.

Muscular layer( Muscularis propria) - consists of an outer layer of

longitudinal muscle fibers, a middle layer of circular smooth muscle fibers an

inner layer of tranverse fibers. These three muscle layers contract to produce

the peristaltic motion of the stomach while it churns and compresses the food

during digestion

Sub mucosa - composed mainly of areolar connective

tissue. It contains the blood vessels, lymphatic and nerves.

Mucosa - lines the interior of the stomach. Contains several types of

epithelial cells. When it filled, the stomach interior has a series of wrinkled

ridges called rugae. The rugae allow the stomach to distend to hold a large

quantity of food without any substantial increase in pressure, thus helping to

control the rate at which food enters the duodenum.

2. NERVE SUPLLY

NERVE SUPLLY TO THE STOMACH

Parasympathetic innervations of the stomach is the vagus nerve. Over the

lower esophagus, the vagus nerves split.

The anterior vagus divides into anterior gastric and hepatic branches.

The posterior vagus also divides into two branches:-

a. Supplies the posterior wall of the fundus and the body of the stomach which

primarily stimulates acid secretion.

b. Supplies the posterior wall of the antrum which stimulates motility.

Sympathetic innervations of the stomach is derived from the greater splenic

nerves and the celiac ganglia.

The afferent fibers conduct visceral gastric pain impulses.

 the efferent fibers inhibits gastric secretion and motility

. Intrinsic innovation of the stomach involves:-

i. Auerbach’s plexuses influences gastric motility

ii. Meissner’s plexuses involved in gastrin release.

The primary function of the stomach is to initiate digestion by using both

chemical secretions and mechanical movements.

Gastric secretions also promote the absorption of vitamin B12,

In addition serves as a reservoir for ingested food and liquid and

regulates their entry into the duodenum.

BLOOD SUPLLY

BLOOD SUPPLY TO THE STOMACH

The stomach receive arterial blood from the celiac axis, which sends

branches to the lesser and greater curvatures.

Along the lesser curvature the left gastric artery flows down from the cardia.

At the points it joins with the right gastric artery.

The greater curvature receives blood from the gastroepiploic artery, which run

from the fundus to the pylorus.

Short gastric arteries derived from the splenic artery supply blood to the

fundus of the stomach. Blood is drained from the stomach via the portal vein.

The greater curvature is drained by the right and left gastroepiploic veins and

the lesser curvature is drained by both the gastric vein and the coronary vein.
SECRETION

Stomach Secretions and it’s Glands

The mucosa contains three types of glands, which differ from one region of the

stomach to another:

I. Cardiac glands

located just distal to the esophagogastric junction.

This glands secrete mucus and pepsinogens, which are converted

by hydrochloric acid to pepsin.

II. Oxyntic glands

The proximal two thirds of the stomach area. Consist of four types

of cells:
 Zymogenic or chief cells - secrete pepsinogens,

Mucous neck cells

Endocrine or endocrine-like cells

III. Parietal cells

secrete hydrochloric acid and intrinsic factor, which is a

glycoprotein for the absorption of vitamin B12

IV. Pyloric glands

located at the antrum and pylorus.

These gland contain mucous cells, which secrete mucus and

pepsinogens, and G cells, which secrete gastrin.

 The pyloric and oxyntic glands also have enterochromaffin cells, which

secrete serotonin.

 The cardiac, oxyntic and pyloric glandular mucosa contain at least nine

different types of endocrine cells, which secrete hormonal products such as

somatostatin and glucagon.

 The parietal and pyloric glands both secrete bicarbonate.

 In rest normal secretions occur at a rate of about 0.5ml/min. With food in the

stomach, secretions increase to about 3ml/min. the stomach secretes

approximately 1500 to 3000 ml of gastric juice daily.

motility

Contractions of gastric smooth muscle serves two basic functions:

ingested food is crushed, ground and mixed, liquefying it to form what is

called chyme.

Chyme is forced through the pyloric canal into the small intestine, a process

called gastric emptying.

The stomach can be divided into two regions on the basis of motility pattern:

an accordian-like reservoir that applies constant pressure on the lumen and a

highly contractile grinder.

The upper stomach, composed of the fundus and upper body, shows low

frequency, sustained contractions that are responsible for generating a basal

pressure within the stomach. Importantly.

these tonic contractions also generate a pressure gradient from the stomach

to small intestine and are thus responsible for gastric emptying. Interestingly,

swallowing of food and consequent gastric distention inhibits contraction of this

region of the stomach, allowing it to balloon out and form a large reservoir without a

significant increase in pressure. The lower stomach, composed of the lower body

and antrum, develops strong peristaltic waves of contraction that increase in

amplitude.
 As they propagate toward the pylorus. These powerful contractions constitute

a very effective gastric grinder; they occur about 3 times per minute in people.

Gastric distention strongly stimulates this type of contraction, accelerating

liquefaction and hence, gastric emptying. The pylorus is functionally part of this

region of the stomach - when the peristaltic contraction reaches the pylorus, its

lumen is effectively obliterated - chyme is thus delivered to the all intestine in spurt.
 Gastric motility is controlled by a very complex set of neural and hormonal

signals. Nervous control originates from the enteric nervous system as well as

parasympathetic (predominantly vagus nerve) and sympathetic systems.

 A large battery of hormones have been shown to influence gastric motility - for

example, both gastrin and cholecystokinin act to relax the proximal stomach

and enhance contractions in the distal stomach.

 The bottom line is that the patterns of gastric motility likely are a result from

smooth muscle cells integrating a large number of inhibitory and stimulatory

signals.

 Liquids readily pass through the pylorus in spurts, but solids must be reduced

to a diameter of less than 1-2 mm before passing the pyloric gatekeeper.

 Larger solids are propelled by peristalsis toward the pylorus, but then

refluxed backwards when they fail to pass through the pylorus - this

continues until they are reduced in size sufficiently to flow through the

pylorus.
What is the peptic ulcer?

Peptic ulcer disease refers to painful sores or ulcers in the lining of the stomach or

first part of the small intestine, called the duodenum.

Anotomy and physiology of duodenum

Duodenum is the first part of the small intestine (5 – 7 cm).Followed by the jejunum

and ileum.also widest and shortest (25cm) part of the smal intestine.Duodenum is a

C – shaped or horseshoe – shaped structure that lies in the upper abdomen near

the midline.

it receives partially digested food (known as cyme) from the stomach and plays a

vital role in the chemical digestion of cyme in preparation for absorbtion in the small

intestine.many chemical secretions from the pancreas,liver and gallbladder mix with

the chyme in the duodenum to facilitate chemical digestion.

The pancreas,liver and gallbladder all deliver their digestive secretions into the

duodenum through an orifice known as th ampula of vater,which is located roughly in

the middle of the duodenum on the left side.

The wall duodenum aremade of four layers of tissue that are consistent with the

structure of the gastrointestinal tract.:

The innermost layer (mucosa)

line the inner surface of the duodenum and is in contact with chyme passing

through the intestinal lumen.it is simple columnar epithelial tissue with

microvilli on its surface to increase surface area and improve the absorption of

nutrients.mucus glands secrete mucus into the lumen to lubricate the

intestinal wall and protect it from friction and acidic chyme.

The mucosa layer is the submucosa

layer of connective tissue that supports the otherbtissue layers.blood vessels

and nerve pass through the submucosa.protein fibers give strength and

elasticity to the duodenum.

Muscularis

surrounding the submucosa is the muscularis layer contains layer smooth

muscle tissue of the duodenum.contraction s of the muscularis mix chyme

and propel it through the duodenum toward the rest of the small intestine.

Serosa

Is the outermost layer of the duodenum that acts as the outer skin of the

intestine.serous membrane made of simple squamous epithelium provides a

smooth,slick surface to prevent friction between the duodenum and

surrounding organs.the serosa also secretes serous fluid to further reduce

friction and keep the duodenum’s surface moist.

After being stored and mixed with hydrochloric acid in the stomach for about 30 to

60 minutes.chyme slowely enter to the duodenum through the pyloric

sphincter.Brunner’s glands in the mucosa of the duodenum secrete alkaline mucus

containing a high concentration of bicarbonate ions to neutralize the hydrochloric

acid present in the chyme.the alkaline mucus both protects the walls of the

duodenum and helps the chyme to reach a PH conducive to chemical digestion in

small intestine.

When reaching the ampula of vater in the middle of the duodenum,chyme will mixed

with bile from the liver and gallbladder , follow by as pancreatuc juice produced by

the pancreas.yhese secretion complete the process of chemical digestion that began

in the mouth and stomach by breaking complex macromolecules into their basic

units.bile produced in the liver and stored in the gallbladdder acts as an emulsifier,

breaking lipids into smaller globules to increase their surface area.pancreatic juice

contains many enzymes to breakdown carbohyrates , lipids , proteins and nucleic

acids.example pancreatic lipase breaks trigicerides or fats , into glycerol and fatty

acids an it can be absorbs into the bloodstream by th intestinal wall.

Slow waves of smooth muscle contraction known as peristalsis flow down the length

of the gastrointestinal tracc to push chyme though the duodenum.each wave brgins

at the stomach and pushes chyme a short distance toward the jejunum.small

regional contractions of the intestinal wall known as segmentations, help to mixe

chyme with the digestive secretions in the duodenum and increase the rate of

digestion.segmentations also increase the contact of chyme with the mucosal cells to

increase the absorbtion of nutriens through the intestinal wall.

What are the part of duodenum?

The pylorus of the stomach leads to the duodenum,which has the following 4 parts:
First part (superior) or duodenal buld (5cm)

 which is connected to the undersurface of the liver (porta hepatis) by

the hepatoduonal ligament (HDL).

 containing the proper hepatic artery , portal vein , and common bile

duct(CBD)

 the quadrate lobe of the liver and gallbladder are in front.

 Whereas t he CBD,the portal vein and the gastroduodenal artery are

behind the first part of the duodenum.

Second (descending) part ( 7.5cm)

 which has an upper and lower (flexure.

 the transverse mesocolon and transverse colon are infront.

 the right kidne

 y and inferior vena cava ( IVC) are behind.

 The head of the pancreas lies in the concavity of the duodenal .

Third (horizontal part ( 10cm)

  from right to left in front of the inferior vena cava ( IVC) and aorta.

 Th superior mesenteric vessels ( the vein on the right and the artery

on the left) in front of it.

Fourth ( ascending) part 2.5cm

 Continues as th jejunum.

Pathophysiology of the disease Duodenal ulcer

Common etiologies of helicobacter pylori infection some 12 years ago,three

major disturbances in gastric physiology had been identified in patients with

duodenal ulcer disease.these abnormalities were impaired acid inhibition of

gastrin release from the antral mucosa, increased basal and stimulated acid

secretion by the body of the stomach and increase acid load in the

duodenum.some of these abnormalities in gastric function can now be

explained by the effects of H.pylori infection.the increased release of gastrin

by the antral mucosa in duodenal ulcer patients , for example can be entirely

explained by the effects of this organism..other abnormalities appear to have

a genetic basis or may be due to enviromental factors.much work has been

conducted on the relationship between H.pylori and the development of the

duodenal ulcer disease.

Site (gastroduodenal mucosa

 Inability to withstand the digestive action of gastric acid (HCI)

and pepsin

Increased concentration or activity of acid – pepsin and

decreased resistance of the mucosa

Erosion / damage of the mucosa

Inability to secrete enough mucus to act as a barrier against

HCI

Hypersecretion of gastric juice, duodenal ulcers , and

gastrinomas (islet cell tumors )in the pancreas

Epigastric pain

What are the risk factor of duodenal ulcer?

Helicobacter pylori
 H.pylori is a spiral rod shaped bacterium that thrive in microaerophillic conditions

( requiring low oxygen concentration ,much like our stomach enviroment). It also

equipped with tail – like “FLAGELLA “ used for navigation in the stomach. It is

thought bugs propel themselves quickly away from acidic conditions of the

stomach.Stomach contents mucosal lining which is less acidic.once H.Pylori

estabilsh in the mucosal lining it cause inflammation and damagging deeper

stomach lining layers causing ulcers and gastric pains.

H.Pylori or “Corkscrew Bugs “can found in the enviroment.it also can happen to

people who may poor hygiene.some can be infected and contaminated water , or

food. People colonized with H.Pylori have a 10%-20% chance of developing

stomach ulcers.1% - 2% risk of gastric cancer.

NSAIDS

Frequent used aspirin , ibuprofen and other anti – inflamammatory drugs (can

increase in women and people over age of 60).

Mucosa protected from gastric acid via mucus secreation that stimulate by certain

prostoglandin.

Mucosa exposed – erosion happen.

Stress

 Due to health problem. Such as severe trauma , who have ongoing sepsis .

 Those who have significant burn injuries (Curling’s ulcer).

 Those who sustain intracranial trauma such as craniotomy (Cushing’s ulcer)

Drinking alcohol overload can causes ulcer.

Smoking and cancer (gastromonas , are rare gastrin secreating tumours

radiation therapy

Family history of gastric ulcer

What are symptoms?

The most common symptom of a peptic ulcer is burning abdominal pain extends

from navel to the chest it can be mild to severe pain.Some cases the pain can be till

night.Small peptic ulser may not produce any symptoms in the early phases.
 Changes in appetiteNausea

bloody or dark stools (melena)

Weight lossIndigestion

Vomiting

chest pain

complication of peptic ulcer is:

hemorrhage

 approximately 15% of ulcer patients ,causing hematemesis or melena stool.

 Life – threatening hemorrhage is the first indication of ulcer.

Perforation

 Less commom in about 7% of peptic ulcer patients..

 Gastric ulcers tend to perforate along the anterior wall of the lesser curvature

of the stomach.

 Patients who may perforation experience upper abdominal

pain,guarding,rebound tenderness and absent bowel sounds.

 Surgery required.

Penetration

 Similir to perforation.the ulcer crater extends into an adjacent organ,most

common left lobe of the liver.

  Rarely gastric ulcers can penetrate into the colon into colon resulting in

gastrocolic fistula.

 Symptoms can be back pain , night distress ,changing epigastric pain.,

vomitting

Gastric outlet obstruction

 Antral motility cause by inflammation and edema of the ulcer.

 Symtoms it can be abdominal distension.vague abdominal pain and early

satiety may be symptoms of partial obstruction.

 Obstruction treated by decompressing the stomach using nasogastric

aspiration,restoring fluid and electrolyte balance and administering iv

Histamine 2 blockers.

 Surgery may be indicated if these therapies fail.

TREATNENT

Proton pump inhibitor (PPI) ,

 PPI reduce acid levels and allow the ulcer to heal.

The medication include Omeprazole (losec), lansoprazole (Prevacid), or

Esomeprazole (controloc)

H2 Blockers,

such as Cimetidine (tagamet), famotidine (Pepcid), ranitidine

(Zantac), reduce the amount of gastric produced by the stomach by binding

the histamine receptor on parietal cells and blocking histamine-stimulated

acid production.

Antacids

 act to neutralize gastric acid, strengthen the gastric mucosal barrier

and heighten the tone of LES. Example of antacids such as Gaviscon.

Sucralfate (carafate)

 is a complex of Aluminium hydroxide and sulfated sucrose, form a protective

gel at the site of disrupted mucosa, thus providing a protective covering for

the ulcer.

 Upper endoscope(OGDS) is the procedure of choice for a patient with active

Bleeding.

Surgery
 is often required for patient who have perforation; patient may experience

upper abdominal pain, guarding, rebound tenderness and absent bowel

sounds.

Avoid smoking, tea, coffee and soft drink containing caffeine, alcohol,

aspirin and NSAIDs.

Self-help measures include eating several small meals a day at regular

times.

Prostaglandins misoprostol (Cytotec) have anti secretory and

cytoprotective effects.

Investigational drugs include both Tricyclic compounds, which block

acid production by interfering with acetylcholine – stimulated acid

secretion and colloidal bismuth compounds, which act by coating the

ulcer.

CLASSIFICATION ULCERS
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PATIENT PARTICULARS:
 NAME MISS.K

IDENTITIY CARD NUMBER 550103 – 12 – XXXX

DATE OF BIRTH 03 JANUARY 1955

AGE 61 YEARS OLD

GENDER FEMALE

RACE CHINESE

HOME ADDRESS PENAMPANG

MARRITAL STATUS MARRIED

DATE OF ADMISSION 7 APRIL 2016

WARD GASTRO MEDICAL WARD

DATE OF PROCEDURE 8 APRIL 2016

DISCHARGE DATE 11 APRIL 2016

MEDICAL DIAGNOSIS PRE--OGDS UGIB secondary PUD (Peptic Ulcer

Disease

MEDICAL DIAGNNOSIS POST -

OGDS UGIB Secondary Forrest 2A

TREATMENT ADRENALINE INJECTION, HEATER

PROBE

REASON FOR ADMISSION

 Miss. K direct to the emergency department Hospital Queen Elizabeth on 7th

April 2016 at 9.50PM ,accompanied by daughter. She complained of SOB ,

palpitation after vomiting of blood clot 2 times at home after taking herbal

medication pass two days ago but no fresh blood. First day miss K took Herbal

Medication no reaction happening after taken medication. Second day only she got

reaction and realize that after taking herbal medication she vomiting blood clot at

7pm. on 6th April 2016..Follow by around 11.30pm vomiting again with moderate

amount blood clot. After that miss K waking up her daughter and informing that she

was vomiting blood clot two time. Than immediately her daughter bring miss k to

Hospital Queen Elizabeth for get immediate treatment to save the life patient. She

mention stool was black in color , no dizziness , no abdominal pain and sweating her

daughter was mention. Doctor M examine Miss K and instructed to give IV

Pantoprazole 80mg stat every hourly and IV normal saline 0.9% 5 paint / 5%

Dextrose a day running 2hourly.Keep patient nil by mouth. Blood for group and

cross match (GXM) was done to detect blood loss and further

management such as blood transfusion. Vital sign was checked for baseline

as below:

 Blood pressure : 143/80mmHg

 Pulse rate : 80 beat per minutes

 Respiration : 24 per minutes

 O2 saturation : 98%
 Temperature : 36.7 ‘c

 Plan was made

 Admit in gastro medical ward

 General condition alert and concious

 FBC/ PTT/ PT / INR /BUSE

 Keep nil by mouth

 IV normal saline 5 paint / Dextrose 5% over 24 hours

 Refer gastroenterologist for OGDS

 Initial diagnosis : UGIB 2’ Herbal Medication (before procedure)

Doctor M (gastroenterologist on call) was noted regarding patient condition.

He instructed to sent patient to Endoscopy department for urgent OGDS.

Meanwhile her daughter doing admission for her mother to get the bed from

gastro ward. Patient was sent to endoscopy department at 10am. On arrival

she was pallor and lethargy looking. She was alert and conscious.

Observations was done and documented as:

Blood pressure: 114 /62mmhg

Pulse rate: 80 beat per minutes

 Respiration: 23 per minutes

Oxygen saturation: 99%

Assessment was done and documented.

PATIENT ASSESMENT
MEDICAL HISTORY MISS. K
 Hypertension ( HPT) for pass 10 years on Tablet Amlodipine 10 mg daily.

Diabetes (DM) for pass 10 years on tablet metformin 1g BD and tablet

gliclazide 80mg BD.

Bilateral OA knee for pass 3years on tablet calcium lactate 600mg OD but

stop taking of NSAID’S pass tree month. continue taking herbal medication by

own.

Dyslipidemia for past 2 years but not on treatment.

SURGICAL HISTORY

Surgery was not done bilateral OA knee .

SOCIAL HISTORY

Not smoking.

Not taking alcohol.

As a housewife.

Married with 2 children and stay with him.

PHYSICAL ASSESMENT

Miss K was pallor and lethargy looking may be due to excessive blood lost

MEDICATION HISTORY

Tab amlodipine 10mg BD

Tablet metformin 1g BD

Tablet gliclazide 160mg BD

Tab calcium lactate 600mg OD

MANAGEMENT AND INVESTIGATION OF MISS.K

INVESTIGATION

ECG : NORMAL SINUS RYTHYM

CHEST X-RAY : NORMAL / CLEAR

BLOOD INVESTIGATION DATE ( 7 april 2016) NORMAL RANGE

HEMOGLOBIN 8.6 mmol 12.1 – 15.1 g/dl (Female)

13.8 - 17.2 g/dl (man)

PLATLET 303 142 – 424 (10^3/UL)

WBC 15 3.6 – 11.0 (10^/UL)

SODIUM 141 135 – 145 (mEq/L)

RED BLOOD CELL 4.88 12.2 (10^6/UL)

PTT 25 25 – 35 SCC

PT 13 12 – 13

INR 1.03 0.9 – 1.2

INDICATION FOR ENDOSCOPIC OGDS

 PROCESS FOR OGDS

Miss k planed for OGDS

OGDS ( oesophago gastroduodenoscopy) is a diagnostic  procedure that visualizes

the upper part of the gastrointestinal tract up to the duodenum. Its perform by using

a thin , flexible fiber –optic instrument which is passed through the mouth and allow

the lining of these parts of the gut to be visualized inside stomach to detect any

abnormalities.

1)Diagnostic OGDS miss k

 Unexplained anemia  (usually along with a colonoscopy)

 Upper gastrointestinal bleeding as evidenced by hematemasis or melena.

 Persistent dyspepsia in patients over the age of 45 years.

 Heartburn and chronic acid reflux - this can lead to a precancerous lesion

called Barrett’s esophagus.

 Persistent vomiting

 Dysphagia - difficulty in swallowing

 Odynophagia - painful swallowing

 IBD (Inflammatory Bowel Diseases)

2)Therapeutic OGDS

 Oesophageal varices

 Gastric /duodenal ulcer ( Miss k was diagnosed Upper GI Bleeding)

 Oesophageal stricture

 Removal of foreign body

Diagnostic OGDS contraindication;

 Uncooperative patient

 Shock

 Seizure

 Recent myocardial infarction

 Respiratory compromise

 Acute oral or oesophagus inflammation

Equipment ready for OGDS procedure:

endoscope(OGDS) monitor and light source

1. upper endoscope

2. light source

3. sterile water bottle with sterile water

4. biopsy forceps

5. bite block

6. topical anesthetic
 7. suction equipment

ADDITIONAL EQUIPMENT THAT MAY BE NEEDED

(therapeutic procedure)

1. injector 21G or 23G

2. heater probe applicator and diathermy machine

3. hemoclip

4. bottles of formalin and labels for biopsy specimen

5. histocryl and lipodol

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Trolley preparation

Top trolley

Bottom trolley
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PREPARATION OF DRUGS

SEDATION – Analgesic sedation given to patient to relax muscle during procedure

PETHIDINE

MIDAZOLAM

ANTIDOTE – to reverse sedative may due to allergic or overdose for

counteracting
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PREPARATION ACSESORY
NALAXON
OXYGEN SYILINDER HUMUDIFIRE NASALPRONE

PREPARATION OGDS FOR MISS. K

Miss. K was ordered for OGDS. Miss K had a episode of vomiting of blood

clot OGDS is an indication to check along the GI track to examine the bleeding site

and causes of the bleeding . Miss. K was send to endoscopy department for urgent

OGDS. Miss. K came by stretcher along escort by staff nurse and her daughter from

emergency department. Assessment and data collection was done on Miss. K as

the most important and priority to be taken immediately before the procedure and

nursing early intervention.

Physical assessment and patient complain must be the priority for immediate

nursing intervention and preparation for procedure. General condition miss K alert

and conscious. Miss K looked pink in color and warm to touching. Vital sign such as

blood pressure, pulse rate and oxygen saturation to be done as a baseline and to

detect any abnormalities or changes during the procedure. All the reading must be

documented as a reference.
 Identify past medical and surgical history to prevent any complication during

the procedure. Miss k was nil by mouth since midnight prior day of procedure. This

to prevent complication of aspiration, difficulty on perform any therapeutic procedure

such as injection . This also important for doctor to visualize the upper GI track

clearly.

Identify current drugs that Miss K on medication such as tablet amlodipine

1mg, tab metformin 1g,tab gliclozide ,tab calcium lactate 3mg Miss K withhold prior

OGDS. In general situation, patient must be stop taking this pills at least at one nite

before the test to prevent bleeding during therapeutic procedure.

Miss K safety, ensure that she already removed denture before procedure

to prevent aspiration and accidently swallowed his denture. Keep all the valuable

such as ring or chain to prevent burn during procedure. Miss K was examine by

doctor and explanations given regarding procedure.

Inform consent taken by doctor, allowed doctor performed the procedure. Full

explanation regarding procedure (OGDS) given by doctor or staff nurse to miss K

and her daughter. Miss K was alert and understand of the procedure. A complication

of the procedure also explained by nurses as patient information. It’s also to check

patient understanding, patient’s anxiety and cooperation when the procedure was

performed. Patient are entitled to be fully informed of the reason why a procedure is

recommended and its expected benefits. The potential risks, its limitation and other

alternatives. Miss K also explained exactly what happen and the chance to ask

questions.
 Printed brochures can be facilitate this education process and was given to

Miss k and her daughter well in advance of the procedure, so that they can be

studied carefully and digest.

Pathophysiology related to Miss. K case

The lining of the stomach is usually protected from the damaging effects of

stomach acid. When that protection fails, an ulcer forms. There are a few different

ways this happens.

Helicobacter pylori (H. pylori)

H. pylori, a type of bacteria, is responsible for most ulcers. This

organism weakens the protective coating of the stomach and first part

of the intestine and allows damaging digestive juices to eat away at the

sensitive lining below. H pylori test (pronto dry) was not taken on Miss

K because of internal bleeding.

 Nonsteroidal anti-inflammatory drugs (NSAIDs) –

Long-term taking herbal medication of these pain relievers is the

second most common cause of ulcers. These drugs block

prostaglandins, substances in the stomach that help maintain blood flow

and protect the area from injury. Some people are more susceptible to

this side effect of NSAIDs than others.

Miss. K was send to endoscopy department by stretcher accompany by her

daughter. General condition was alert and conscious but a bit pale because blood

loss. Miss. k. Vital sign was taken and recorded as:

Blood Pulse rate Oxygen Respiration Oxygen

pressure saturation (rate/min)

114/62mmhg 80bpm 99% 22 3 liter

.
 PRE PROCEDURE

Miss K arrive in endoscopy procedure room at 10.20am . she was get ready

for OGDS which is in room 4. All equipment such as biopsy forceps , injector,

adrenaline, heater probe and hemoclip was prepared well standby. Scope and the

monitor was checked and ready to be used.

A pre procedure assessment was perform :

Ask Miss K about :

Medical history: Diabetes Mellitus, Hypertension, dyslipidemia

Surgical history: no surgery done before

Address and record his phone number and relative

Document drug daily medication including dose and frequency.

 Daily drugs taking by MISS.K

Vital signs - To assess any abnormalities before procedure.

BLOOD

TIME PRESSURE SPO2 RESPIRATION PULSE

10.20 AM 148/77mmHg 99% 22permin ate 96 bpm

I make sure all blood investigation for Miss K such as FBC, PT / PTT/ INR/

GXM taken . All result are normal and patient can proceed OGDS.

I also make sure Miss K was fasted from 12 midnight (NBM) prior to the

procedure to prevent patient vomiting and aspiration pneumonia.

Verified the consent by asking the name and correct case note.
 I checked the consent was ready and taken by the Doctor. The purpose

of consent to protect right patient understand regarding procedure,

complication and post OGDS care.

Ensure Miss. K to remove his denture to prevent dislodged and may

cause blocking of airway. All accessories such watch ,ring are removed to

avoid accidentally burning during diathermy or therapeutic procedure.

Explaining procedure to Miss K to allay anxiety and fear to obtain

confident and cooperation during procedure.

I documented all relevant in the pre procedural checklist form.

IV LINE

IV line Miss K must patency before administrating the medication. Such as iv

midazolam 5ml and 50 mg of IV Pethidine be ready before procedure and get ready

antidote of iv midazolam and iv pethidine.

IV midazolam given shortly before a procedure produces sedation (induction of

sleepiness or drowsiness and relief of apprehension).

preoperative impairment of memory IV Pethidine given reacted as an analgesic

effect. It’s relief moderate to severe pain.

 INTRA PROCEDURE

Topical anaesthesia spray (xylocaine 10%) was spray to the back of

throat of Miss K to facilitate insertion of the endoscope – notice feeling

numbness.

Turn Miss K to the left position to facilitate drainage of pharyngeal

secretions.

Mouth piece was placed to avoid Miss K bite the fiberscope.

Miss K experience some abdominal discomfort during the insertion of the

endoscope. She was allayed to relax and take a deep breath to relax the

abdominal muscles.

Procedure was start under sedation. Iv Midazolam 3mg and iv

pethidine 25mg given as ordered by Doctor. During procedure I call

 Miss K weather responding or not. i ask miss K having stomach pain

or not. Miss K tolerating our procedure until finish the case.

During procedure I observe any allergic reaction off the drugs to the

miss K around the topical skin.

Vital sign monitoring was check such as blood pressure, pulse rate,

respiration rate, oxygen saturation, level of consciousness and

documented every 5 minutes or more often if patient condition

warrant.

TIME BLOOD PULSE RESPIRATION OXYGEN OXYGEN LEVEL OF

PRESSURE SATURATION SEDATION
(MMHG)

11.50 hrs 176/101mmhg 87 /min 20 /min 3L 100% Conscious (0)

11.55 hrs 197/89mmhg 97 /min 22 /min 3L 100% Drowsy (1)

12.10 hrs 168/97mmhg 86 min 20 /min 3L 100% Drowsy (1)

I gave oxygen 3L/min via nasal prong to prevent hypoxia due to side

effect of sedation and to maintain oxygen saturation.

Frequently suctioning was done to keep airway clear and prevent

aspiration.

Emergency trolley and reversal IV Flumazenil must be ready

available in the procedure room in case of patient’s condition worsen

due to complication happen.

I help in assisting Doctor during therapeutic procedure – preparing

injector needle adrenaline and heater probe.

Miss K was observed for any complication such as bleeding, hypoxia,

cardiac arrest and abdomen distended. No sign of condition noted.

Patient safety

Reassuring to Miss K and obtained confident and cooperation during

procedure.

Documented all relevant finding in intra procedural checklist

Upon the procedure Forest II a non bleeding visible vessel gastric

ulcer was noted at the lesser curvature.

THERAPEUTIC TREATMENT

INJECTION ADRENALINE

Therapeutic procedure was performed for miss K using adrenaline injection and

heater probe. Followed by classification of forest 11a (Non bleeding visible

vessel).Injection of adrenaline diluted (1:10,000 to 1:20,000 dilution) for endoscopic

hemostasis treatment is the oldest endoscopic method with typical injection volumes

less than 10mls. Adrenaline contain citric acid , sodium citrate , sodium chloride ,

sodium bisulfate , hydrochloric acid and water. Injection adrenaline works as

vasoconstriction and activates platelet coagulation, reducing blood flow to the

bleeding site using. Injection. There is evidence using higher volumes ( exp :20ml to
40ml ) for injection therapy may be more effective at reducing re bleeding than the

conventional relatively low volume . Although overall clinical outcomes including

surgery rates and mortality have not been shown to be improved (Gastrointestinal

Endosc,2004 Dec). Higher doses of injecting adrenaline are more likely to cause

Cardiovascular side effects , particularly when injected around the region of

gastroesophageal junction and the distal esophagus.

HEATER PROBE

After the injection of the adrenaline, heater probe was applied. The heater probe

comes with its own power unit, while multi polar electro coagulation probes. BICAP

or Gold probe ,have power supplied by standard electrocautery unit. The larger

heater probe is a 3.2 mm diameter. Heater probe recommended using for slow and

improved control during thermo coagulation with a heater probe in UGIB. Fifty - six

patients with actively bleeding peptic ulcers were treated with the heater probe unit.

Initial hemostasis was achieved in patients (85.7).The setting heater probe

applications is 25 – 30 j. Heater probe treatment is an effective and safe haemostatic

method for control actively bleeding ulcers. Effective hemostasis is suggested by

whitening of the lesion and flattening of a non - bleeding visible vessel or clot remain.

In a controlled randomized, study of 101 patients with non-bleeding visible vessels.

The rate of re-bleeding was 10% after heater probe therapy compared with 26% in

the control group who received non - endoscopic therapy. In a trial of 43 patients

with an active bleeding ulcer or non-bleeding visible vessels, 0% of patients

undergoing heater probe therapy re-bleed compared 21.7% of patients undergoing

endoscopy therapy.

Two method of therapeutic procedure done to miss K on the day is:

 1) Injection adrenaline

Injection adrenaline 1:10 000 by 10mls .During procedure

injection adrenaline 8mls are used to miss K and bleeding

manage to stop and secured.

2) Heater probe

Heater probe applied to miss K to ensure bleeding ulcer under control and to avoid

high risk of re-bleeding . The heater probe is inserted through an endoscope channel

to control GI hemorrhage and bleeding. Heater probe are available with diameter of

3.2mm and normal setting of coagulation therapy 30 joules for miss K therapeutic

endoscope GIF –ITQ 160 was used. Finally once procedure complete I remove all

blood pressure cuff, pulse saturation from the hand and arm. After that i waking up

miss K . She respond went I’m calling than I inform her that procedure was done.

Than only I push miss K to recovery area for monitoring vital signs.
FINDING POST OGDS MISS K

.
POST

PROCEDURE

Miss K was kept in recovery area until she fully awake and able to control

secretion.

Miss was observed in recovery area to monitor vital sign, blood pressure,

pulse rate, respiration rate, oxygen saturation and level of consciousness

until it returned to baseline.

TIME BLOOD PULSE RESPIRATION OXYGEN OXYGEN

PRESSURE SATURATION

(MMHG)

12.20hrs 166/70mmhg 102 /min 20 /min 2 liter 100%

12.30hrs 159/86mmhg 100 /min 20 /min 2 liter 99%

Continued oxygen 2L/min via nasal prong to provide oxygenation and

avoid respiratory distress.

I observed sign and symptoms of complication such as vomiting, abdominal

pain and abdominal distended. Doctor will notified if these complication were

suspected.
 Before patient discharge from recovery bay, I gave health education

regarding his disease. (Refer to Health Education Form)

Documented all relevant finding in the post procedural checklist form

Miss K was sent back to the ward at about 13.30 hrs accompanied by staff

nurse.

OGDS procedure for Miss K takes about 35 minutes. After that Miss .K sent

to recovery area for observation until she’s fully awake. Miss K was closed monitor

for vital sign, blood pressure, pulse, oxygen saturation, level of consciousness until

he have returned to baseline. Miss K still continue with oxygen with 2 liter nasal

prong. Observed for any sign of bleeding, vomiting and changes in vital sign, severe

pain and abdominal pain. If this occurred immediately informed the doctor for further

management as this is sign and symptoms of complication.

Miss K was reminded nil by mouth until review by doctor. Miss K was kept

lateral position and prop up the head to prevent aspiration pneumonia, and able to

control secretion until gag reflux return which takes about 1 to 2 hour. To make sure

that Miss K is save, cord side must be put up for safety purpose, as he was drowsy

for side effect of sedation.

After Miss K was fully awake, she was sent to gastro medical ward 6 for

further observation and treatment before she was safe for discharge. Miss K was

ready send to ward by bed escort by staff nurse from gastro ward. Before that make

sure all documentation was passed to staff nurse who fetch the patient.

WARD PROGRASS

DAY 1 (8 APRIL 2016)

 Miss K was send to ward at 13.30 hrs company by her daughter to reduce

anxiety to her mother. General condition Miss K stable, alert and conscious but look

paler. No active bleeding noted. KIV transfuse blood if HB low. Keep Miss K Nil by

mouth (NBM).Continue Iv drip 4 paint Normal saline @ 24hrs still in progressing well

together with iv Pantoprazole 8mg / hourly. Iv dextrose saline 5% QID only. Keep

Miss K saturation > 95% – 100%..To Trace FBC.( hemoglobin)

Vital sign was checked to Miss K :

Blood Pulse rate Respiration Temperature Pulse Pain score

pressure rate saturation (1 – 10)

146 / 67mmhg 100 /min 22 /min 36.7 C 96% 0

At 15.00hrs Miss K hemoglobin traced. The latest result is 6.6mmol called

up Doctor M and informed the hemoglobin result .Doctor M ask to transfused 1

paint of packed cell today. Before I transfuse packed cells to Miss K I checked

packed cells with another staff nurse witness to checking name of patient , identity

card number , blood group, expiry date and rhesus factor to prevent error. Iv line in

patency .Same was transfuse 1 paint ( in progress ).

Vital sign before transfuse Packed Cells is:

 Blood Pulse rate Respiration Temperature Pulse Pain score

peressure rate saturation (1 – 10)

137 69mmhg 99 /min 20 /min 36.9 C 99% 1

Observation continue until finishing the 1paint of packed cells. During

transfusion no allergic reaction I seen to Miss. K. She very comfortable

and tolerating with transfusion we are giving. After few hours blood

transfusion finishing without any complication.

Vital sign after transfuse packed cells is :

Blood Pulse rate Respiration Temperature Pulse Pain score

pressure rate saturation (1 – 10)

139/68mmhg 85 /min 19 /min 37* C 99% 1

Currently miss K in condition conscious , alert with full GCS 15/15 and comfortable

in room air. She rest in bed with bed cot side up to prevent fall from bed. To continue
medication as per chart ordered by Doctor M. Keep Miss K nil by mouth and to

repeat post transfusion hemoglobin (FBC) coming morning. If HB <8 to transfuse

packed cells. Otherwise Miss K sleep well, no nausea and vomiting. I noted no active

bleeding tendency after post OGDS 1st day. All documented.

DAY 2 ( 9 April 2016)

General condition Miss K, stable , alert and conscious. Miss K daughter around and

she ambulating her mother with minimal supporting. Iv pantaprazole and Iv normal

saline still on progress. I seen no active bleeding post OGDS 2 nd day. Miss K blood

taken early in the morning and send to laboratory to check post transfusion blood

result
The post blood transfusion result is below :

BLOOD TEST RESULT NORMAL RANGE

WBC 11.06 4.0 -10.0 (10^3/ul)

RBC 2.21 3.8 - 4.8( 10^6/ul)

HGB 6.7 12 -15 (g/dl)

HCT 20.2 36 - 46.0 %

MCV 91..4 83.0 -101.0 fL

MCH 30.3 27.0 - 32.0 pg

Miss K was started 2nd paint of packed cells .packed cells al ready

screened. Before start transfuse as a nurse checked again with staff nurse as a

witness to checking the name of patient , identity card number , blood group and

rhesus factor to prevent error. Iv line in patency .Same was transfuse 2 nd paint

packed cells ( in progress ).

Vital sign before transfuse Packed Cells is:

Blood Pulse rate Respiratio Temperature Pulse Pain score

peressure n rate saturation (1 – 10)

112/72mmh 84 /min 20 /min 36.8 C 98% 0

 g

Currently Miss K looked alert , conscious comfortable rest in bed with tolerating

well blood transfusion without any complaining. During transfusion no allergic

reaction I seen to the patient. Observation continue until finishing packed of

blood. After few hours blood transfusion finishing without any complication.

Vital sign after transfuse packed cells is :

Blood Pulse rate Respiration Temperature Pulse Pain score

pressure rate saturation (1 – 10)

136/70mmhg 85 /min 29 /min 37.3* C 99% 0

Currently miss K in good condition conscious , alert with full GCS 15/15 and

comfortable in room air. She rest in the bed with bed cot side up to prevent fall from

bed. To continue medication as per chart ordered by Doctor M .Such as iv

pantaprazole 8mg / hourly. To repeat post transfusion hemoglobin (FBC) level. If

Hemoglobin <8 to transfuse packed cells. Otherwise Miss K sleep well, no nausea

and vomiting. I noted no active bleeding tendency after transfusing. Doctor M

ordered Miss K can allowed orally..At the same time Doctor M ask to of iv normal

saline once Miss K tolerating oral intake. She was tolerating well without no
vomiting. Keep Miss K saturation > 95% – 100%. To off oxygen. To Trace FBC.

( hemoglobin).All documented for medical legal.

DAY 3 ( 10 April 2016)

Generally patient condition well , alert , conscious. Miss K ambulating well without

calling help. She well tolerating oral soft diet. At moment she no nausea and

vomiting noted. I notice no active bleeding in tendency. Continue medication as per

chart Doctor M ordered. Iv pantaprazole 8mg/ hourly once complete of f iv drip. Post

transfusion last night she tolerating without any reaction.

post blood transfusion result is below :

 BLOOD TEST RESULT NORMAL RANGE

WBC 10.07 4.0 -10.0 (10^3/ul)

RBC 2.97 3.8 - 4.8( 10^6/ul)

HGB 9.1 12 -15 (g/dl)

HCT 27.8 36 - 46.0 %

MCV 93..6 83.0 -101.0 fl

MCH 30.6 27.0 - 32.0 pg

Post hemoglobin Miss K level are increase up to 9.1(g / dl).Doctor M and

Miss K was very happy with it. Doctor M planned discharged coming morning..Doctor

M advise Keep Miss K one more day to see any complication. Vital sign was done

and documented.

Vital sign below:

Blood Pulse rate Respiration Temperature Pulse Pain score

pressure rate saturation (1 – 10)

 134/76mmhg 82 /min 18 /min 36.5* C 100% 0

DAY 4 ( 11 April 2016)

Patient condition stable ,alert and conscious. Patient was not complaining

made. She tolerating orally very well. No bleeding noted. Miss K very happy today

going back to home. She and her daughter very thank full for nurses and doctors

treatment are giving. Miss K daughter said safe my mother life. I advise Miss K take

care of yourself and continue taking medication as doctor purchasing.

 Vital sign all are stable before discharge:

Blood Pulse rate Respiration Temperature Pulse Pain score

pressure rate saturation (1 – 10)

128/72mmhg 78 /min 20 /min 36.3 C 99% 0

Follow up to see Doctor after three month. She will repeat OGDS three moths later

under gastroenterologist to progressing after taking medication. On discharge

medication as below:

Tablet Calcium Lactate 600mg OD

Tablet Amlodipine 10mg OD

Metformin 1g BD

Table Gliclazide 160g BD

Tablet Pantoprazole 40 mg BD
Upon discharge ( 11 April 2016 ), health education was given to Miss K:

COMPLICATION

Miss K to remain alert for any sign and symptom of perforation and bleeding
such as blackish stool, abdominal pain and abdominal distended, fever and
vomiting of blood.
 To come immediately to the hospital if sign and symptom occur.

MEDICATION

Advice Miss K to take all the medication that prescribed by doctor for the
healing ulcer. He was given tablet Pantaprazole 40mg BD, Tablet Calcium
Lactate 600mg OD ,Tablet Amlodipine 10mg OD. Tablet Metformin 1g BD,
Tablet Gliclazide 160g BD , Tablet Pantoprazole 40 m BD.
Advice her should not taken any other medication without prescribed by
doctor especially traditional medication or herbs.

LIFE STYLES

Advice Miss K to stop smoking and stop drinking alcohol that may cause
delay healing of the ulcer and recurrent bleeding ulcer.
Advise Miss K and her daughter to take balance diet to promote healing of the
ulcer.
Avoid peppermint, caffeine (coffee, tea, chocolate) and citrus fruits and
juices, tomatoes to inhibit the production of gastric juice.

FOLLOW UP

Remind Miss K and her daughter to come again for repeat OGDS after 3
month to inspect and the healing process of the ulcer.
MISS. K
 Date Result Result Result Result Normal

Test 7/4/2016 8/4/2016 9/4/2016 10/4/2016 range

WBC 4.0 -10.0

15 11.06 10.07 (10^3/ul)

RBC 3.8 - 4.8(

4.88 2.21 2.97 10^6/ul)

HGB 12 -15
8.6 6.6 6.7 9.1 (g/dl)

HCT 20.2 27.8 36 - 46.0

%

MCV 91..4 93..6 83.0

-101.0 fL
 PTT 25

PT 13

INR 1.02

SUMMARY

Miss K was direct to emergency department Hospital Queen Elizabeth,

because vomiting blood clot two times at home. She is pale looking and anxious.

Miss K was diagnose of upper gastrointestinal bleeding. After seen by

gastroenterologist, Doctor M was proceed for OGDS to find out the bleeding site

and for treatment. OGDS finding was Forest 2a ulcer at the lesser curvature due to

either prolonged taking herbal medication without seen doctor. Therapeutic

procedure was done which is injection of adrenaline, and heater probe applied to

stop the bleeding and promote healing of the ulcer . Miss. K send back to ward for

closed monitoring. After patient stable and no present of any complication she was
discharge. Medication was prescribed and appointment was fixed for repeat OGDS

procedure. Health education was given upon discharge.

CONCLUSION

From the case study I can learn more about gastric ulcer. An ulcer is a sore or

lesion that forms in the lining of the stomach or duodenum where the digestive fluids

acid and pepsin are present. Most ulcers develop as a result of infection with

bacteria called Helicobacter pylori (H. pylori). The bacteria produce substances

that weaken the stomach's protective mucus and make the stomach more

susceptible to damaging effects of acid and pepsin . H. pylori can also cause the

stomach to produce more acid.

Although acid and pepsin and lifestyle factors such as stress and smoking

cigarettes play a role in ulcer formation, H. pylori is now considered the primary

cause. Non-steroidal anti-inflammatory drugs such as aspirin make the stomach

vulnerable to the harmful effects of acid and pepsin, leading to an increased chance

of stomach ulcers.

Ulcers do not always cause symptoms. When they do, the most common

symptom is a gnawing or burning pain in the abdomen between the breastbone and

naval. Some people have nausea, vomiting, and loss of appetite and weight.

Bleeding from an ulcer may occur in the stomach and duodenum. Symptoms may

include weakness and stool that appears tarry or black. However, sometimes people

are not aware they have a bleeding ulcer because blood may not be obvious in the

stool. Ulcers are diagnosed usually by endoscopy. The presence of H. pylori may be

diagnosed with a blood test, Urea breath test, or tissue test.

Once an ulcer is diagnosed and treatment begins, the doctor will usually

monitor progress. Doctors treat ulcers with several types of medicines aimed at

reducing acid production, including H2-blockers, acid pump inhibitors, and

mucosal protective drugs. When treating H. pylori, these medications are used in

combination with antibiotics. Surgery may be necessary if an ulcer recurs or fails to

heal or if complications such as bleeding, perforation, or obstruction develop.

Although ulcers may cause discomfort, rarely are they life threatening. With

an understanding of the causes and proper treatment, most people find relief.

Eradication of H. pylori infection is a major medical advance that can permanently

cure most peptic ulcer disease.

Nevertheless, other cause such as NSAIDs, herbal medication cause of Miss

K in trouble with gastric duodenal ulcer.

BIBILIOGRAFI

http://.wikipedia.org/wiki/stomach

http://www.patient.co.uk/health/Stomach-(Gastric)-Ulcer.htm.Retrieved

http://www.webmd.com/digestive-disorders/digestive-diseases-peptic-

ulcer-disease.

http://www.about.com.biology
Amy carpenter Aquino, MS. Gastroenterology Nursing A Core

Curriculum: fourth edition; Society of Gastroenterology Nursing and

Associates, Inc.

John Hopkins: Manual of Gastrointestinal Endoscopic Procedures,

second edition; SLACK Incorporated.

Peter B Cotton, Christopher B .Williams, Robert H. Hawes, Brian P.

Saunders: Practical Gastrointestinal Endoscopy, sixth edition; The

Fundamental.