GI

Peptic Ulcer • An Ulcer is … Erosion in the lining of the stomach or the first part of the small
intestine, an area called the duodenum. Ulcers damage the mucosa of the alimentary tract, which
extends through the muscularis mucosa into the sub mucosa or deeper.
4. Ulcers that form in the stomach are called gastric ulcers; in the duodenum, they are called
duodenal ulcers. Both types are referred to as peptic ulcers.
5. Peptic UlcerPeptic Ulcer
6. • The gastroduodenal mucosal integrity is determined by protective (defensive) & damaging

(aggressive) factors.
7. Mucosal damage erosions & ulcerations
8. Causes gastric and duodenal ulcer • In the past it was believed lifestyle factors, such as stress and
diet caused ulcers. Later, researchers determined that stomach acids -- hydrochloric acid and pepsin --
contributed to ulcer formation. • Today, research shows that most ulcers (80 percent of gastric ulcers
and 90 percent of duodenal ulcers) develop as a result of infection with a bacterium called
Helicobacter pylori (H. pylori). • It is believed that, although all three of these factors -- lifestyle, acid
and pepsin, and H. pylori -- play a role in ulcer development, H. pylori is considered to be the primary
cause.
9. Cont…
10. Factors in the development of peptic ulcers • Factors for the development of peptic ulcers include:
• Helicobacter pylori Research shows that most ulcers develop as a result of infection with bacterium
called Helicobacter pylori (H. pylori). The bacterium produces substances that weaken the stomach's
protective mucus and make it more susceptible to the damaging effects of acid and pepsin, as well as
produce more acid.
11. Conti…. • Smoking: Studies show smoking increases the chances of getting an ulcer, slows the
healing process of existing ulcers, and contributes to ulcer recurrence. • Caffeine: Caffeine seems to
stimulate acid secretion in the stomach, which can aggravate the pain of an existing ulcer. However,
the stimulation of stomach acid cannot be attributed solely to caffeine
12. Conti… • Alcohol no proven link between alcohol consumption and peptic ulcers, ulcers are more
common in people who have cirrhosis of the liver, a disease often linked to heavy alcohol
consumption. • Stress Although emotional stress is no longer thought to be a cause of ulcers, people
with ulcers often report that emotional stress increases ulcer pain.
13. Conti… • Acid and pepsin It is believed that the stomach's inability to defend itself against the
powerful digestive fluids, hydrochloric acid and pepsin, contributes to ulcer formation. • Nonsteroidal
anti-inflammatory drugs (NSAIDs) These drugs (such as aspirin, ibuprofen, and naproxen sodium)
make the stomach vulnerable to the harmful effects of acid and pepsin. They are present in many
non-prescription medications used to treat fever, headaches, and minor aches and pains.
14. Symptoms of gastric and duodenal ulcer • The following are the most common symptoms for
ulcers, however, each individual may experience symptoms differently. • Belching • Nausea •
Vomiting • Poor appetite • Loss of weight • Feeling tired and weak
15. Complication of ulcer • Bleeding. • Perforation. • Narrowing and obstruction.
16. Diagnosis • Diagnostic procedures include: • Barium Swallow • Endoscopy - a small flexible
instrument with a camera on the end is inserted through the mouth into the esophagus, stomach, and
duodenum to view the entire upper GI tract. • Blood tests - performed to detect the presence of H.
pylori.
17. Treatment • Lifestyle changes: In the past, physicians advised people with ulcers to avoid spicy,
fatty, or acidic foods. • Smoking: Smoking has been shown to delay ulcer healing and has been linked
to ulcer recurrence; therefore, people with ulcers should not smoke.
18. Conti… • Medications: Physicians treat stomach and duodenal ulcers with several types of
medications, including: • H2-blockers to reduce the amount of acid the stomach produces by blocking
histamine, a powerful stimulant of acid secretion. E.g. Cimetidine, Ranitidine, and Famotidine. •
Proton pump inhibitors to more completely block stomach acid production by stopping the stomach's
acid pump -- the final step of acid secretion. E.g. Omeprazol.
19. Cont… • Mucosal protective agents to shield the stomach's mucous lining from the damage of acid,
but do not inhibit the release of acid. E.g. Bismuth, Sucralfate • When treating H. pylori, these
medications are often used in combination with antibiotics. • Antibiotics: The discovery of the link
between ulcers and H. pylori resulted in a probable new treatment option -- antibiotics for patients
with H. pylori.
20. H. pylori Therapy: • Triple therapy: Proton pump inhibitor Clarithromycin Amoxicillin.
21. Surgery • At present, surgery is performed to treat ulcers. Types of surgery include: • Vagotomy •
Pyloroplasty • Antrectomy
22. Vagotomy • Vagotomy: a surgical operation in which one or more branches of the vagus nerve are
cut, typically to reduce the rate of gastric secretion (e.g. in treating peptic ulcers).
23. Pyloroplasty • Pyloroplasty is surgery to widen the opening in the lower part of the stomach
(pylorus) so that stomach contents can empty into the small intestine (duodenum). The pylorus is a
thick, muscular area. When it thickens, food cannot pass through.
24. Antrectomy • Surgical removal of the walls of an antrum, especially the antrum of the stomach.
25. Nursing diagnosis • Pain related to the wound in the stomach, primary to HCl secretion. •
Vomiting related to indigestion of food. • Loss appetite related to ulceration of the stomach. • Loss of
weight related decreased nutrients intake secondary to peptic ulcer. • Stress and anxiety related to
disease process.
26. Nursing interventions. • Support the patient emotionally. • Administer prescribed medications. •
Provide small meals a day or small hourly meals as ordered. • Schedule care so that the patient gets
plenty of rest. • Monitor the effectiveness of administered medications, and also watch for adverse
reactions. • Assess the patient’s nutritional status and the effectiveness of measures used to maintain
it. Weigh him regularly.
27. Cont… • Teach the patient about peptic ulcer disease, and help him to recognize its signs and
symptoms. • Instruct the patient to take antacids 1 hour after meals. • Warn the patient to avoid
aspirin containing drugs because they irritate gastric.
Break in the gastrointestinal mucosaexposed to the aggressive action of acid-peptic juices. Common
sites are the first part of the duodenum and the lesser curve of the stomach.
4. The gastroduodenal mucosal integrity isdetermined by protective (defensive) &damaging

(aggressive) factors.
5. • Bicarbonate • Helicobacter pylori• Mucus layer • NSAIDs• Prostaglandins • Pepsins• Mucosal

blood flow • Bile acids• Epithelial renewal • Smoking and alcoholDefensive Aggressive Mucosal
damage erosions & ulcerations
6. H. Pylori Infection NSAIDs Smoking & Alcohol Acid Hypersecretion StressFamily History of PUD.
7. Duodenal Ulcer Gastric ulcer Age Any age specially 30-40 middle age 50-60 Sex More in male More
in maleOccupation Stress job eg. Manager Same Pain Epigastric , discomfort Epi. Can radiate to back
Onset 2-3 hours after eating & Immediately after midnight eating Agg.by Hunger Eating
8. Duodenal Ulcer Gastric ulcerRelived by Eating Lying down or vomitingDuration 1-2 months Few
weeksVomiting Uncommon Common(to relieve the pain)Appetite Good Pt. afraid to eatDiet Good ,
eat to relieve the pain Avoid fried foodWeight No wt. loss wt. LossHematemesis 40% 60%Melena 60%
40%
9. Stool fecal occult blood.CBC CBL.Rapid Urease test, ureabreath test H. Pylori.Upper GI
Endoscopy.Barium meal X-Ray.
10. Any patient >50 y/o with new onset of symptoms In all patients with “Alarmingsymptoms”
endoscopy is required. Dysphagia. Weight loss. Vomiting. Anorexia. Hematemesis or Melena.
11. Life Style Change.Medical.Surgical.
12. Discontinue NSAIDsSmoking cessation. Alcohol cessation. Stress reduction.
13. Antacids H2-receptor blocking agents. Proton pump inhibitors. Cytoprotective and
antisecretory drugs. Antibiotics.
14. H. pylori Eradication Therapy:• Triple therapy: Proton pump inhibitor . 2 Antibiotics: •
Metronidazole + Clarithromycin. • Clarithromycin + Amoxicillin. » In some regimens, H2-receptor
blockers, e.g. ranitidine, are used instead of PPI.
15. Indications: Failure of medical treatment. Development of complications High level of gastric
secretion and combined duednal and gastric ulcer. Principle: Reduce acid and pepsin secretion.
16. Vagotomy: Truncal Vagotomy with drainage. Highly selective Vagotomy. Combination of vagal
denervation (vagotomy) + anterctomy.
17. Truncal vagotomy with drainage:Resect the major trunk of the vagus tothe stomach this will lead
to: Decrease acid and pepsin secretion. Impair antral motility and drainage. – Two types of drainage:
Pyloroplasty. Gastrojejnostomy.
18. Highly selective vagotomy: • It is a parietal cells vagotomy. • It can be done with or without
drainage. • It is done by cut a branch of vagus of the body and the fundus this will lead to decrease
HCl production.
19. Combination of vagotomy+anterctomy: Combination of vagal denervation & removal of the major
area of gastric production.
20. Gastrointestinal continuity is restored bygastroduodenal (Billroth 1) anastomosisOR gastrojejunal

(Billroth 2)anastomosis.
21. Dehiscence. Stenosis of anastomosis. Bleeding. Injury to neighbour tissues. Dumping

syndrome
22. HemorrhagePerforation peptic ulcerGastric outlet obstruction
reatment of Peptic Ulcer 1) Reduction of gastric acid secretion A) H2 antihistamines- (R2FC) Ranitidine,
Roxatidine, Famotidine, Cimetidine. B) Proton Pump Inhibitors (PPI)- (PRO-LE) Pantoprazole,
Rabeprazole, Omeprazole, Lansoprazole, Esomeprazole. C) Anticholinergics -(PPO) Pirenzepine,
Propantheline, Oxyphenonium. D) Prostaglandin Analogue- Misoprostol
15. Treatment of Peptic Ulcer Cont… 2) Neutralization of Gastric acid (Antacids)- a) Systemic- Sod. bi
carbonate, Sod. Citrate. b) Nonsystemic- Mag Hydroxide, Mag tricilicate, Al hydroxide gel, Calcium
carbonate, Magaldrate. 3) Ulcer Protectives- Sucralfate, Collidal bismuth subcitrate. 4) Anti
Helicobacter pylori Drugs- Amoxicillin, Clarithromycin, Metronidazole, Tinidazole, Tetracycline.
istamine Receptors •H1 receptors – Smooth muscle – Nerves •H2 receptors – Parietal cells
17. Histamine H2 Antagonists Decrease Acid Output Histamine Protein Kinase ATP cAMP K+ H+
Histamine Antagonist PP
18. 1. Reduction of gastric acid secretion Histamine H2 Antagonists 4 drugs are available- Ranitidine,
Roxatidine, Famotidine & Cimetidine. & have competitive interaction with H2 receptors. Cimetidine
was the 1st H2blocker to be introduced & Prototype.. All H2 antagonist block histamine induced
gastric secretion. The ulcer healing dose produces 60-70% inhibition of 24 hr acid output.
Cimetidine is absorbed orally (bioavailability is 60-80% d/t 1st pass hepatic metabolism). Mild
adverse effects in 5% is common- headache, dizziness, bowel upset, CNS effects- restlessness,
19. Drugs for Acid-Peptic Disorders - Cimetidine Additional Side effects: • In some patients, cimetidine
acts as a nonsteroidal antiandrogen (i.e., interferes with estrogen metabolism). decrease in male
sexual function gynecomastia (swelling of the breasts and soreness of the nipples in males) • Can
produce confusion and disorientation in elderly patients; • Diarrhea, rash and miscellaneous other
effects in a small number of patients.
20. Interactions- Antacids reduces absorption of all H2 blockers. A gap of 2 hr is recommended for
concurrent use with antacids. Cimetidine dose – 400mg BD or 800mg HS. Orally for stress ulcer –
50mg/hr IV Ranitidine 5 times more potent than cimetidine with a lower incidence of side effects.
Dose – 150 mg BD or 300mg HS or 50mg IM / slow IV in 6-8 hr. Roxatidine- Pk, Pd & side effect
profile is similar to Ranitidine bt its twice as potent & longer acting. Dose – 75 mg BD or 150 mg HS
21. Famotidine- It is 5-8 times more potent than ranitidine Dose- 20 mg BD or 40 mg HS or 20mg
I.V. / 12 hr. Proton Pump Inhibitors (PRO-LE) Omeprazole- Inhibits final common step in gastric acid
secretion & have overtaken H2 blockers for acid –peptic disorders. Bioavailability of all PPIs is
reduced by food, hence they should be taken as empty stomach. Uses- Duodenal Ulcers, Gastric
Ulcers, Stress Ulcers, GERD (gastroesophageal reflux disesse) Dose- 40mg/Day
22. Interaction- Omeprazole inhibits oxidation of certain drugs like Diagepam, Phenytoin and
warfarin levels may be increased. Clarithromycin inhibits omeprazole metabolism & increases its
plasma concentration. Esomeprazole- It is S-enantiomer of omeprazole, have higher bioavailability
& to produce better control of intragastric pH than omeprazole in GERD. Dose- 20-40 mg OD
23. Lansoprazole More potent than omeprazole. Higher bioavailability. Dose should be reduced in
liver diseases. Side effects are similar bt drug interactions are less significant. Dose- 15-30 mg OD.
Pantoprazole It is more acid stable & has higher bioavilability. It is also available for I.V.
Administration. Dose- 20mg OD.
24. Strategies for Inhibiting Parietal Cell Acid Secretion Gastrin Histamine Acetylcholine Ca2+ Protein
Kinase ATP cAMP Prostaglandin Agonists (-) K+ H+ PP H2M3 CCK2 EP3 Ca2+
25. Drugs for Acid-Peptic Disorders - Prostaglandins Misoprostol (Cytotec): • Synthetic Analog of
Prostaglandin E1 • Anti-acid secretory • 0.1 to 0.2 mg results in 85% to 95% acid reduction •
Prevention of NSAID gastric ulcers Side Effects • Diarrhea • Abortion • Exacerbate IBD and should not
be given
26. Neutralization of gastric acid Drugs for Acid-Peptic Disorders - Antacids • Antacids are weak bases
that neutralize HCl in the stomach; • They do not decrease the secretion of acid, and in some cases
increase secretion; • They do not suppress nocturnal acid secretion 1. Neutralize acid 2. Decrease acid
load to duodenum 3. Diminish pepsin activity
27. Drugs for Acid-Peptic Disorders - Antacids • Magnesium hydroxide • Magnesium trisilicate •
Magnesium-aluminum mixtures • Calcium carbonate • Sodium bicarbonate
28. Characteristics of Common Antacids Feature Sodium Bicarbonate Calcium Magnesium Hydroxide
Aluminum Onset of action rapid intermediate rapid slow Duration of action short moderate moderate
moderate Systemic alkalosis yes ? no no Effect on stool --- constipating laxative constipating
29. Ulcer Protectives Drugs for Acid-Peptic Disorders – Sucralfate • Sucralfate is a basic aluminum salt
of sucrose octasulfate; • In the presence of acid (pH < 3-4) some of the aluminum ions dissociate and
the resulting negatively charged molecule polymerizes to form a viscous paste-like substance; • This
substance adheres strongly to gastric and duodenum mucosa and adheres even more strongly to
partially denatured proteins such as those found at the base of the ulcer.
30. Drugs for Acid-Peptic Disorders - Sucralfate (Carafate) •This compound does not decrease the
concentration or total amount of acid in the stomach; •Sucralfate protects the gastric and duodenal
mucosa from acid/pepsin attack. Side effects: • The compound is not really absorbed and, therefore,
side-effects are minimal: – constipation – diarrhea – nausea
31. Anti H. pylori drugs • Helicobacter Pylori (H. pylori) –Most ulcers are the result of infection with H.
pylori –Not all of those infected with H. pylori develop ulcers – H. pylori MAY result in a weakening of
the mucosal defense systems, allowing for development of ulcer subsequent to acid/pepsin
aggression; by producing ammonia which maintains a neutral micro environment around the bacteria
& promotes back diffusion of H+ions.
32. Helicobacter pylori Spiral shaped, flagellated, Gram negative bacterium
33. Helicobacter pylori on gastric mucus- secreting epithelial cells
34. Role of H. pylori in Peptic Ulcer Disease •The host reaction to H. pylori determines the outcome of
the infection: – Gastritis – GERD – Gastric & Duodenal Ulcers – Gastric Cancer (?)
35. Role of H. pylori in Peptic Ulcer Disease •Treatment –If H. pylori detected, eradication of the
bacteria, along with inhibition of acid. –Eradication of H. pylori is a cure as reinfection rates in
Western countries is less than 1%.
36. Role of H. pylori in Peptic Ulcer Disease •Combination therapy with Omeprazole and Amoxycillin
37. H. pylori Eradication Rates with Either Dual, Triple or Quad Therapy (1999) Treatment Pooled
Eradication Rate Dual Therapy 72% Triple Therapy 85% Quad Therapy 90%
38. H. pylori Eradication Rates with Either Dual, Triple or Quad Therapy (1999) GENERIC NAME
DOSING DURATION CURE RATE (%) Dual therapies omeprazole 500 mg TID 14 days 70-80 amoxycillin
1,000 mg TID 14 days ranitidine 400 mg BID 28 days 73-84 clarithromycin 500 mg TID 14 days
lansoprazole 30 mg TID 14 days 66-77 amoxycillin 1,000 mg TID 14 days
39. H. pylori Eradication Rates with Either Dual, Triple or Quad Therapy (1999) Cont. GENERIC NAME
DOSING DURATION CURE RATE (%) Triple therapies lansoprazole 30 mg BID 14 days 86-92 amoxycillin
1,000 mg BID 14 day clarithromycin 500 mg BID 14 days
40. H. pylori Eradication Rates with Either Dual, Triple or Quad Therapy (1999) Cont. GENERIC NAME
DOSING DURATION CURE RATE (%) Quad therapies bismuth subsalicylate Two tablets 7 days 85-95
525 mg QID metronidazole 250 mg QID 7 days tetracycline 500 mg QID 7 days omeprazole 20 mg BID
7 days or lansoprazole 30 mg BID 7 days
41. New Strains of H. pylori • Recently a more virulent genetic strain of H. Pylori known as
cytotoxin-associated gene A (cagA) has been found in some people with peptic ulcers
42. Functional Disorders of the GI • Primary –infection, inflammation, congenital defects (disorders of
the neuronal/muscular activity); • Secondary –metabolic disorders (hypo- or hyper-parathyroidism,
hypercalcemia), neurologic (diabetes mellitus - damage to vagal and sympathetic extrinsic nerves,
intrinsic nerves; MS, heavy metal toxicity, carcinoma); • Examples of colonic dysfunction: –IBS;
chronic constipation; Hirschsprung’s disease (agangliosis of myenteric plexus); sphincter dysfunction,
etc.
SYMPTOMS <ul><li>Burning abdominal pain </li></ul><ul><li>Haematemesis

</li></ul><ul><li>Melena </li></ul><ul><li>Nausea or vomiting </li></ul><ul><li>Unexplained weight
loss </li></ul><ul><li>Anorexia </li></ul><ul><li>Abdominal fullness </li></ul>
13. DIAGNOSIS <ul><li>Endoscopy: </li></ul><ul><li>Flexible tube fitted with camera is threaded

down the esophagus in to stomach to see the ulcer by physician </li></ul><ul><li>Barium meal:
</li></ul><ul><li>Barium liquid is drunk making ulcer visible on X-ray </li></ul>
14. <ul><li>Test for diagnosing H.pylori </li></ul><ul><li>Breath test :by measuring the amount of co
2 in exhaled breath. </li></ul><ul><li>Blood test : by identifying H.pylori antibodies by ELISA test.
</li></ul><ul><li>Stool test :stool sample tested with H.pylori antigen. </li></ul>
15. LIFE-STYLE MODIFICATION IN PUD <ul><li>Doubtful efficacy </li></ul><ul><ul><li>REST

</li></ul></ul><ul><ul><li>RELAXATION </li></ul></ul><ul><ul><li>GOOD SLEEP
</li></ul></ul><ul><ul><li>DIET INDICATION </li></ul></ul><ul><ul><ul><li>Balanced diet
</li></ul></ul></ul><ul><ul><ul><li>Frequent small meal </li></ul></ul></ul><ul><ul><ul><li>fiber
</li></ul></ul></ul><ul><ul><ul><li>vitamin E and dietary fatty acids
</li></ul></ul></ul><ul><ul><ul><li>fat diet </li></ul></ul></ul><ul><ul><li>CONTRAINDICATION
</li></ul></ul><ul><ul><ul><li>caffeine-containing beverages
</li></ul></ul></ul><ul><ul><ul><li>spices </li></ul></ul></ul><ul><ul><ul><li>Alcohol
</li></ul></ul></ul>
16. ANTI ULCER DRUGS <ul><li>REDUCTION OF GASTRIC ACID SECRETION </li></ul><ul><li>Histamine

antagonist : Cimetidine, ranitidine </li></ul><ul><li>Proton pump inhibitors : omeprazole,
pantaprazole </li></ul><ul><li>Acetyl choline antagonist : pirenzepine, propantheline
</li></ul><ul><li>Prostaglandin analogue : misoprostol </li></ul>
17. ANTIULCER DRUGS <ul><li>Neutralization of gastric acid(antacids) Systemic : Sodium bicarbonate,

Sodium citrate </li></ul><ul><li>Nonsystemic : Magnesium hydroxide , Aluminium hydroxides
</li></ul><ul><li>Ulcer protectives : Sucralfate </li></ul><ul><li>Anti helicobacter pylori: amoxicillin,
clarithromycin etc </li></ul>
18. HISTAMINE ANTAGONIST <ul><li>Cimetidine </li></ul><ul><li>.Histamine antagonists inhibit the

action of histamine on the acid-producing cells of the stomach and reduce stomach acid </li></ul>
19. CIMETIDINE <ul><li>SIDE EFFECTS ; it include constipation , diarrhea, fatigue , headache, insomnia,
muscle pain, and vomiting. Major side effects include confusion and hallucinations, gynacomastia
(enlargement of the breasts); impotence. </li></ul><ul><li>USES: it is used in treatment of duodenal
ulcer, </li></ul><ul><li>Gastric ulcer, stress ulcer, GERD, zollinger ellison syndrome </li></ul>
20. PROTON PUMP INHIBITORS <ul><li> </li></ul><ul><li>Proton pump inhibitors act by irreversibly
blocking the hydrogen/potassium adenosine triphosphatase enzyme system of the gastric parietal
cells. </li></ul><ul><li>The proton pump is the terminal stage in gastric acid secretion </li></ul>
21. PROTON PUMP INHIBITORS <ul><li>OMEPRAZOLE </li></ul><ul><li>Omeprazole is inactive at

neutral pH, but at pH<5 rearranges to two charged cationic forms(a sulphenic acid and a
sulphenamide configurations)that react covalently with SH groups of the H + K + ATPase enzyme and
inactivate it irreversibly, especially when two molecules of omeprazole react with one molecule of the
enzyme </li></ul><ul><li>SIDE EFFECTS Stomach pain, Diarrhea,Constipation,Dizziness,Pain,Hives,
Itching,seizures </li></ul>
22. ACETYL CHOLINE ANTAGONIST <ul><li>PIRENZEPINE </li></ul><ul><li>MECHANISM:

</li></ul><ul><li>It selectively block M1 muscaranic recptors and inhibits gastric secretion.
</li></ul><ul><li>Because of their relatively poor efficacy, side effects, and risk of blood disorders,
they are rarely used today </li></ul>
23. AGENTS THAT ENHANCE MUCOSAL DEFENSE <ul><li>Prostaglandin Analogs:

</li></ul><ul><li>prostaglandins are produced in the gastric </li></ul><ul><li>mucosa and appear to
serve a protective role by inhibiting acid secretion and promoting mucus </li></ul><ul><li>and
bicarbonate secretion. </li></ul><ul><li>In addition, PGs inhibits gastrin production, increase mucosal
blood flow and probably have an ill defined cytoprotective action. </li></ul><ul><li>DRUGS :
Misoprostol </li></ul>
24. MISOPROSTOL <ul><li>MECHANISM: </li></ul><ul><li>Misoprostol acts upon gastric parietal cells ,

inhibiting the secretion of gastric acid via G-protein coupled receptor-mediated inhibition of
adenylate cyclase , which leads to decreased intracellular cyclic AMP levels and decreased
</li></ul><ul><li>pump activity at the apical surface of the parietal cell </li></ul><ul><li>Side effects
</li></ul><ul><li>Diarrhea. </li></ul><ul><li>Other common side effects include: abdominal pain,
nausea, flatulence, headache, dyspepsia, vomiting, and constipation. </li></ul>
25. ULCER PROTECTIVES <ul><li>SUCRALFATE </li></ul><ul><li>MECHANISM:

</li></ul><ul><li>Sucralfate is a locally acting substance that in an acidic environment (pH < 4), reacts
with hydrochloric acid in the stomach to form a cross-linking, viscous , paste-like material capable of
acting as an acid buffer for as long as 6 to 8 hours after a single dose . It also attaches to proteins on
the surface of ulcers, such as albumin and fibrinogen , to form stable insoluble complexes. These
complexes serve as protective barriers at the ulcer surface, preventing further damage from acid ,
pepsin , and bile . </li></ul>
26. <ul><li>Side effects </li></ul><ul><li>The most common side effects seen are constipation . Less
commonly reported include flatulence, cephalalgia (headache), xerostomia (dry mouth).
</li></ul><ul><li>USES: </li></ul><ul><li>It is used in treatment of </li></ul><ul><li>Gastritis,
</li></ul><ul><li>Stress ulcers. </li></ul>
27. SODIUM BICARBONATE (ANTACID) <ul><li>It is water soluble, acts instantaneously, but duration
of action is short. It is a potent neutralizer , pH may raises above 7. </li></ul><ul><li>Adverse
reactions </li></ul><ul><li>It causes systemic alkalosis, gastric distention, rebound acidity and
milk-alkali syndrome </li></ul><ul><li>Uses </li></ul><ul><li>It is restricted to casual treatment of
heartburn and to treat acidosis </li></ul>
28. ANTI H.PYLORI DRUGS <ul><li>Anti microbials that have been found clinically effective against
H.pylori are: amoxicillin, clarithromycin, tetracycline and metronidazole. </li></ul><ul><li>A
combination regimen is preferred, using gastric acid inhibitors and antibiotics.
</li></ul><ul><li>Example: </li></ul><ul><li>A proton pump inhibitor or H2 blocker + amoxicillin +
clarithromycin or metronidazole </li></ul>
H. pylori Gram (-) rod Associated with gastritis, gastric & duodenal ulcers, gastric adenocarcinoma
Transmission route fecal-oral Secretes urease → convert urea to ammonia Produces alkaline
environment enabling survival in stomach Higher prevalence in Low SES
43. Who are they ? Barry J Marshall J. Robin Warren Nobel Laureates of Medicine – 2005 Discovery of
H. pylori & its role in peptic ulcer
44. Triple Therapy The BEST among all the Triple therapy regimen is: Omeprazole / Lansoprazole - 20 /
30 mg bd Clarithromycin - 500 mg bd Amoxycillin / Metronidazole - 1gm / 500 mg bd Given for 14
days followed by P.P.I for 4 – 6 weeks Short regimens for 7 – 10 days not very effective
45. Other 2 weeks regimen(mg) Amoxicillin 750/ + Tinidazole 500 +omeprazole 20 mg/ lansoprazole
30 mg BD clarithromycin 250 + Tinidazole 500/amoxicillin 1000 + lansoprazole 30 mg BD
. Classification of drugs used in peptic ulcer 1. Drugs that inhibit gastric acid secretion 2. Drugs that neutralize
gastric acid (Antacids) 3. Ulcer protectives 4. Anti H. pylori drugs
. 7. Classification (Contd.) Drugs that inhibit gastric acid secretion H2 receptor blockers: Cimetidine,
Ranitidine, Famotidine Proton pump inhibitors: Omeprazole, Pantoprazole, esomeprazole
Anticholinergics : Pirenzepine Prostaglandin analogues: Misoprostol
. 8. Classification (Contd..) Drugs that neutralize gastric acid (Antacids) Systemic: • Sodium bicarbonate,
sodium citrate Non systemic: • Magnesium hydroxide, Mag. Trisilicate, Aluminium hydroxide gel,
Magaldrate
. 9. Classification (Contd..) Ulcer protectives Sucralfate Colloidal Bismuth Sulfate (CBS) Anti H.
pylori drugs Amoxicillin, Clarithromycin, Metronidazole, Tinidazole, Tetracycline
. 10. H2 ANTAGONISTS
. 11. Mechanism of action Competitively block H2 receptors on parietal cell & inhibit gastric acid production
Supress secretion of acid in all phases but mainly nocturnal acid secretion Also reduce acid secretion
stimulated by Ach, gastrin, food, etc.
. 12. Pharmacokinetics Absorption is not interfered by food Can cross placental barrier and reaches milk,
Poor CNS penetration The serum half-lives range from 1.1 to 4 hours; Cleared by a combination of
hepatic metabolism, glomerular filtration, and renal tubular secretion. Dose reduction needed in moderate
to severe renal insufficiency
. 13. Bioavailability 80 50 40 >90 Relative Potency 1 5 -10 32 5 -10 Half life (hrs) 1.5 - 2.3 1.6 - 2.4 2.5 - 4 1.1
-1.6 DOA (hrs) 6 8 12 8 Inhibition of 1 0.1 0 0 CYP 450 Dose mg (bd) 400 150 20 150 Cimetidine Ranitidine
Famotidine Nizatidine Comparison of H2 antagonists
. 14. H2 antagonists - Uses Promote the healing of gastric and duodenal ulcers Duodenal ulcer – 70 to 90%
at 8 weeks Gastric Ulcer – 50 to 75% NSAID ulcers induced ulcers Stress ulcer and gastritis GERD
Zollinger-Ellison syndrome Prophylaxis of aspiration pneumonia
. 15. Adverse effects Headache, dizziness, bowel upset, dry mouth CNS: Confusion, restlessness
Bolus IV – release histamine – bradycardia, arrhythmia, cardiac arrest Cimetidine has antiandrogenic
actions
. 16. Drug interactions Cimetidine inhibits several CYP-450 isoenzymes and reduces hepatic blood flow, so
inhibits metabolism of many drugs like theophylline, metronidazole, phenytoin, imipramine etc. Antacids
reduce the absorption of all H2 blockers
. 17. Proton Pump Inhibitors Most effective drugs in antiulcer therapy Prodrugs requiring activation in
acid environment Activated forms binds irreversibly to H+K+ATPase and inhibit it Omeprazole
Pantoprazole Lansoprazole Esomeprazole
. 18. Mechanism of Action Prodrugs inactive at neutral pH At pH < 5 rearranges to two charged cationic
forms (sulfenamide + sulphenic acid) that bind covalently with SH groups of H⁺ K⁺ ATPase and inactivate it
irreversibly Also inhibits gastric mucosal carbonic anhydrase
. 19. Pharmacokinetics - PPI Available as enteric coated tablets They should be given 30 minutes to 1
hour before food intake half life is very short and only 1-2 Hrs Still the action persists for 24 Hrs to 48 hrs
after a single dose Action lasts for 3-4days even after stoppage of the drug
. 20. PPI – contd. Therapeutic uses: 1. Gastroesophageal reflux disease (GERD) 2. Peptic Ulcer - Gastric
and duodenal ulcers 3. Bleeding peptic Ulcer 4. Zollinger Ellison Syndrome 5. Prevention of recurrence of
nonsteroidal antiinflammatory drug (NSAID) - associated gastric ulcers in patients who continue NSAID use.
6. Reducing the risk of duodenal ulcer recurrence associated with H. pylori infections 7. Aspiration
Pneumonia
. 21. Comparative success of therapy with PPI and H2 antagonist
. 22. Adverse Effects Nausea, loose stools, headache abdominal pain, constipation, Muscle & joint pain,
dizziness, rashes Rare Gynaecomastia, erectile dysfunction Leucopenia and hepatic dysfunction
Osteoporosis in elderly on prolonged use Hypergastrinemia
. 23. Drug interactions Omeprazole inhibits the metabolism of warfarin, phenytoin, diazepam, and
cyclosporine. However, drug interactions are not a problem with the other PPIs.
. 24. PPI – Dosage schedule Omeprazole 20 mg o.d. Lansoprazole 30 mg o.d. Pantoprazole 40 mg o.d.
Rabeprazole 20 mg o.d. Esomeprazole 20-40 mg o.d
. 25. Proton Pump Inhibitors Lansoprazole : Partly reversible, more potent, slightly more against H pylori,
Higher BA, rapid onset. Pantoprazole: More acid stable, I.V, CYP450 less affinity Rabeprazole:
claimed to most rapid Es-omeprazole Better intragastric pH , higher healing rates.
. 26. Muscarinic antagonists Block the M1 class receptors Reduce acid production, Abolish
gastrointestinal spasm Pirenzepine and Telenzepine Reduce meal stimulated HCl secretion by reversible
blockade of muscarinic (M1) receptors on the cell bodies of the intramural cholinergic ganglia Unpopular
as a first choice because of high incidence of anticholinergic side effects (dry mouth and blurred vision)
. 27. Prostaglandin analogues- Misoprostol Inhibit gastric acid secretion Enhance local production of
mucus or bicarbonate Help to maintain mucosal blood Therapeutic use: Prevention of NSAID-induced
mucosal injury (rarely used because it needs frequent administration – 4 times daily)
. 28. Misoprostol Doses: 200 mcg 4 times a day ADRs: Diarrhoea and abdominal cramps Uterine
bleeding Abortion Exacerbation of inflammatory bowel disease and should be avoided in patients with
this disorder Contraindications: 1. Inflammatory bowel disease 2. Pregnancy (may cause abortion)
. 29. Antacids Weak bases that neutralize acid Also inhibit formation of pepsin (As pepsinogen converted
to pepsin at acidic pH) Acid Neutralizing Capacity: Potency of Antacids Expressed in terms of Number
of mEq of 1N HCl that are brought down to pH 3.5 in 15 minutes by unit dose of a preparation (1 gm)
. 30. Systemic antacids Sodium Bicarbonate: Potent neutralizing capacity and acts instantly ANC: 1
gm = 12 mEq DEMERITS: Systemic alkalosis Distension, discomfort and belching – CO2 Rebound
acidity Sodium overload
. 31. Non systemic antacids Insoluble and poorly absorbed basic compounds React in stomach to form
corresponding chloride salt The chloride salt again reacts with the intestinal HCO3- so that HCO3- is not
spared for absorption
. 32. Non systemic Antacids Magnesium hydroxide (ANC 30 mEq) Aqueos suspension is called Milk of
magnesia Magnesium trisilicate (ANC 10 mEq) Aluminium Hydroxide (ANC 1-2.5mEq/g) (Magaldrate –
hydrated hydroxy magnesium aluminate)
. 33. Non systemic antacids Duration of action : 30 min when taken in empty stomach and 2 hrs when taken
after a meal Adverse effects: Aluminium antacids – constipation (As they relax gastric smooth muscle &
delay gastric emptying) – also hypophosphatemia and osteomalcia Mg2+ antacids – Osmotic diarrhoea
In renal failure Al3+ antacid – Aluminium toxicity & Encephalopathy
. 34. Miscellaneous drugs Simethicone: Decrease surface tension thereby reduce bubble formation -
added to prevent reflux Alginates: Form a layer of foam on top of gastric contents & reduce reflux
Oxethazaine: Surface anaesthetic
. 35. Chemical reactions of antacids with HCl in the stomach
. 36. Drug interactions By raising gastric pH & forming insoluble complexes ↓ absorption of many drugs
Tetracyclines, iron salts, H2 Blockers, diazepam, phenytoin, isoniazid, ethambutol
. 37. Sucralfate – ulcer protective Aluminium salt of sulfated sucrose MOA: In acidic environment ( pH
<4) it polymerises by cross linking molecules to form sticky viscous gel that adheres to ulcer crater - more on
duodenal ulcer Astringent action and acts as physical barrier Dietary proteins get deposited on this layer
forming another coat
. 38. Sucralfate – contd. Concurrent antacids avoided, (as it needs acid for activation) Uses:
Prophylaxis of Stress ulcers Bile reflux gastritis Topically – burn, bedsore ulcers, excoriated skins
Dose: 1 gm 1 Hr before 3 major meals and at bed time for 4-8 weeks ADRs: Constipation,
hypophosphatemia Drug interactions : adsorbs many drugs and interferes with their absorption
. 39. Colloidal Bismuth Subcitrate (CBS) Mechanism of action CBS and mucous form glycoprotein bi
complex which coats ulcer crater ↑ secretion of mucous and bicarbonate, through stimulation of mucosal
PGE production Detaches H.pylori from surface of mucosa and directly kills them
. 40. Colloidal Bismuth subcitrate Dose: 120 mg 4 times a day Adverse effects blackening of tongue,
stools, dentures Prolonged use may cause osteodystrophy and encephalopathy Diarrhoea, headache,
dizziness
. 41. Eradication of H.pylori No acid No ulcer OLD TESTAMENT No HP No ulcer NEW TESTAMENT
. 42. H. pylori Gram (-) rod Associated with gastritis, gastric & duodenal ulcers, gastric adenocarcinoma
Transmission route fecal-oral Secretes urease → convert urea to ammonia Produces alkaline
environment enabling survival in stomach Higher prevalence in Low SES
Peptic ulcers are produced by an imbalance between the gastroduodenal mucosal defense mechanisms and
damaging forces of gastric acid and pepsin, combined with superimposed injury from environmental or immunologic
agents. ♥The mucous membrane lining the digestive tract erodes and causes a gradual breakdown of tissue. This
breakdown causes a gnawing or burning pain in the upper middle part of the belly (abdomen).
lassification ₪ Stomach (called gastric ulcer) ₪ Duodenum (called duodenal ulcer) ₪ Oesophagus (called
Oesophageal ulcer) ₪ Types of peptic ulcers: ₪ Type I: Ulcer along the lesser curve of stomach ₪ Type II: Two ulcers
present - one gastric, one duodenal ₪ Type III: Prepyloric ulcer ₪ Type IV: Proximal gastroesophageal ulcer ₪ Type V:
Anywhere.
. YMPTOMS
. 10. Gastric versus duodenal ulcer — Although there is much overlap, symptoms of a gastric ulcer may be
different than those of a duodenal ulcer. Duodenal ulcer — "Classic" symptoms of a duodenal ulcer include
burning, gnawing, aching, or hunger-like pain, primarily in the upper middle region of the abdomen below the
breastbone (the epigastric region). Pain may occur or worsen when the stomach is empty, usually two to five
hours after a meal. Symptoms may occur at night between 11 PM and 2 AM, when acid secretion tends to be
greatest. Feel better when you eat or drink and then worse 1 or 2 hours later (duodenal ulcer) Gastric ulcer —
Symptoms of a gastric ulcer typically include pain soon after eating. Symptoms are sometimes not relieved
by eating or taking antacids. Feel worse when you eat or drink (gastric ulcer)
. 11. SYMPTOMS Burning painBurning pain bloatingbloating NauseaNausea water brashwater brash
Unexplained weight lossUnexplained weight loss hematemesis (vomiting of blood)hematemesis (vomiting of
blood) Appetite changesAppetite changes MelinaMelina vomitingvomiting Blood in the stoolsBlood in the
stools low blood cell count (anemia)low blood cell count (anemia) Stomach pain wakes you up at
nightStomach pain wakes you up at night frequent burping or hiccuppingfrequent burping or hiccupping An
early sense of fullness with eatingAn early sense of fullness with eating
. 12. CAUSESCAUSES
. 13. stretch receptors Medulla oblongata endocrine cells gastrinCirculatory system stomach secretes gastric
juice
. GOALS OF TREATMENT ☻ lowering the amount of acid that stomach makes, ☻neutralizing the acid ☻
protecting the injured area so it can heal ☻ It's also very important to stop smoking and drinking alcohol
☻Prevent complications (bleeding, perforation, penetration, obstruction) ☻Minimize recurrences ☻Reduce
financial costs
. 39. Antibiotic medications. Doctors use combinations of antibiotics to treat H. pylori because one antibiotic
alone isn't always sufficient to kill the organism. Antibiotics prescribed for treatment of H. pylori include
amoxicillin (Amoxil), clarithromycin (Biaxin) and metronidazole (Flagyl). Combination drugs that include two
antibiotics together with an acid suppressor or cytoprotective agent (Helidac, Prevpac) have been designed
specifically for the treatment of H. pylori infection. Acid blockers. Acid blockers — also called hista
Bowel rest: Bed rest and clear fluids with no food at all for a few days. This gives the ulcer a chance to start healing
without being irritated. ♪ Nasogastric tube: Placement of a thin, flexible tube through your nose and down into your
stomach. This also relieves pressure on the stomach and helps it heal. ♪ Urgent endoscopy or surgery if indicated:
Damaged, bleeding blood vessels can usually be repaired with an endoscope. The endoscope has a small heating
device on the end that is used to cauterize a small wound.
41. SurgerySurgery Vagotomy Antrectomy Pyloroplasty Tying off an artery Acupuncture Chiropractic Homeopathy
Herbs Other modes Of treatment
42. LIFE STYLE AND HOME REMEDIESLIFE STYLE AND HOME REMEDIES
43. Don't smokeDon't smoke Limit or avoid alcoholLimit or avoid alcohol Avoid nonsteroidalAvoid nonsteroidal
anti-inflammatoryanti-inflammatory drugs (NSAIDs)drugs (NSAIDs) Fruits andFruits and VegetablesVegetables
LessLess Coffee andCoffee and CarbonatedCarbonated BeveragesBeverages Use of Olive OilUse of Olive Oil
ExerciseExercise Stress ReliefStress Relief
. Depth till submucosa </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>In any part of GI tract exposed

to aggressive action of acid pepsin juices. </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Can be
acute or chronic </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Both can penetrate muscularis
mucosae.. </li></ul></ul></ul></ul></ul>
. 3. SITES <ul><ul><ul><ul><ul><li>Gastric and duodenal – 98 %
</li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Ratio of 1:4
</li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Duodenum:1 st part >95%
</li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> :ant & post walls
</li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Gastric :junctn b/w antrum &acid secr. mucosa
</li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>:lesser curvature
</li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> </li></ul></ul></ul></ul></ul>
. 4. Pathomorphology <ul><li>Round </li></ul><ul><li>Punched out craters </li></ul><ul><li>2 to 4 cm
diameter </li></ul>Margins – Perpendicular - No Elevatn or Beading Mild oedema of immediate adj. mucosa
Surrounding Mucosal folds Radiate like Wheel Spokes Base Remarkably Clean
. 5. Duodenal ulcer Gastric ulcer Patho physiology <ul><li>Major </li></ul><ul><li>causes
</li></ul><ul><li>Gastric </li></ul><ul><li>acid </li></ul><ul><li>Gastric </li></ul><ul><li>emptying
</li></ul>increasd decreased rapid delayed Bicarbonate secretion remarkably decreased H.pylori & NSAID
H.pylori & NSAID Abnormal resting & stimulated Pyloric sphincter pressure
. 6. ETIOLOGY <ul><ul><li>Predisposing factors </li></ul></ul><ul><ul><li>Age :young in DU and peak inc.
at 6 th decade in GU. </li></ul></ul><ul><ul><li>Sex :GU commoner in males
</li></ul></ul><ul><ul><li>Causes </li></ul></ul><ul><ul><li>H.Pylori </li></ul></ul><ul><ul><li>NSAID
</li></ul></ul><ul><ul><li>Infection: CMV,herpes simplex,etc.. </li></ul></ul><ul><ul><li>Other drug/toxin:
bisphosphonates, chemo, clopidogrel , glucocorticoids
</li></ul></ul><ul><ul><li>Misc.:crohn,neoplasm,ashemia,infiltrating diseases,duodenal obstruction,etc..
</li></ul></ul>
. 7. <ul><li>Smoking </li></ul><ul><li>Genetic : increased freq of blood group O and non secretor status
</li></ul><ul><li>Stress </li></ul><ul><li>Diet : alcohol and caffeine </li></ul><ul><li>Associations
</li></ul><ul><li>Systemic mastocytosis </li></ul><ul><li>CRF, nephrolithiasis
</li></ul><ul><li>Hyperparathyroidism </li></ul><ul><li>Cirrhosis </li></ul><ul><li>Alpha antitrypsin
deficiency </li></ul><ul><li>CAD, pancreatitis, polycythaemia vera </li></ul>Pathogenetic factors not related
to h.pylori & NSAID
. 8. <ul><li>Gram –ve </li></ul><ul><li>S-shaped , flagellate </li></ul><ul><li>Lies b/w mucous layer &
gastric epithelium </li></ul><ul><li>1 st antrum then proximal segments. </li></ul><ul><li>Dormant state –
coccoid form </li></ul><ul><li>Genome—1500 proteins </li></ul><ul><li>Transmission:oral-oral/faeco-oral
</li></ul>H.pylori
. 9. Cytokines-IL 1 α / β , IL6,IL2, IL8(recruits act. neutrophils) TNF- α ,IFN- γ <ul><li>HOST FACTORS
</li></ul><ul><li>Duration </li></ul><ul><li>Location </li></ul><ul><li>Apoptosis </li></ul><ul><li>Cag PAI
</li></ul><ul><li>Mucosal nd systemic </li></ul><ul><li>humoral response </li></ul>cagA into host cells
<ul><li>BACTERIAL FACTORS </li></ul><ul><li>1st : Outer membrane proteins </li></ul><ul><li>2
nd :gastric residence-- Urease </li></ul><ul><li>3 rd :Mucosal damage </li></ul><ul><ul><ul><li>vacA
</li></ul></ul></ul><ul><ul><ul><li>cagA </li></ul></ul></ul><ul><ul><ul><li>Pathogenecity island cag
</li></ul></ul></ul><ul><ul><ul><li>Catalase, lipase, adhesins, </li></ul></ul></ul><ul><ul><ul><li>platelet
activating factors </li></ul></ul></ul><ul><li>Proteases nd phospholipases
</li></ul><ul><ul><ul><li>Breaks glycoprotein lipid complex of mucous gel
</li></ul></ul></ul><ul><ul><ul><li>Damage surface epi. cells </li></ul></ul></ul><ul><li>inflammatn
</li></ul><ul><li>Chronic gastritis </li></ul><ul><li>Peptic ulcer </li></ul><ul><li>Gastric MALT lymphoma
</li></ul><ul><li>Gastric adenocarcinoma </li></ul>V I R U L E N C E Pathophysiology of H.pylori ulcer
. 10. <ul><li>Gastric metaplasia </li></ul><ul><li>Increased acid production </li></ul><ul><li>Decreased
duodenal mucosal bicarbonate production </li></ul>Then how does it cause Ulcers in duodenum?????
. 11. <ul><li>Endothelial defects </li></ul><ul><li>Stasis--ischemia </li></ul>Direct toxicity by Ion trapping
<ul><li>Epithelial effects </li></ul><ul><li>Due to PG depletion </li></ul><ul><li>HCL
</li></ul><ul><li>mucin </li></ul><ul><li>bicarbonate </li></ul><ul><li>Epi. cell
</li></ul><ul><li>proliferation </li></ul>ULCER erosions Healing (spontaneous Or therapeutic) NSAID
induced PUD Pathophysiology Epithelial effects Due to PG depletion
. 12. Clinical features <ul><li>Abdominal pain * </li></ul><ul><li>Epigastric </li></ul><ul><li>Burning or
gnawing discomfort* </li></ul><ul><li>90 min to 3 h after meal </li></ul><ul><li>Frequently relieved by
antacids or food in DU.* </li></ul><ul><li>Awakes the pt from sleep b/w midnight & 3 am.
</li></ul><ul><li>Nausea </li></ul><ul><li>Weight loss </li></ul><ul><li>Dyspepsia </li></ul><ul><li>if not
relieved by food antacids , </li></ul><ul><li>radiates to back—penetrating ulcer </li></ul>
. 13. <ul><li>Perforation: </li></ul><ul><li>Gastric outlet obstruction </li></ul><ul><li>Bleeding
</li></ul>Symptom : sudden continuous generalized abd pain Examn : severly tender board like abdomen
Common in elderly and with NSAID Penetration Complications Symptoms : Pain worsening with meals,
nausea and vomiting of undigested food Examn : succusion splash Symptoms : Tarry stools or coffee ground
emesis Acute hematemesis Anemia Examn : tachycardia and orthostasis suggesting dehydration
. 14. <ul><li>NUD : non ulcerative dyspepsia </li></ul><ul><li>D/D OF ULCER LIKE SYMPTOMS
</li></ul><ul><li>Proximal GI tumors </li></ul><ul><li>Gastro esophageal reflux </li></ul><ul><li>Vascular
disease </li></ul><ul><li>Pancreaticobiliary disease </li></ul><ul><li>Crohn’s disease </li></ul>Differential
diagnosis
. 15. <ul><li>D/D OF EPIGASTRIC PAIN </li></ul><ul><li>Gastric </li></ul><ul><li>Duodenal
</li></ul><ul><li>Gall bladder </li></ul><ul><li>Pancreas </li></ul><ul><li>Colon
</li></ul><ul><li>Superficial / radicular pain </li></ul><ul><li>Nervous dyspepsia </li></ul>
. 16. Diagnostic Evaluation
. 17. <ul><li>Barium studies of proximal GI </li></ul><ul><li>Endoscopy </li></ul><ul><li>Tests for detection
of H.Pylori </li></ul><ul><li>Occasionally serum gastrin level </li></ul><ul><li>gastric acid analysis
</li></ul><ul><li>screen for NSAIDs </li></ul>Non invasive: serology Urea breath test Stool antigen
Invasive : rapid urease histology culture Duodenal ulcer Gastric ulcer
. 18. Treatment
. 19. <ul><li>Cimetidine 400mg bid </li></ul><ul><li>Ranitidine 300mg hs </li></ul><ul><li>Famotidine
40mg hs </li></ul><ul><li>Nizatidine 300mg hs </li></ul>: Magnesium Hydroxide ,Aluminum Hydroxide ,
Sodium Bicarbonate , Calcium Carbonate :100 – 150 meq/l 1 & 3 hrs after the meal & hs <ul><li>Acid
Suppressing Drugs </li></ul><ul><li>Antacids </li></ul><ul><li>H2 Receptor antagonists
</li></ul><ul><li>Proton Pump </li></ul><ul><li>Inhibitors (PPIs) </li></ul><ul><li>Omeprazole 20mg/day
</li></ul><ul><li>Lansoprazole 30mg/day </li></ul><ul><li>Rabiprazole 20mg/day
</li></ul><ul><li>Pantoprazole 40mg/day </li></ul><ul><li>Esomeprazole 20mg/day </li></ul>
. 20. <ul><li>Mucosal Protective Agents </li></ul><ul><li>Sucralfate </li></ul><ul><li>Prostaglandin
Analogue </li></ul><ul><li>Bismuth Containing Compounds </li></ul>-Sucralfate – 1gm qid -Misoprostol -
200 μ g qid
. 21. Regimens for Eradication Of H.Pylori <ul><li>Triple Therapy </li></ul><ul><li>Bismuth Subsalicylate +
-2 tablets qid </li></ul><ul><li>Metronidazole + -250mg qid </li></ul><ul><li>Tetracycline -500mg qid
</li></ul><ul><li>2 . Ranitidine Bismuth Citrate + -400mg bid </li></ul><ul><li>Tetracycline + -500mg bid
</li></ul><ul><li>Clarithromycin / Metronidazole -500mg bid </li></ul>
. 22. Regimens for Eradication Of H.Pylori 3. Omeprazole + - 20mg bid Claithromycin + -250/500mg bid
Metronidazole / -500mg bid Amoxicillin - 1gm bid
. 23. <ul><li>Quadruple therapy </li></ul><ul><li>Treatment of complications </li></ul><ul><li>Therapy for
NSAID injury </li></ul><ul><li>Surgical Therapy </li></ul>
. 24. Surgical Therapy <ul><li>Duodenal Ulcer </li></ul><ul><li>Vagotomy & Drainage (By Pyroloplasty ,
Gastrodudenostomy , Gastrojejunostomy) </li></ul><ul><li>Highly Selective Vagotomy (does not require
drainage procedure) </li></ul><ul><li>Vagotomy with Antrectomy </li></ul>
. 25. Surgical Therapy <ul><li>Gastric Ulcer </li></ul><ul><li>Antral Ulcer – Antrectomy with Billroth I
</li></ul><ul><ul><ul><ul><ul><li> anastomosis </li></ul></ul></ul></ul></ul><ul><li>Ulcer Excision with
Vagotomy & Drainage </li></ul><ul><li>3.High GU – Csende’s Procedure
</li></ul><ul><ul><ul><ul><ul><li>Subtotal Gastrectomy with a Roux-en-Y Oesophagogastrojejunostomy
</li></ul></ul></ul></ul></ul><ul><li>Kelling Madlener Procedure </li></ul><ul><li>antrectomy + intraop.
ulcer biopsy + </li></ul><ul><li>vagotomy </li></ul>
. 26. Surgical complications <ul><li>Recurrent ulceration </li></ul><ul><li>Afferent loop syndromes
</li></ul><ul><li>Dumping syndromes </li></ul><ul><li>Post vagotomy diarrhea </li></ul><ul><li>Bile reflux
gastropathy </li></ul><ul><li>Maldigestion & malabsorption </li></ul><ul><li>Gastric adenocarcinoma
</li></ul>
GI tract Hollow muscular tube, lumen surrounded by 4 tissue layers: Mucosa- innermost, thin layer of smooth
muscle and exocrine cells Submucosa- connective tissue Muscularis- smooth muscle Serosa-
outermost, connective tissue 
4. GI tract Function: Secretion- secretes HCL acid, digestive enzymes Digestion- mechanical and
chemical, food is broken down to chyme Absorption- from GI tract to blood supply Motility Elimination 
5. GI tract Nerve Supply Intrinsic stimulation by myenteric plexus in smooth muscle and submucosa plexus
in inner layer Autonomic system- Parasympathetic stimulation by vagus nerve, connects with intrinsic system Vagus-stimulates motor and secretory activity and relaxes spinchters Sympathetic system- thoracic and lumbar
splanchnic nerves slows movement, inhibits secretions and contracts spinchters 
6. Nerves of GI tract 
7. Mouth Function: Mastication, taste, begin movement Glands produce 1 L of saliva/day Saliva
contains mucin and salivary amylase with begins to break down CHO Oral preparatory phase- food is softened,
made into a “bolus” and tongue moves to the back of the mouth Oral phase- tongue presses bolus against hard
palate, elevates the larynx and forces the food bolus to the pharynx, triggering swallowing Pharyngeal phase- soft
palate elevates and seals nasal cavity, inhibits respirations and allows esophagus to open Esophageal phase- is
when bolus enter at cricopharyngeal juncture, peristalsis now takes food to the stomach All this takes about 10
seconds ! 
8. Esophagus Canal about 10 in long, passes through the center of the diaphragm Upper end is the upper
esophageal sphincter, at rest it is closed to prevent air from entering the esophagus Lower end is the lower
esophageal sphincter, it sits at the gastroesophageal junction, at rest it is closed to prevent reflux of gastric contents,
this is where GERD occurs Function- to propel food and fluids and prevent reflux Mucous is secreted to
move the food along Cardiac sphincter of the stomach opens to allow the food to enter 
9. Stomach Digestive and endocrine organ, in midline and LUQ Four regions: Cardia- narrow part that
is distal to the gastroesophageal junction Fundus- left above the GE junction Body or corpus- largest area Antrum- pylorus, is the distal portion and is separated from the duodenum by the pyloric sphincter, prevents backflow
from the duodenum Surface is covered in rugae or folds and have smooth muscle for motility Has intrinsic
and extrinsic nerves 
10. Stomach <ul><li>Function:
11. Parietal cells secrete HCL acid and intrinsic factor, which absorbs B 12, without it, what anemia can occur?
12. Chief cells secrete Pepsinogen pepsin
13. Cephalic phase- sight, smell and taste of food, regulated by vagus, begin secretory and contractile activity
14. Gastric phase- G cells in the antrum secrete gastrin, which causes HCL and pepsinogen to be released. HCL
changes pepsinogen to pepsin, which digest proteins. Mucous and Bicarb are secreted to protect the stomach wall
15. Intestinal phase- chyme produced empties into the duodenum and causes distention, this produces secretin, which
stops the acid production and gastric motility !</li></li></ul><li>Stomach 
16. Small Intestine Longest portion of the GI tract, 16-19 ft. Made up of 3 sections: Duodenum- first 12”
and is attached to the pylorus. The CVD and pancreatic duct join to form the ampulla of Vater and empty into the
duodenum at the duodenal papilla. This surrounded by a muscle, called the Sphincter of Oddi Jejunum- middle 8
ft portion Ileum- last 8-12 ft. The ileocecal valve separates the ileum form the cecum of the large intestine Inner lining is made up of intestinal villi and folds of mucosa and submucosa for digestion. 
17. Small Intestine 3 main functions: Movement- mixing and peristalsis Moves chyme by segmental
contractions and mixes with enzymes Digestion- enzymes produced by the intestinal cells make: Enterokinase, peptidases, lactase, maltase and sucrase Help to digest, CHO, proteins and lipids Absorption- absorbs most of the nutrients from food, takes 3-10 hours for the contents to pass through Major
organ for absorption 
18. Small intestine 
19. Large Intestine Ileocecal valve to the anus, 5-6’, lined with columnar epithelium tha thas absorptive and
mucous cells. Cecum- is the beginning, dilated pouch like structure, appendix is attached to the base Colon
has 4 divisions: Ascending, transverse, descending and sigmoid Rectum- last 6-8” to the sphincter muscles
and anus 
20. Large Intestine Function: Movement- segmental contractions, to allow time for the water and electrolytes
to be absorbed Absorption- absorbs most of water and electrolytes, reduces fluid volume of chyme and creates a
more solid mass for elimination Elimination- 3-4 strong peristaltic contraction /day triggered by colonic distention
in proximal large intestine to propel contents to rectum, until urge to defecate. 
21. Nursing Assessment Family history- GI disorders, cancer Personal history- what kinds of things? Diet history- anorexia, dyspepsia- what is that? What should you question them on for diet history? Health
history- diarrhea, constipation, # and color of stools, change in wt. or appetite Abdominal pain- P-
precipitating Q-quality- how intense, severe, type R-region or radiation S- severity scale- 0-10 T-timing- when did it first occur, duration and frequency 
22. Physical Assessment Abdomen: Inspection- skin, symmetry, rashes, lesions, scars Auscultation-
all four quadrants, normally heard in 5-15 seconds, normal, hypoactive or hyperactive, listen 1 full minute. What is
borborygmus? Why would bruits be heard? Why would there not be bowel sounds heard? Percussion- tympanic-
air filled, dull- organ Palpation- light and deep palpation, masses, tenderness, look for guarding 
23. Lab tests CBC- anemia Oncofetal antigens- CA19-9 and CEA, used to monitor for cancer in the GI
tract Ca- decreased in malabsorption K – decreased with vomiting, diarrhea Xylose absorption-
decreased indicates possible malabsorption in the small intesting Stool for Occult blood Stool for ova and
parasite- infection Stool for fecal fat- increased with Crohn’s disease and malabsorption 
24. Radiology Abdominal films- air in bowel and masses Upper GI and small bowel- pharynx to
duodenojejunal junction, barium swallow and SBFT NPO 8 hours before, drink barium, then lie, stand and turn in
multiple directions to view movement of barium SBFT- drink more barium and view passage After drink fluids
to pass barium Barium enema Large intestine, done for obstructions, masses, not done is perforated colon
or fistulas Only clear liquids for 12-24 hours prior, NPO, given bowel prep like Golytely Insert rectal catheter
with a balloon and give 500-1500 ml of barium and hold Can be uncomfortable, must take a laxative after 
25. UGI exam 
26. Diagnostic Tests EGD- esophagogastroduodenoscopy Visualize esophagus to duodenum, NPO prior,
given versed and fentanyl, maybe cetacaine to inhibit gag reflex, pass tube and visualize structures, can take
biopsies Gag reflex may not return for 1-2 hours after, so no eating or drinking until then Colonoscopy- large
bowel, take biopsies and remove polyps, have a bowel prep prior, given versed and fentanyl prior; Capsule
enteroscopy is now done to visualize, apply a data recorder to the abdomen and the patient swallows the capsule Proctosigmoidoscopy- like colonoscopy, only a rigid tube, less invasive and does not require the cleansing of the
colonoscopy 
27. Colonoscopy 
28. Case Study 72 year old male admitted with chest pain and nausea. He states that he awakens in the night with
pain in his chest and nausea. What would you do first to evaluate his condition? What diseases could he
have? What kind of lab work would you like to obtain? What past medical history do you need? 
29. Case Study Your patient starts to have hematemesis. What does this mean? Is this
life-threatening? What interventions should be done? What could have caused this condition? 
30. Case Study It is determined that your patient can be treated non-surgically. What medications would be given?
(should have 3) What type of teaching would be done for prevention? If he needed surgery, what could have
been done? 
31. Esophageal Problems GERD- gastroesophageal reflux disease Reflux causes esophageal mucosa to be
irritated by the effects of gastric and duodenal contents, results in inflammation Causes: Inappropriate
relaxation of the LES, sphincter tone is decreased Irritation from refluxed material Delayed gastric emptying,
gastric volume or intra-abdominal pressure is increased Abnormal esophageal clearance 
32. GERD Refluxed material has a pH of 1.5-2, whereas the esophagus normally has a pH of 6-8 erosive
esophagitis, once inflammed, the mucosa can’t eliminate the material as quickly. This leads to increased blood flow and
more erosion. Gastric acid and Pepsin cause the tissue injury. Can lead to Barrett’s epithelium- thicker, but can be
cancerous, can also cause hemorrhage, aspiration pneumonia, asthma, laryngitis and dental deterioration. 
33. GERD 
34. GERD Physical Manifestations: Dyspepsia- heartburn, substernal or retrosternal burning that moves up
and down in wavelike fashion, pain may radiate to neck or jaw or back, worsens when bends over, strains or lies on
their back, occurs after meals and last 1-2 hours, helped by fluids and staying upright Regurgitation- food entering
throat without nausea, watch for cough, hoarseness or wheezing Hypersalivation- water brash in response to
reflux, fluid without sour or bitter taste 
35. GERD Physical Manifestations Dysphagia and Odynophagia- difficulty swallowing, esophagus may be
narrowed by inflammation or tumor, odynophagia- means what? Chronic cough, mostly at night Atypical
chest pain Belching and flatulence or bloating Diagnosis: Endoscopy, 24 hour ambulatory pH
monitoring- pass a small tube into esophagus and monitor pH levels 
36. GERD Nursing Diagnoses: What diagnoses would apply to these patients? 1. 2. 3. Interventions: Diet therapy- what type of dietary modifications would be appropriate? Certain foods
decrease LES pressure- chocolate, fat and mints. Also, smoking and alcohol decrease Spicy foods irritate the
esophagus and Carbonated can increase gastric pressure 
37. GERD Lifestyle changes: How should they sleep? What things increase intra-abdominal
pressure? Drug therapy: Goal is to inhibit gastric acid secretion, accelerate gastric emptying and protect the
gastric mucosa Antacids: Elevate the pH and deactivate pepsin, good for heartburn, take 1 hour before and
2-3 hr after a meal Name 2 antacids. 
38. GERD Drug therapy: Histamine Receptor Antagonists Decrease acid, help promote healing of the
esophagus Name 2 common ones sold OTC (generic ends in “dine”) Proton Pump Inhibitors Main
treatment for GERD, long acting inhibition of gastric acid secretions by inhibiting protom pump of parietal cell, can
reduce by 90%/ day Name 2 proton pump inhibitors (generic ends in “zole”) 
39. GERD Other therapies: Consider medications that may lower LES pressure- oral contraceptives,
anticholinergics, sedative, tranquilizers, B-adrenergic agonists, nitrates and Ca channel blockers Prokinetic
drugs- for emptying and peristalsis- metoclopramide (reglan) Endoscopic: Enteryx procedure- spongy
material in LES to tighten it Stretta procedure- radiofrequency energy through needles to inhibit the vagus nerve Surgical: Laparoscopic Nissen Fundoplication Angelchik esophageal antireflux- anchors the LES in the
abdomen to increase sphincter pressure 
40. Hiatal Hernia Protrusion of stomach through the esophagus Sliding or Rolling hernias Symptoms
are similar to GERD patient Nonsurgical management is like GERD Surgical: Lap Nissen
Fundoplication- reinforces the LES, wraps a portion of the stomach around the distal esophagus to anchor it Post
op- risk for bleeding, infection and respiratory complications Have an NGT, begin PO once BS return Watch
for gas-bloat syndrome and air swallowing 
41.
42.
43.
44.
45. Nursing Diagnosis: GERD Impaired Nutrition: less than body requirements What things can be done to
improve their intake and decrease pain? What would be the expected outcomes? How would you monitor
their progress? Acute Pain r/t irritation of the esophagus What interventions can be performed? Risk for
aspiration r/t reflux of gastric contents How can you determine that this does not occur? 
46. Peptic Ulcer Disease Mucosal lesion of the stomach or duodenum Peptic can be gastric or duodenal PUD- gastric mucosal defenses become impaired and they can no longer protect the epithelium from acid and
pepsin Three main types of ulcers: Gastric Duodenal Stress 
47. Peptic Ulcers 
48. Gastric Ulcers Gastric mucosa is protected by mucous and bicarbonate that maintain a normal pH on the
gastric tissue and protects it from acid Gastromucosal prostaglandins increase the barrier’s resistance to
ulceration by producing mucous Integrity is improved by a rich blood supply to the mucosa If there is a break
in the mucosal barrier, HCL acid damages the epithelium. Gastric ulcers result from back-diffusion of acid or
dysfunction of the pyloric sphincter. 
49. Gastric Ulcers If the pyloric sphincter doesn’t function, bile backs up into the stomach, produces H+ ion back
diffusion and mucosal inflammation Toxic agents and bile destroy the lipid plasma membrane of the mucosa.
Delayed gastric emptying also affects. What drug can be given to improve emptying? Gastric Ulcers are deep and
penetrating and usually are in the lesser curvature of the stomach, near the pylorus 
50. Duodenal Ulcers Occur in the first portion of the duodenum. Deep lesions that penetrate through the
mucosa and submucosa into the muscle layer. The floor of the ulcer consists of a necrotic area on granulation tissue
and surrounded by fibrosis High gastric acid secretion, pH levels are low for long periods Protein rich meals,
calcium and vagal excitation stimulate acid secretion Hypersecretion, rapid emptying of food from stomach
reduces the buffering effect of food and delivers a large acid bolus to the duodenum Inhibitory secretory
mechanisms and pancreatic secretion may be insufficient to control the acid Many patients have H. pylori infection.
H. pylori produces urease changes urea to ammonia, H+ ions released contribute to damage 
51.
52. Stress Ulcers Acute gastric mucosal lesions occurring after and acute medical crisis or trauma Associated with head injury, major surgery, burns, respiratory failure, shock and sepsis Bleeding is the principle
manifestation Multifocal areas often in the proximal portion of the stomach and duodenum Usually elevated
HCL acid levels and hospital stay longer than 11 days 
53. Complications of Ulcers Hemorrhage: 15-25% of patients with PUD, most serious complication Most often with gastric ulcers and elderly After initial bleed, 40% have a recurrence if untreated, especially if H.
pylori untreated and no H2 antagonist Have Hematemesis- bleeding at or above the duodenojejunal junction Smaller amounts of bleeding are seen as melena, more often seen in duodenal ulcers, stool may appear black. 
54. Complications of Ulcers Perforation Gastric or duodenal may perforate or bleed Stomach or
duodenal contents can leak into the abdomen, acid peptic juice, bile and pancreatic juice empty through the anterior
wall of the stomach into the peritoneal cavity Sudden, sharp pain in midepigastric region and spread over the
abdomen Amount of pain correlates with the amount and type of GI contents spilled Abdomen is tender, rigid
and boardlike, go into a fetal position to decrease tension of abdomen Chemical peritonitis, bacterial septicemia
and hypovolemic shock follow paralytic ileus and possible death 
55. Perforated ulcer 
56. Complications of Ulcers Pyloric obstruction Small number of patients, vomiting caused by stasis and
gastric dilation Obstruction occurs at the pylorus and is caused by scarring, edema, and/or inflammation Gastric outlet obstruction abdominal bloating, nausea and vomiting May go into metabolic alkalosis from loss
of large quantities of acid gastric juice (H+ and Cl-) Hypokalemia may result from the vomiting 
57. Complications of Ulcers Intractable disease Disease may recur throughout life, stressors, inability to
adhere to therapy, no longer responds to management Cause: Use of NSAID’s- break down the mucosal
barrier and disrupt the protection by COX inhibition. Cause the depletion of prostaglandins, have a high rate of
recurrence Drugs such as Theophylline, corticosteroids and caffeine stimulate HCL acid production H pylori
infection is transmitted person to person 50% of people with PUD have a first or second line relative with PUD,
usually the same type of ulcer 
58. Physical Manifestations Epigastric tenderness, midline between the umbilicus and xiphoid process May
begin as hyperactive BS, then diminish if perforation Dyspepsia- discomfort around the epigastrium, sharp,
burning or gnawing Gastric- occurs in upper epigastrium with localization to the left of the midline and may be
relieved by food Duodenal- located to the right of the epigastrium, occurs 90 min to 3 hours after eating and
awaken at night, may be aggravated by spicy foods, onions, alcohol, caffeine and ASA, NSAIDS 
59. Physical Manifestations Vomiting may occur Appetite is maintained, unless pyloric obstruction occurs Fluid volume deficit, if bleeding, take orthostatic BPs Watch for Hematemesis and melena Monitor H &
H Dx- barium swallow and EGD Test for H. pylori is IgG serologic testing and urea breath testing 
60. Nursing Diagnoses Name 5 diagnoses r/t PUD 1. 2. 3. 4. 5. What would be an
expected outcome for this disorder? 
61. Nursing Interventions Drug Therapy Goals: Provide pain relief, eradicate H. pylori, heal ulcerations,
prevent recurrence Eliminate H. pylori- triple treatment: Bismuth product (pepto-bismol) or a a proton pump
inhibitor and two antibiotics (metronidazole (Flagyl) and tetracycline or amoxicillin) May have to take medications
4 x’s/day for 14 days and often they don’t complete the series 
62. Nursing Interventions Drug therapy: Hyposecretory drugs- reduce gastric acid secretions Antisecretory agents- proton pump inhibitors, “zole” ending, suppress H, K-ATP ase enzyme system of gastric acid
production, can be given IV or PO H2 receptor antagonists- block histamine-stimulated gastric secretions, “dine”
ending Prostaglandin analogues- reduce gastric acid secretion and enhance gastric mucosal resistance to tissue
injury, Misoprostol (Cytotec) helps prevent NSAID induced ulcers, does cause uterine contraction and can not be given
to pregnant women 
63. Nursing Interventions Antacids Buffer gastric acid and prevent formation of pepsin, heal duodenal
ulcers Aluminum hydroxides and magnesium hydroxide, may affect those with renal impairment Take 2
hours after meals to reduce the H+ion load Calcium carbonate (TUMS) is an antacid, but it triggers gastrin release
and causes a rebound acid secretion Antacids can interact with other drugs- tetracycline, dilantin, also may have
a high sodium content Mucosal Barrier fortifiers- sucralfate (Carafate) supplies a protect coating by forming a
complex with proteins, binds with bile acids and pepsin, should be given on an empty stomach and not within 1 hour of
eating or taking antacids 
64. Nursing Interventions Diet therapy Bland diet may help to relieve symptoms Food may help to
neutralize acids, rebound may follow when more acid is released Avoid foods that stimulate gastric acid
release They are?? Yoga for stress relief, herbals, such as licorice and vitamins may help 
65. Gastrointestinal Bleeding What would be a nursing diagnosis for GI Bleeding? 1. 2. What
would be the expected outcome and how would you know that this was met? 
66. GI bleeding 
67. Gastrointestinal Bleeding Hypovolemia Management Monitor vital signs and I&O, assess for bleeding
and vomiting, monitor CBC Fluid and electrolyte replacement is necessary, usually NSS or LR, may give PRBC’s
or FFP Watch for signs of shock, what are they?? Bleeding reduction Monitor labs, insert and NGT to
decompress the stomach, give an H2 blocker, may need gastric lavage, what is that?? 
68. Nursing Interventions for GI bleeding Endoscopic therapy EGD, can do: cautery on the bleeding
sites inject a sclerosing agent with diluted epipherine Laser therapy Clip the bleeding vessel Somastatin Analogue- Sandostatin may be used to suppress gastric acid secretion on parietal and chief cells,
vasoconstricts the splanchnic arteries which reduce hemorrhage 
69. Surgical management of GI bleeding MIG- minimally invasive gastrectomy- laproscopic to remove chronic
gastric ulcer or treat hemorrhage, make several small incisions, may partially remove the stomach and/or vagotomy to
control acid secretion Gastroenterostomy- creates a passage between the body of the stomach and jejunum,
reduces motor activity in the pyloroduodenal area, diverts acid, a vagotomy may be done with it to decrease secretion.
Can do truncal, selective or proximal. Billroth I- connect to duodenum, Billroth II connects to jejunum Pyloroplasty-
widens the exit of the pylorus and empties the stomach 
70. Billroth 1 
71. Postop care for GI surgery NGT management Monitor for complications of: Dumping syndrome-
vasomotor symptoms, rapid emptying of gastric contents into the small intestine, shifts fluid into the gut and cause
abdominal distention, 30 min after eating have vertigo, tachycardia, syncope, sweating, pallor, palpitations. 90 min later
have excessive amount of insulin released, this dizziness, palpitations, diaphoresis and confusion Should eat
smaller amounts, take less liquid with food, high protein and fat, low CHO diet, sandostatin may be given and pectin
with food 
72. Postop Care of GI surgery Reflux gastropathy- bile reflux, when pylorus is bypassed, bile in stomach and have
abdominal discomfort and vomiting Delayed gastric emptying- usually resolves in 1 week, edema at the
anastomosis or adhesions may occur, hypokalemia, hypoproteinemia and hyponatremia may also cause Afferent
loop syndrome- duodenal loop is partially obstructed, pancreatic and biliary secretions fill the intestinal loop, it becomes
distended painful contractions, bloating and pain 20-60 min after eating 
73. Post op GI surgery Recurrent ulceration- occurs in 5% of patients, may have ulcers at the anastomosis Nutritional management: Deficiencies of B12, folic acid and iron Impaired Ca metabolism and reduced
absorption of Ca and vitamin D Shortage of intrinsic factor, r/t the resection and rapid emptying of the food 
pernicious anemia- weak, anemic, atrophic glossitis- beefy shiny tongue Give back B12 and folic acid 
74. Pernicious anemia 
75. Irritable Bowel Syndrome Chronic GI disorder, with chronic or recurrent diarrhea, constipation, abdominal pain
and bloating Spastic colon, impairment of the motor/sensory function diarrhea alternating with constipation Usually begin as a young adult Stress, anxiety and familial factors may predispose patient 
76. IBS Assessment: History of bowel pattern Manning criteria- abdominal pain relieved by defection,
abdominal distention, sensation of incomplete evacuation of stool, presence of mucus with the stool Pain in LLQ
and cramps, may be tenderness and air in bowels Dx- flexible sigmoidoscopy or colonoscopy if >40 Barium
enema 
77. IBS Interventions Diet therapy- limit caffeine, alcohol, beverages with sorbitol, take in fiber and bulk,
30-40 gm/day Drug therapy: Bulk forming laxatives (Metamucil) antidiarrheals (loperamide) anticholinergics (bentyl) antidepressants (elavil) 5-HT4 agonists(Zelnorm) for prokinetic activity, imitates
serotonin to stimulate peristalsis Stress management- relaxation techniques 
78. Nursing Diagnoses Constipation r/t low residue diet and stress What can be done to manage this? Diarrhea r/t increased motility of intestines How can this be corrected or treated? What can be done to
correct constipation and impaction? What role may analgesics play in constipation? 
79. Colorectal Cancer 95% are adenocarcinomas, most come from adenomatous polyps 2/3 occur in
rectosigmoid region Can metastasize through blood and lymph, liver most common site with 15-30% spread there,
can also go to the lungs, brain, bones and adrenals May form fistulas into bladder and vagina Genetics-
autosomal dominant disorder- familial adenomatous polyposis only 1%, 100% malignant, usually starting at age 20.
Also, hereditary nonpolyposis colorectal cancer- autosomal dominant, 10% of cancers, develop by age 45 
80. Colorectal cancer 75% have no known cause Age is a risk factor Dietary- decreased bowel
emptying time, foods with carcinogens- red meat, fatty food, fried meats and fish, concentrated sweets High fat
diet increases bile acid secretion and anaerobic bacteria Irritable bowel diseases Third most common
malignancy 
81. Colorectal Cancer 
82. Colorectal cancer Manifestations: Rectal bleeding, anemia and change in stool Gas pains,
cramping or incomplete evacuation Hematochezia- bright red blood when in rectum Tumors can grow large
when in upper abdomen, mostly liquid stool, more pain when in lower Tests- stool for occult blood, CEA, barium
enema, CT of abdomen Colonoscopy or sigmoidoscopy 
83. Colorectal cancer Nursing Diagnoses- Name 4 diagnoses, associated with colorectal cancer 1. 2. 3. 4. What would be the expected outcomes? 
84. Colorectal cancer Nonsurgical management: Duke’s staging classification A- tumor has penetrated
into, but not through the bowel wall B- tumor has penetrated through the bowel wall C-tumor has penetrated
through the bowel wall and there is lymph node involvement D- tumor has metastasized to distant sites Radiation therapy Drug therapy-chemotherapy IV 5-FU and leucovorin, side effects are diarrhea, mucositis,
leucopenia and mouth ulcers Eloxatin, Camptosar, Avastin are also being used, along with monoclonal
antibodies- cetuximab 
85. Colorectal cancer Surgical management: Colon resection- removal of tumor and lymph nodes Colectomy- colon removal Abdominal perineal resection- removes sigmoid colon, rectum and anus, colostomy
is performed Colostomies may be ascending, descending, sigmoid, transverse or double barreled Stool
returned depends on the site of the colostomy 
86. Colostomy 
87. Colorectal cancer Postoperative Care: Colostomy management What types of nursing diagnoses
may accompany this procedure? How should the stoma appear? Report any bleeding, breakdown of the
sutures from the wall and signs of ischemia or necrosis Wound care management- JP drains, monitor for
infection Fluid volume deficit and electrolyte imbalance 
88. Colorectal cancer Teaching: Colostomy care- what kinds of things should be covered? Dietary
measures to control stool and gas, what would they be? Psychological adjustment to the colostomy, what
diagnosis relates to this? Grief and family coping- what resources may be needed? Genetic testing if familial
type 
89. Intestinal Obstruction Partial or complete Mechanical- bowel is physically obstructed by adhesions,
tumors Nonmechanical- paralytic ileus or adynamic ileus, neuromuscular distrubance- slow movement or
backup Contents accumulate at or above the obstruction distention, peristalsis increases to aid movement,
stimulates more secretions more distention edema of the bowel, increased capillary permeability 
90. Intestinal Obstruction Plasma leaks into the peritoneal cavity and trapped fluid decreases the absorption of
fluid and electrolytes into the vascular space reduced blood volume and electrolyte imbalances, can hypovolemic
shock Can also lead to metabolic alkalosis if high and there is a loss of gastric acid, if low, metabolic acidosis
occurs with the loss of alkaline fluids Bacterial peritonitis and septic shock can also occur from the release of
endotoxins 
91. Intestinal obstruction 
92.
93. Intestinal Obstruction Adhesions account for 45-60%, r/t scar tissue Intussusception- telescoping bowel
and volvulus- twisting of the bowel Paralytic ileus- decreased peristalsis from trauma, toxin or autonomic, can
result from surgery, MI’s, rib fracture, pneumonia, peritonitis and vascular insufficiency from heart failure or shock 
94. Intestinal Obstruction Assessment: History of symptoms and occurrence Abdominal pain and
cramping Obstipation, vomiting with brown and foul smelling Borborygni above the obstruction, then
absent Abdominal distention and tympanic abdomen Abdominal films and CT of abdomen WBC
elevated in some cases 
95. Intestinal Obstruction Nonsurgical management: NGT to decompress to LCS Nasointestinal tubes-
Miller-Abbott, mercury balloons and migrate down the intestine by peristalsis, don’t irrigate with fluid- it will increase
edema at the obstruction Fluid and electrolyte replacement- NPO, give NSS or LR, replace K Pain control-
not normally given opioids, mask pain and peritonitis Antibiotics if suspect perforation Surgical
management: Exploratory laparotomy 
96. Case Study 24 year old female admitted with frequent bloody diarrhea stools, weight loss and anemia. What do you suspect? What labwork should you do? What treatment may be needed? 
97. Case Study Your patient tells you that the diarrhea has been occurring for months. How do you
differentiate between U.C. and Crohn’s disease? What may be her treatment options? 
98. Case Study How do you help your patient decide about a colostomy? If she does want a colostomy, what
type of teaching needs to be done? 
99. Chronic Inflammatory Bowel Disease Ulcerative Colitis and Crohn’s Ulcerative Colitis: Remissions
and exacerbations Loose stools with blood and mucous 10-20/day Poor absorption of nutrients and
thickening of the colon wall Abdominal distention and cramping Complications are: hemorrhage, perforation,
fistulas and nutritional deficiencies May be familial tendency, inflammation r/t response to normal flora 
100. Ulcerative Colitis 
101. Chronic Inflammatory Bowel Disease Crohn’s disease Terminal ileum, patching involvement through all
layers of the bowel Deep fissures and ulcers occur 5-8 loose stools/day, rarely bloody Complications
are: Fistulas, nutritional deficiencies Cause is thought to be mycobacterium paratuberculosis, genetic
predisposition 
102. Crohn’s Disease Garrard Crohn's story 
103. Ulcerative Colitis Manifestations: Abdominal pain, bloody diarrhea, tenesmus- uncontrolled straining Dx- barium enema Nursing Diagnoses: Diarrhea r/t inflammation of the bowel Acute and chronic
pain Imbalance nutrition: less than body requirements Disturbed body image 
104. Ulcerative Colitis Diarrhea management- Drugs- salicylate compounds- Sulfasalazine (Azulfidine)
inhibits prostaglandins to reduce inflammation, also use Asacol, Pentasa Corticosteroids- Prednisone to decrease
edema Immunosuppressive- cyclosporine Antidiarrheals Monoclonal antibody- Remicade neutralizes
the activity of tumor necrosis factor and prevents toxic megacolon 
105. Ulcerative Colitis Diet therapy: NPO at first, then TPN, may have low fiber or low residue, what foods
would be included? Surgical management: Total Proctocolectomy with permanent Ileostomy Total
colectomy with a continent ileostomy Total colectomy with ileoanal anastomosis and ileoanal reservoir or
pouch Postop- teaching for ostomy, pain control and monitoring for GI bleeding and fluid volume deficit 
106.
107.
108. Crohn’s Disease Aggravated by bacterial infection, inflammation and smoking History of fever,
abdominal pain and loose stools, weight loss Steatorrhea is common- fatty stools Fistulas may occur
between bladder and vagina Drug therapy- same as UC, except may take metronidazole if fistulas and imuran as
an immunosuppressant Diet therapy- may be on TPN, supplements like ensure, vivonex 
109. Crohn’s Disease Monitor for fistulas- infections, skin problems, malnutrition, fluid and electrolyte
imbalances Fluid and electrolyte therapy- what would this entail? Name one antidiarrheal. Surgical
management: Bowel resections Fistula repairs Ileostomies may also be required to rest the bowel or
repair damaged areas. 
GI tract Hollow muscular tube, lumen surrounded by 4 tissue layers: Mucosa- innermost, thin layer of smooth
muscle and exocrine cells Submucosa- connective tissue Muscularis- smooth muscle Serosa-
outermost, connective tissue 
4. GI tract Function: Secretion- secretes HCL acid, digestive enzymes Digestion- mechanical and
chemical, food is broken down to chyme Absorption- from GI tract to blood supply Motility Elimination 
5. GI tract Nerve Supply Intrinsic stimulation by myenteric plexus in smooth muscle and submucosa plexus
in inner layer Autonomic system- Parasympathetic stimulation by vagus nerve, connects with intrinsic system Vagus-stimulates motor and secretory activity and relaxes spinchters Sympathetic system- thoracic and lumbar
splanchnic nerves slows movement, inhibits secretions and contracts spinchters 
6. Nerves of GI tract 
7. Mouth Function: Mastication, taste, begin movement Glands produce 1 L of saliva/day Saliva
contains mucin and salivary amylase with begins to break down CHO Oral preparatory phase- food is softened,
made into a “bolus” and tongue moves to the back of the mouth Oral phase- tongue presses bolus against hard
palate, elevates the larynx and forces the food bolus to the pharynx, triggering swallowing Pharyngeal phase- soft
palate elevates and seals nasal cavity, inhibits respirations and allows esophagus to open Esophageal phase- is
when bolus enter at cricopharyngeal juncture, peristalsis now takes food to the stomach All this takes about 10
seconds ! 
8. Esophagus Canal about 10 in long, passes through the center of the diaphragm Upper end is the upper
esophageal sphincter, at rest it is closed to prevent air from entering the esophagus Lower end is the lower
esophageal sphincter, it sits at the gastroesophageal junction, at rest it is closed to prevent reflux of gastric contents,
this is where GERD occurs Function- to propel food and fluids and prevent reflux Mucous is secreted to
move the food along Cardiac sphincter of the stomach opens to allow the food to enter 
9. Stomach Digestive and endocrine organ, in midline and LUQ Four regions: Cardia- narrow part that
is distal to the gastroesophageal junction Fundus- left above the GE junction Body or corpus- largest area Antrum- pylorus, is the distal portion and is separated from the duodenum by the pyloric sphincter, prevents backflow
from the duodenum Surface is covered in rugae or folds and have smooth muscle for motility Has intrinsic
and extrinsic nerves 
10. Stomach <ul><li>Function:
11. Parietal cells secrete HCL acid and intrinsic factor, which absorbs B 12, without it, what anemia can occur?
12. Chief cells secrete Pepsinogen pepsin
13. Cephalic phase- sight, smell and taste of food, regulated by vagus, begin secretory and contractile activity
14. Gastric phase- G cells in the antrum secrete gastrin, which causes HCL and pepsinogen to be released. HCL
changes pepsinogen to pepsin, which digest proteins. Mucous and Bicarb are secreted to protect the stomach wall
15. Intestinal phase- chyme produced empties into the duodenum and causes distention, this produces secretin, which
stops the acid production and gastric motility !</li></li></ul><li>Stomach 
16. Small Intestine Longest portion of the GI tract, 16-19 ft. Made up of 3 sections: Duodenum- first 12”
and is attached to the pylorus. The CVD and pancreatic duct join to form the ampulla of Vater and empty into the
duodenum at the duodenal papilla. This surrounded by a muscle, called the Sphincter of Oddi Jejunum- middle 8
ft portion Ileum- last 8-12 ft. The ileocecal valve separates the ileum form the cecum of the large intestine Inner lining is made up of intestinal villi and folds of mucosa and submucosa for digestion. 
17. Small Intestine 3 main functions: Movement- mixing and peristalsis Moves chyme by segmental
contractions and mixes with enzymes Digestion- enzymes produced by the intestinal cells make: Enterokinase, peptidases, lactase, maltase and sucrase Help to digest, CHO, proteins and lipids Absorption- absorbs most of the nutrients from food, takes 3-10 hours for the contents to pass through Major
organ for absorption 
18. Small intestine 
19. Large Intestine Ileocecal valve to the anus, 5-6’, lined with columnar epithelium tha thas absorptive and
mucous cells. Cecum- is the beginning, dilated pouch like structure, appendix is attached to the base Colon
has 4 divisions: Ascending, transverse, descending and sigmoid Rectum- last 6-8” to the sphincter muscles
and anus 
20. Large Intestine Function: Movement- segmental contractions, to allow time for the water and electrolytes
to be absorbed Absorption- absorbs most of water and electrolytes, reduces fluid volume of chyme and creates a
more solid mass for elimination Elimination- 3-4 strong peristaltic contraction /day triggered by colonic distention
in proximal large intestine to propel contents to rectum, until urge to defecate. 
21. Nursing Assessment Family history- GI disorders, cancer Personal history- what kinds of things? Diet history- anorexia, dyspepsia- what is that? What should you question them on for diet history? Health
history- diarrhea, constipation, # and color of stools, change in wt. or appetite Abdominal pain- P-
precipitating Q-quality- how intense, severe, type R-region or radiation S- severity scale- 0-10 T-timing- when did it first occur, duration and frequency 
22. Physical Assessment Abdomen: Inspection- skin, symmetry, rashes, lesions, scars Auscultation-
all four quadrants, normally heard in 5-15 seconds, normal, hypoactive or hyperactive, listen 1 full minute. What is
borborygmus? Why would bruits be heard? Why would there not be bowel sounds heard? Percussion- tympanic-
air filled, dull- organ Palpation- light and deep palpation, masses, tenderness, look for guarding 
23. Lab tests CBC- anemia Oncofetal antigens- CA19-9 and CEA, used to monitor for cancer in the GI
tract Ca- decreased in malabsorption K – decreased with vomiting, diarrhea Xylose absorption-
decreased indicates possible malabsorption in the small intesting Stool for Occult blood Stool for ova and
parasite- infection Stool for fecal fat- increased with Crohn’s disease and malabsorption 
24. Radiology Abdominal films- air in bowel and masses Upper GI and small bowel- pharynx to
duodenojejunal junction, barium swallow and SBFT NPO 8 hours before, drink barium, then lie, stand and turn in
multiple directions to view movement of barium SBFT- drink more barium and view passage After drink fluids
to pass barium Barium enema Large intestine, done for obstructions, masses, not done is perforated colon
or fistulas Only clear liquids for 12-24 hours prior, NPO, given bowel prep like Golytely Insert rectal catheter
with a balloon and give 500-1500 ml of barium and hold Can be uncomfortable, must take a laxative after 
25. UGI exam 
26. Diagnostic Tests EGD- esophagogastroduodenoscopy Visualize esophagus to duodenum, NPO prior,
given versed and fentanyl, maybe cetacaine to inhibit gag reflex, pass tube and visualize structures, can take
biopsies Gag reflex may not return for 1-2 hours after, so no eating or drinking until then Colonoscopy- large
bowel, take biopsies and remove polyps, have a bowel prep prior, given versed and fentanyl prior; Capsule
enteroscopy is now done to visualize, apply a data recorder to the abdomen and the patient swallows the capsule Proctosigmoidoscopy- like colonoscopy, only a rigid tube, less invasive and does not require the cleansing of the
colonoscopy 
27. Colonoscopy 
28. Case Study 72 year old male admitted with chest pain and nausea. He states that he awakens in the night with
pain in his chest and nausea. What would you do first to evaluate his condition? What diseases could he
have? What kind of lab work would you like to obtain? What past medical history do you need? 
29. Case Study Your patient starts to have hematemesis. What does this mean? Is this
life-threatening? What interventions should be done? What could have caused this condition? 
30. Case Study It is determined that your patient can be treated non-surgically. What medications would be given?
(should have 3) What type of teaching would be done for prevention? If he needed surgery, what could have
been done? 
31. Esophageal Problems GERD- gastroesophageal reflux disease Reflux causes esophageal mucosa to be
irritated by the effects of gastric and duodenal contents, results in inflammation Causes: Inappropriate
relaxation of the LES, sphincter tone is decreased Irritation from refluxed material Delayed gastric emptying,
gastric volume or intra-abdominal pressure is increased Abnormal esophageal clearance 
32. GERD Refluxed material has a pH of 1.5-2, whereas the esophagus normally has a pH of 6-8 erosive
esophagitis, once inflammed, the mucosa can’t eliminate the material as quickly. This leads to increased blood flow and
more erosion. Gastric acid and Pepsin cause the tissue injury. Can lead to Barrett’s epithelium- thicker, but can be
cancerous, can also cause hemorrhage, aspiration pneumonia, asthma, laryngitis and dental deterioration. 
33. GERD 
34. GERD Physical Manifestations: Dyspepsia- heartburn, substernal or retrosternal burning that moves up
and down in wavelike fashion, pain may radiate to neck or jaw or back, worsens when bends over, strains or lies on
their back, occurs after meals and last 1-2 hours, helped by fluids and staying upright Regurgitation- food entering
throat without nausea, watch for cough, hoarseness or wheezing Hypersalivation- water brash in response to
reflux, fluid without sour or bitter taste 
35. GERD Physical Manifestations Dysphagia and Odynophagia- difficulty swallowing, esophagus may be
narrowed by inflammation or tumor, odynophagia- means what? Chronic cough, mostly at night Atypical
chest pain Belching and flatulence or bloating Diagnosis: Endoscopy, 24 hour ambulatory pH
monitoring- pass a small tube into esophagus and monitor pH levels 
36. GERD Nursing Diagnoses: What diagnoses would apply to these patients? 1. 2. 3. Interventions: Diet therapy- what type of dietary modifications would be appropriate? Certain foods
decrease LES pressure- chocolate, fat and mints. Also, smoking and alcohol decrease Spicy foods irritate the
esophagus and Carbonated can increase gastric pressure 
37. GERD Lifestyle changes: How should they sleep? What things increase intra-abdominal
pressure? Drug therapy: Goal is to inhibit gastric acid secretion, accelerate gastric emptying and protect the
gastric mucosa Antacids: Elevate the pH and deactivate pepsin, good for heartburn, take 1 hour before and
2-3 hr after a meal Name 2 antacids. 
38. GERD Drug therapy: Histamine Receptor Antagonists Decrease acid, help promote healing of the
esophagus Name 2 common ones sold OTC (generic ends in “dine”) Proton Pump Inhibitors Main
treatment for GERD, long acting inhibition of gastric acid secretions by inhibiting protom pump of parietal cell, can
reduce by 90%/ day Name 2 proton pump inhibitors (generic ends in “zole”) 
39. GERD Other therapies: Consider medications that may lower LES pressure- oral contraceptives,
anticholinergics, sedative, tranquilizers, B-adrenergic agonists, nitrates and Ca channel blockers Prokinetic
drugs- for emptying and peristalsis- metoclopramide (reglan) Endoscopic: Enteryx procedure- spongy
material in LES to tighten it Stretta procedure- radiofrequency energy through needles to inhibit the vagus nerve Surgical: Laparoscopic Nissen Fundoplication Angelchik esophageal antireflux- anchors the LES in the
abdomen to increase sphincter pressure 
40. Hiatal Hernia Protrusion of stomach through the esophagus Sliding or Rolling hernias Symptoms
are similar to GERD patient Nonsurgical management is like GERD Surgical: Lap Nissen
Fundoplication- reinforces the LES, wraps a portion of the stomach around the distal esophagus to anchor it Post
op- risk for bleeding, infection and respiratory complications Have an NGT, begin PO once BS return Watch
for gas-bloat syndrome and air swallowing 
41.
42.
43.
44.
45. Nursing Diagnosis: GERD Impaired Nutrition: less than body requirements What things can be done to
improve their intake and decrease pain? What would be the expected outcomes? How would you monitor
their progress? Acute Pain r/t irritation of the esophagus What interventions can be performed? Risk for
aspiration r/t reflux of gastric contents How can you determine that this does not occur? 
46. Peptic Ulcer Disease Mucosal lesion of the stomach or duodenum Peptic can be gastric or duodenal PUD- gastric mucosal defenses become impaired and they can no longer protect the epithelium from acid and
pepsin Three main types of ulcers: Gastric Duodenal Stress 
47. Peptic Ulcers 
48. Gastric Ulcers Gastric mucosa is protected by mucous and bicarbonate that maintain a normal pH on the
gastric tissue and protects it from acid Gastromucosal prostaglandins increase the barrier’s resistance to
ulceration by producing mucous Integrity is improved by a rich blood supply to the mucosa If there is a break
in the mucosal barrier, HCL acid damages the epithelium. Gastric ulcers result from back-diffusion of acid or
dysfunction of the pyloric sphincter. 
49. Gastric Ulcers If the pyloric sphincter doesn’t function, bile backs up into the stomach, produces H+ ion back
diffusion and mucosal inflammation Toxic agents and bile destroy the lipid plasma membrane of the mucosa.
Delayed gastric emptying also affects. What drug can be given to improve emptying? Gastric Ulcers are deep and
penetrating and usually are in the lesser curvature of the stomach, near the pylorus 
50. Duodenal Ulcers Occur in the first portion of the duodenum. Deep lesions that penetrate through the
mucosa and submucosa into the muscle layer. The floor of the ulcer consists of a necrotic area on granulation tissue
and surrounded by fibrosis High gastric acid secretion, pH levels are low for long periods Protein rich meals,
calcium and vagal excitation stimulate acid secretion Hypersecretion, rapid emptying of food from stomach
reduces the buffering effect of food and delivers a large acid bolus to the duodenum Inhibitory secretory
mechanisms and pancreatic secretion may be insufficient to control the acid Many patients have H. pylori infection.
H. pylori produces urease changes urea to ammonia, H+ ions released contribute to damage 
51.
52. Stress Ulcers Acute gastric mucosal lesions occurring after and acute medical crisis or trauma Associated with head injury, major surgery, burns, respiratory failure, shock and sepsis Bleeding is the principle
manifestation Multifocal areas often in the proximal portion of the stomach and duodenum Usually elevated
HCL acid levels and hospital stay longer than 11 days 
53. Complications of Ulcers Hemorrhage: 15-25% of patients with PUD, most serious complication Most often with gastric ulcers and elderly After initial bleed, 40% have a recurrence if untreated, especially if H.
pylori untreated and no H2 antagonist Have Hematemesis- bleeding at or above the duodenojejunal junction Smaller amounts of bleeding are seen as melena, more often seen in duodenal ulcers, stool may appear black. 
54. Complications of Ulcers Perforation Gastric or duodenal may perforate or bleed Stomach or
duodenal contents can leak into the abdomen, acid peptic juice, bile and pancreatic juice empty through the anterior
wall of the stomach into the peritoneal cavity Sudden, sharp pain in midepigastric region and spread over the
abdomen Amount of pain correlates with the amount and type of GI contents spilled Abdomen is tender, rigid
and boardlike, go into a fetal position to decrease tension of abdomen Chemical peritonitis, bacterial septicemia
and hypovolemic shock follow paralytic ileus and possible death 
55. Perforated ulcer 
56. Complications of Ulcers Pyloric obstruction Small number of patients, vomiting caused by stasis and
gastric dilation Obstruction occurs at the pylorus and is caused by scarring, edema, and/or inflammation Gastric outlet obstruction abdominal bloating, nausea and vomiting May go into metabolic alkalosis from loss
of large quantities of acid gastric juice (H+ and Cl-) Hypokalemia may result from the vomiting 
57. Complications of Ulcers Intractable disease Disease may recur throughout life, stressors, inability to
adhere to therapy, no longer responds to management Cause: Use of NSAID’s- break down the mucosal
barrier and disrupt the protection by COX inhibition. Cause the depletion of prostaglandins, have a high rate of
recurrence Drugs such as Theophylline, corticosteroids and caffeine stimulate HCL acid production H pylori
infection is transmitted person to person 50% of people with PUD have a first or second line relative with PUD,
usually the same type of ulcer 
58. Physical Manifestations Epigastric tenderness, midline between the umbilicus and xiphoid process May
begin as hyperactive BS, then diminish if perforation Dyspepsia- discomfort around the epigastrium, sharp,
burning or gnawing Gastric- occurs in upper epigastrium with localization to the left of the midline and may be
relieved by food Duodenal- located to the right of the epigastrium, occurs 90 min to 3 hours after eating and
awaken at night, may be aggravated by spicy foods, onions, alcohol, caffeine and ASA, NSAIDS 
59. Physical Manifestations Vomiting may occur Appetite is maintained, unless pyloric obstruction occurs Fluid volume deficit, if bleeding, take orthostatic BPs Watch for Hematemesis and melena Monitor H &
H Dx- barium swallow and EGD Test for H. pylori is IgG serologic testing and urea breath testing 
60. Nursing Diagnoses Name 5 diagnoses r/t PUD 1. 2. 3. 4. 5. What would be an
expected outcome for this disorder? 
61. Nursing Interventions Drug Therapy Goals: Provide pain relief, eradicate H. pylori, heal ulcerations,
prevent recurrence Eliminate H. pylori- triple treatment: Bismuth product (pepto-bismol) or a a proton pump
inhibitor and two antibiotics (metronidazole (Flagyl) and tetracycline or amoxicillin) May have to take medications
4 x’s/day for 14 days and often they don’t complete the series 
62. Nursing Interventions Drug therapy: Hyposecretory drugs- reduce gastric acid secretions Antisecretory agents- proton pump inhibitors, “zole” ending, suppress H, K-ATP ase enzyme system of gastric acid
production, can be given IV or PO H2 receptor antagonists- block histamine-stimulated gastric secretions, “dine”
ending Prostaglandin analogues- reduce gastric acid secretion and enhance gastric mucosal resistance to tissue
injury, Misoprostol (Cytotec) helps prevent NSAID induced ulcers, does cause uterine contraction and can not be given
to pregnant women 
63. Nursing Interventions Antacids Buffer gastric acid and prevent formation of pepsin, heal duodenal
ulcers Aluminum hydroxides and magnesium hydroxide, may affect those with renal impairment Take 2
hours after meals to reduce the H+ion load Calcium carbonate (TUMS) is an antacid, but it triggers gastrin release
and causes a rebound acid secretion Antacids can interact with other drugs- tetracycline, dilantin, also may have
a high sodium content Mucosal Barrier fortifiers- sucralfate (Carafate) supplies a protect coating by forming a
complex with proteins, binds with bile acids and pepsin, should be given on an empty stomach and not within 1 hour of
eating or taking antacids 
64. Nursing Interventions Diet therapy Bland diet may help to relieve symptoms Food may help to
neutralize acids, rebound may follow when more acid is released Avoid foods that stimulate gastric acid
release They are?? Yoga for stress relief, herbals, such as licorice and vitamins may help 
65. Gastrointestinal Bleeding What would be a nursing diagnosis for GI Bleeding? 1. 2. What
would be the expected outcome and how would you know that this was met? 
66. GI bleeding 
67. Gastrointestinal Bleeding Hypovolemia Management Monitor vital signs and I&O, assess for bleeding
and vomiting, monitor CBC Fluid and electrolyte replacement is necessary, usually NSS or LR, may give PRBC’s
or FFP Watch for signs of shock, what are they?? Bleeding reduction Monitor labs, insert and NGT to
decompress the stomach, give an H2 blocker, may need gastric lavage, what is that?? 
68. Nursing Interventions for GI bleeding Endoscopic therapy EGD, can do: cautery on the bleeding
sites inject a sclerosing agent with diluted epipherine Laser therapy Clip the bleeding vessel Somastatin Analogue- Sandostatin may be used to suppress gastric acid secretion on parietal and chief cells,
vasoconstricts the splanchnic arteries which reduce hemorrhage 
69. Surgical management of GI bleeding MIG- minimally invasive gastrectomy- laproscopic to remove chronic
gastric ulcer or treat hemorrhage, make several small incisions, may partially remove the stomach and/or vagotomy to
control acid secretion Gastroenterostomy- creates a passage between the body of the stomach and jejunum,
reduces motor activity in the pyloroduodenal area, diverts acid, a vagotomy may be done with it to decrease secretion.
Can do truncal, selective or proximal. Billroth I- connect to duodenum, Billroth II connects to jejunum Pyloroplasty-
widens the exit of the pylorus and empties the stomach 
70. Billroth 1 
71. Postop care for GI surgery NGT management Monitor for complications of: Dumping syndrome-
vasomotor symptoms, rapid emptying of gastric contents into the small intestine, shifts fluid into the gut and cause
abdominal distention, 30 min after eating have vertigo, tachycardia, syncope, sweating, pallor, palpitations. 90 min later
have excessive amount of insulin released, this dizziness, palpitations, diaphoresis and confusion Should eat
smaller amounts, take less liquid with food, high protein and fat, low CHO diet, sandostatin may be given and pectin
with food 
72. Postop Care of GI surgery Reflux gastropathy- bile reflux, when pylorus is bypassed, bile in stomach and have
abdominal discomfort and vomiting Delayed gastric emptying- usually resolves in 1 week, edema at the
anastomosis or adhesions may occur, hypokalemia, hypoproteinemia and hyponatremia may also cause Afferent
loop syndrome- duodenal loop is partially obstructed, pancreatic and biliary secretions fill the intestinal loop, it becomes
distended painful contractions, bloating and pain 20-60 min after eating 
73. Post op GI surgery Recurrent ulceration- occurs in 5% of patients, may have ulcers at the anastomosis Nutritional management: Deficiencies of B12, folic acid and iron Impaired Ca metabolism and reduced
absorption of Ca and vitamin D Shortage of intrinsic factor, r/t the resection and rapid emptying of the food 
pernicious anemia- weak, anemic, atrophic glossitis- beefy shiny tongue Give back B12 and folic acid 
74. Pernicious anemia 
75. Irritable Bowel Syndrome Chronic GI disorder, with chronic or recurrent diarrhea, constipation, abdominal pain
and bloating Spastic colon, impairment of the motor/sensory function diarrhea alternating with constipation Usually begin as a young adult Stress, anxiety and familial factors may predispose patient 
76. IBS Assessment: History of bowel pattern Manning criteria- abdominal pain relieved by defection,
abdominal distention, sensation of incomplete evacuation of stool, presence of mucus with the stool Pain in LLQ
and cramps, may be tenderness and air in bowels Dx- flexible sigmoidoscopy or colonoscopy if >40 Barium
enema 
77. IBS Interventions Diet therapy- limit caffeine, alcohol, beverages with sorbitol, take in fiber and bulk,
30-40 gm/day Drug therapy: Bulk forming laxatives (Metamucil) antidiarrheals (loperamide) anticholinergics (bentyl) antidepressants (elavil) 5-HT4 agonists(Zelnorm) for prokinetic activity, imitates
serotonin to stimulate peristalsis Stress management- relaxation techniques 
78. Nursing Diagnoses Constipation r/t low residue diet and stress What can be done to manage this? Diarrhea r/t increased motility of intestines How can this be corrected or treated? What can be done to
correct constipation and impaction? What role may analgesics play in constipation? 
79. Colorectal Cancer 95% are adenocarcinomas, most come from adenomatous polyps 2/3 occur in
rectosigmoid region Can metastasize through blood and lymph, liver most common site with 15-30% spread there,
can also go to the lungs, brain, bones and adrenals May form fistulas into bladder and vagina Genetics-
autosomal dominant disorder- familial adenomatous polyposis only 1%, 100% malignant, usually starting at age 20.
Also, hereditary nonpolyposis colorectal cancer- autosomal dominant, 10% of cancers, develop by age 45 
80. Colorectal cancer 75% have no known cause Age is a risk factor Dietary- decreased bowel
emptying time, foods with carcinogens- red meat, fatty food, fried meats and fish, concentrated sweets High fat
diet increases bile acid secretion and anaerobic bacteria Irritable bowel diseases Third most common
malignancy 
81. Colorectal Cancer 
82. Colorectal cancer Manifestations: Rectal bleeding, anemia and change in stool Gas pains,
cramping or incomplete evacuation Hematochezia- bright red blood when in rectum Tumors can grow large
when in upper abdomen, mostly liquid stool, more pain when in lower Tests- stool for occult blood, CEA, barium
enema, CT of abdomen Colonoscopy or sigmoidoscopy 
83. Colorectal cancer Nursing Diagnoses- Name 4 diagnoses, associated with colorectal cancer 1. 2. 3. 4. What would be the expected outcomes? 
84. Colorectal cancer Nonsurgical management: Duke’s staging classification A- tumor has penetrated
into, but not through the bowel wall B- tumor has penetrated through the bowel wall C-tumor has penetrated
through the bowel wall and there is lymph node involvement D- tumor has metastasized to distant sites Radiation therapy Drug therapy-chemotherapy IV 5-FU and leucovorin, side effects are diarrhea, mucositis,
leucopenia and mouth ulcers Eloxatin, Camptosar, Avastin are also being used, along with monoclonal
antibodies- cetuximab 
85. Colorectal cancer Surgical management: Colon resection- removal of tumor and lymph nodes Colectomy- colon removal Abdominal perineal resection- removes sigmoid colon, rectum and anus, colostomy
is performed Colostomies may be ascending, descending, sigmoid, transverse or double barreled Stool
returned depends on the site of the colostomy 
86. Colostomy 
87. Colorectal cancer Postoperative Care: Colostomy management What types of nursing diagnoses
may accompany this procedure? How should the stoma appear? Report any bleeding, breakdown of the
sutures from the wall and signs of ischemia or necrosis Wound care management- JP drains, monitor for
infection Fluid volume deficit and electrolyte imbalance 
88. Colorectal cancer Teaching: Colostomy care- what kinds of things should be covered? Dietary
measures to control stool and gas, what would they be? Psychological adjustment to the colostomy, what
diagnosis relates to this? Grief and family coping- what resources may be needed? Genetic testing if familial
type 
89. Intestinal Obstruction Partial or complete Mechanical- bowel is physically obstructed by adhesions,
tumors Nonmechanical- paralytic ileus or adynamic ileus, neuromuscular distrubance- slow movement or
backup Contents accumulate at or above the obstruction distention, peristalsis increases to aid movement,
stimulates more secretions more distention edema of the bowel, increased capillary permeability 
90. Intestinal Obstruction Plasma leaks into the peritoneal cavity and trapped fluid decreases the absorption of
fluid and electrolytes into the vascular space reduced blood volume and electrolyte imbalances, can hypovolemic
shock Can also lead to metabolic alkalosis if high and there is a loss of gastric acid, if low, metabolic acidosis
occurs with the loss of alkaline fluids Bacterial peritonitis and septic shock can also occur from the release of
endotoxins 
91. Intestinal obstruction 
92.
93. Intestinal Obstruction Adhesions account for 45-60%, r/t scar tissue Intussusception- telescoping bowel
and volvulus- twisting of the bowel Paralytic ileus- decreased peristalsis from trauma, toxin or autonomic, can
result from surgery, MI’s, rib fracture, pneumonia, peritonitis and vascular insufficiency from heart failure or shock 
94. Intestinal Obstruction Assessment: History of symptoms and occurrence Abdominal pain and
cramping Obstipation, vomiting with brown and foul smelling Borborygni above the obstruction, then
absent Abdominal distention and tympanic abdomen Abdominal films and CT of abdomen WBC
elevated in some cases 
95. Intestinal Obstruction Nonsurgical management: NGT to decompress to LCS Nasointestinal tubes-
Miller-Abbott, mercury balloons and migrate down the intestine by peristalsis, don’t irrigate with fluid- it will increase
edema at the obstruction Fluid and electrolyte replacement- NPO, give NSS or LR, replace K Pain control-
not normally given opioids, mask pain and peritonitis Antibiotics if suspect perforation Surgical
management: Exploratory laparotomy 
96. Case Study 24 year old female admitted with frequent bloody diarrhea stools, weight loss and anemia. What do you suspect? What labwork should you do? What treatment may be needed? 
97. Case Study Your patient tells you that the diarrhea has been occurring for months. How do you
differentiate between U.C. and Crohn’s disease? What may be her treatment options? 
98. Case Study How do you help your patient decide about a colostomy? If she does want a colostomy, what
type of teaching needs to be done? 
99. Chronic Inflammatory Bowel Disease Ulcerative Colitis and Crohn’s Ulcerative Colitis: Remissions
and exacerbations Loose stools with blood and mucous 10-20/day Poor absorption of nutrients and
thickening of the colon wall Abdominal distention and cramping Complications are: hemorrhage, perforation,
fistulas and nutritional deficiencies May be familial tendency, inflammation r/t response to normal flora 
100. Ulcerative Colitis 
101. Chronic Inflammatory Bowel Disease Crohn’s disease Terminal ileum, patching involvement through all
layers of the bowel Deep fissures and ulcers occur 5-8 loose stools/day, rarely bloody Complications
are: Fistulas, nutritional deficiencies Cause is thought to be mycobacterium paratuberculosis, genetic
predisposition 
102. Crohn’s Disease Garrard Crohn's story 
103. Ulcerative Colitis Manifestations: Abdominal pain, bloody diarrhea, tenesmus- uncontrolled straining Dx- barium enema Nursing Diagnoses: Diarrhea r/t inflammation of the bowel Acute and chronic
pain Imbalance nutrition: less than body requirements Disturbed body image 
104. Ulcerative Colitis Diarrhea management- Drugs- salicylate compounds- Sulfasalazine (Azulfidine)
inhibits prostaglandins to reduce inflammation, also use Asacol, Pentasa Corticosteroids- Prednisone to decrease
edema Immunosuppressive- cyclosporine Antidiarrheals Monoclonal antibody- Remicade neutralizes
the activity of tumor necrosis factor and prevents toxic megacolon 
105. Ulcerative Colitis Diet therapy: NPO at first, then TPN, may have low fiber or low residue, what foods
would be included? Surgical management: Total Proctocolectomy with permanent Ileostomy Total
colectomy with a continent ileostomy Total colectomy with ileoanal anastomosis and ileoanal reservoir or
pouch Postop- teaching for ostomy, pain control and monitoring for GI bleeding and fluid volume deficit 
106.
107.
108. Crohn’s Disease Aggravated by bacterial infection, inflammation and smoking History of fever,
abdominal pain and loose stools, weight loss Steatorrhea is common- fatty stools Fistulas may occur
between bladder and vagina Drug therapy- same as UC, except may take metronidazole if fistulas and imuran as
an immunosuppressant Diet therapy- may be on TPN, supplements like ensure, vivonex 
109. Crohn’s Disease Monitor for fistulas- infections, skin problems, malnutrition, fluid and electrolyte
imbalances Fluid and electrolyte therapy- what would this entail? Name one antidiarrheal. Surgical
management: Bowel resections Fistula repairs Ileostomies may also be required to rest the bowel or
repair damaged areas. 
Definition <ul><li>Peptic ulcer disease (PUD) = Mucosal defect in the gastrointestinal tract (gastric or duodenal)
exposed to acid and pepsin secretion </li></ul><ul><li>Gastritis is the precursor to PUD and it is clinically difficult to
differentiate the two </li></ul>
5. Differentiating gastric from peptic ulcer disease <ul><li>Duodenal ulcers - age 25-75 years. </li></ul><ul><li>Gastric
ulcer - age 55-65 years </li></ul><ul><li>Pain awakening patient from sleep between 12-3 a.m. present in 2/3 duodenal
ulcer patients and 1/3 gastric ulcer patients </li></ul>
. Physical Exam Findings <ul><li>In uncomplicated PUD exam findings few and non-specific:
</li></ul><ul><li>Epigastric tenderness - usually mild. </li></ul><ul><li>Bowel sounds - normal.
</li></ul><ul><li>Rectal exam may show melena/guaiac+ stool from occult blood loss
</li></ul><ul><li>Signs of peritonitis with perforation </li></ul>
. 25. If Mr. Jones Hemoccult is Positive <ul><li>What PE findings do you want to specifically document if Mr.
Jones is Heme (+) indicating a possible active GI bleed? </li></ul><ul><li>Look for signs of volume depletion:
tachycardia, hypotension, orthostatics, skin turgor, MM appearance </li></ul><ul><li>Look for signs of
anemia: conjunctiva or skin pallor, new heart murmur </li></ul>
. 26. Lab Studies to Evaluate PUD <ul><li>CBC - evaluate acute/chronic blood loss </li></ul><ul><li>H.
Pylori </li></ul><ul><li>- Serologic antibody test for HP – does not determine if active HP infection
</li></ul><ul><li>- Fecal antigen test tests for active HP </li></ul><ul><li>- Urea breath test tests for active
HP </li></ul>
. 27. Principles in Selecting H. pylori Test <ul><li>Based on the following: </li></ul><ul><ul><li>• Probability
of previously eradicated infection </li></ul></ul><ul><ul><li>• Probability of current active infection
</li></ul></ul><ul><ul><li>• Need to document active infection </li></ul></ul><ul><ul><li>• Need for rapid
result </li></ul></ul><ul><ul><li>• Patient preferences </li></ul></ul><ul><ul><li>• Cost (both of test and
possible unnecessary treatment) </li></ul></ul>
. 28. H. Pylori Serology Antibody Test <ul><li>Office based serology tests faster but less accurate than lab
based ELISA tests </li></ul><ul><li>Sensitivity and specificity of approx 90% </li></ul><ul><li>Not useful for
evaluating eradication - antibody levels can persist for a long time, need serial titers to evaluate </li></ul>
. 29. When is a Serology Test Useful? <ul><li>Not useful in </li></ul><ul><li>Populations with low disease
prevalence </li></ul><ul><li>Elderly populations to detect active disease </li></ul><ul><li>Useful in
</li></ul><ul><li>Patients who never received H. pylori treatment </li></ul><ul><li>Symptomatic patients not
using NSAIDs- if negative serology – unlikely PUD </li></ul>
. 30. H. Pylori Stool Antigen (HpSa) Test <ul><li>Useful in initial diagnosis + confirmation of eradication
</li></ul><ul><li>Sensitivity of 91% and a specificity of 92%* </li></ul><ul><li>Test requires collection of
stool sample- size of an acorn </li></ul><ul><li>Performed in lab or newer POCT available
</li></ul><ul><li>Requires little preparation, however patients may not be compliant with collecting sample
</li></ul><ul><li>*Gisbert JP, Pajares JM. Stool antigen test for the diagnosis of Helicobacter
</li></ul><ul><li>pylori infection: a systematic review. Helicobacter 2004;9(4):347-68 </li></ul>
. 31. Urea Breath Test <ul><li>Useful for initial diagnosis + confirmation of eradication
</li></ul><ul><li>Sensitivity and specificity over 90%* </li></ul><ul><li>Urease activity is present in the
stomach in those infected with H pylori </li></ul><ul><li>Ingest urea labeled with radioactive carbon
</li></ul><ul><li>Hydrolysis of urea -> labeled carbon dioxide (CO2) </li></ul><ul><li>Rapidly absorbed into
bloodstream and within a few minutes, appears in breath </li></ul><ul><li>*Gatta L, Vakil N, Ricci C, et al. A
rapid, low-dose, 13C-urea tablet for the detection of Helicobacter pylori infection before and after treatment.
Aliment Pharmacol Ther 2003;17(6):793-8 </li></ul>
. 32. Breath Test Compared to HpSa <ul><li>Requires more patient preparation </li></ul><ul><li>More
expensive </li></ul><ul><li>Number of drugs can adversely affect accuracy </li></ul><ul><li>Antibiotics and
bismuth -> stop for 4 weeks </li></ul><ul><li>Proton pump inhibitors -> stop for 7 days
</li></ul><ul><li>Patients need to fast for at least 6 hours. </li></ul><ul><li>Breath test cannot be used in
pregnant women </li></ul>
. 33. Imaging Studies <ul><li>Chest x-ray if perforation is suspected to detect free abdominal air
</li></ul><ul><li>Upper gastrointestinal series </li></ul><ul><ul><li>Performed by experienced radiologist is
close to diagnostic accuracy of endoscopy </li></ul></ul><ul><ul><li>Not as sensitive as endoscopy in
diagnosis of small ulcers (<0.5 cm) </li></ul></ul><ul><ul><li>Unable to obtain biopsy to rule out malignancy
</li></ul></ul>
. 34. Endoscopy <ul><li>Endoscopy indicated in following high risk patients: </li></ul><ul><li>>50 years old
with new-onset dyspepsia </li></ul><ul><li>Dyspepsia with dysphasia and/or weight loss
</li></ul><ul><li>Evidence of GI bleeding </li></ul><ul><li>Failed appropriate trial of empiric therapy
</li></ul><ul><li>Using NSAIDs or other high risk meds </li></ul><ul><li>Signs of UGI tract obstruction
(early satiety, vomiting) </li></ul><ul><li>Ethnic background assoc. with increased risk UGI malignancies
</li></ul><ul><li>Excerpts from Guidelines prepared by The Standards of Practice Committee of the
American Society for Gastrointestinal Endoscopy </li></ul>
. 35. Rapid Urease Test and Histopathology <ul><li>Gastric mucosal biopsy obtained during endoscopy:
</li></ul><ul><ul><li>Rapid urease tests (CLOtest, Hpfast, Pyloritek) bacterial urease converts urea
substrate in kit to ammonia -> changes pH producing color change.
</li></ul></ul><ul><ul><li>Histopathology often considered gold standard for diagnosis </li></ul></ul>
. 36. Mr. Jones Prior Ulcer History <ul><li>On further questioning Mr. Jones states he had similar abdominal
pain three years ago and was told by his physician at that time that it was most likely due to an ulcer. He took
“the purple pill” for a month and his symptoms resolved. He had no definitive diagnostic tests done at that
time. </li></ul><ul><li>What would you do at this time? </li></ul>
. 37. Answer <ul><li>H. pylori serology - many patients with history of “ulcer” have not undergone eradication
therapy </li></ul><ul><li>Test for H. pylori antibody and treat if (+) </li></ul><ul><li>Endoscopy if serology
negative or if fails to improve with treatment </li></ul>
. 38. Moving on to Treatment Options……….
. 39. Over The Counter Remedies <ul><li>Aluminum and magnesium hydroxide salt (Maalox ® , Mylanta ® )
Neutralizes gastric acidity. </li></ul><ul><li>Aluminum side effect = constipation
</li></ul><ul><li>Magnesium side effect = diarrhea </li></ul><ul><li>Magnesium and aluminum mixtures
used to avoid side effects </li></ul>
. 40. Over the Counter Remedies cont’d <ul><li>Calcium Carbonate (Tums ®, Rolaids®) – calcium salt
neutralizes acid </li></ul><ul><li>Bismuth subsalicylate (Peptobismol ®) – binds to ulcer base forming a
protective coat, has anti-inflammatory and bacteriocidal properties </li></ul>
. 41. H2-Blockers <ul><li>Selectively block H2-receptors on parietal cells reducing acid secretion
</li></ul><ul><li>Used primarily in ulcer disease not associated with H pylori </li></ul><ul><li>Treatment
duration is 6-8 wk. </li></ul>
. 42. Side Effects of Cimetidine/Tagamet ® <ul><li>Elderly patients – confusion </li></ul><ul><li>Young
males - impotence +/- gynecomastia </li></ul><ul><li>May alter levels of other drug - warfarin, TCA’s,
triamterene, phenytoin, propranolol, metronidazole, antiarrythmics </li></ul><ul><li>May alter renal function
requiring lower doses </li></ul>
. 43. Proton Pump Inhibitors <ul><li>Decreases gastric acid secretion by inhibiting the parietal cell H+/K+
ATP pump </li></ul><ul><li>Relieve pain and heal peptic ulcers more rapidly than H2 blockers
</li></ul><ul><li>Drugs in this class are equally effective </li></ul><ul><li>Four weeks to treat active PUD
</li></ul><ul><li>Eight weeks to treat erosive esophagitis </li></ul>
. 44. Other Pharmacotherapy Agents <ul><li>Sucralfate (Carafate ® ) Binds proteins in exudates and forms a
viscous adhesive that protects GI lining </li></ul><ul><li>Misoprostol (Cytotec ® ) Prostaglandin analog-
protects lining of GI tract by replacing depleted prostaglandin E1. Prevents peptic ulcers in patients taking
NSAIDs </li></ul>
. 45. H. Pylori Triple Therapy Treatment <ul><li>Triple therapy for 14 days is treatment of choice
</li></ul><ul><li>Two forms of triple therapy: PPI–based and bismuth-based </li></ul><ul><li>PPI based =
PPI + 2 antibiotics for 2 wk, cont PPI for additional 2 weeks. </li></ul><ul><li>Bismuth-based = bismuth
subsalicylate and 2 antibiotics, for 2 weeks with addition of H2- blocker to optimize ulcer healing. </li></ul>
. 46. H Pylori Treatment
http://www.drugdigest.org/DD/Comparison/NewComparison/0,10621,550540-21,00.html Cure Rate Side
Effect Rating 81-92% low-medium Prevpak 80-85% medium-high Helidac + H2 blocker Combination
Products 80-90% medium Amoxicillin + Metronidazole + PPI 80-90% medium-low Amoxicillin +
Clarithromycin + PPI 80-90% medium Clarithromycin + Metronidazole + PPI Three Drug Regimens
. 47. H. Pylori Therapy cont’d <ul><li>Successful eradication of H. pylori reduces PUD recurrence rates from
90% to less than 10% per year. </li></ul><ul><li>Patients no longer require ongoing chronic acid
suppression. </li></ul><ul><li>If symptoms return after treatment of PUD, then testing for recurrence should
be pursued </li></ul>
. 48. PUD Complications <ul><li>Hemorrhagic shock/peritonitis from a perforated ulcer
</li></ul><ul><li>Symptomatic relief with PPI may mask symptoms of gastric malignancy
</li></ul><ul><li>Gastritis may present as bleeding, more likely in elderly </li></ul><ul><li>Symptoms of
anemia (fatigue, dyspnea) </li></ul>
. 49. Initial Treatment Plan in the Absence of High Risk Symptoms <ul><li>Based on current evidence, no
single strategy has been demonstrated to be more medically effective than any other.
</li></ul><ul><li>Empiric therapy with acid suppression </li></ul><ul><li>Empiric H pylori testing and
treating strategy </li></ul><ul><li>Early endoscopy </li></ul><ul><li>Excerpts from Guidelines prepared by
The Standards of Practice Committee of the American Society for Gastrointestinal Endoscopy </li></ul>
. 50. Final Recommendations <ul><li>Alarm symptoms = endoscopy. </li></ul><ul><li>No alarm symptoms
= medical management favored approach </li></ul><ul><li>Studies still in progress to evaluate if medical
management versus vs endoscopy is both medically and cost effective in long-term </li></ul><ul><li>Lack of
response or the recurrence of symptoms warrants endoscopy </li></ul>
. 51. Medical Legal Pitfalls <ul><li>Failure to consider non-GI cause of epigastric pain (AMI/AAA)
</li></ul><ul><li>Failure to consider GI bleed in absence of abdominal pain (especially in elderly)
</li></ul><ul><li>Lack of follow-up care resulting in failure to diagnose gastric cancer
</li></ul><ul><li>Failure to recommend endoscopy early in high risk patients </li></ul><ul><li>Failure to
obtain a history regarding NSAID use </li></ul>
. 52. Alternate Scenarios of Mr. Jones Case <ul><li>Mr Jones is a 63 yo male presenting with previously
noted epigastric symptoms and PMH. On physical exam he is noted to have heme (+) stool.
</li></ul><ul><li>What evaluation would you do next? </li></ul>
. 53. Alternate Scenarios to Mr. Jones Case <ul><li>Mr Jones is a 63 yo male presenting with previously
noted epigastric symptoms and PMH. On review of his prior ulcer history he was tested and had a positive H.
pylori serology test. He was treated with triple therapy (PPI and 2 antibiotics) and symptoms resolved.
</li></ul><ul><li>What would you do next? Would you recheck H. pylori serology? Repeat triple therapy?
</li></ul>
. 54. Summary <ul><li>H. pylori is the most common cause of PUD and is a risk factor for gastric cancer
</li></ul><ul><li>H Pylori eradication reduces risk of disease recurrence </li></ul><ul><li>Test-and-Treat
strategy is recommended for patients with undifferentiated dyspepsia </li></ul><ul><li>Intial evaluation with
endoscopy is recommended for those with alarm symptoms or those failing treatment
</li></ul><ul><li>Optimum treatment regimens are 14d multidrug with antibiotics and acid suppressants
</li></ul>
. 55. References <ul><li>http://www.emedicine.com/med/topic1776.htm
</li></ul><ul><li>http://www.mcg.edu/som/pathology/GraduateEducation/Evidence%20Base%20Path/hpsa
1.ppt </li></ul><ul><li>http://www.acg.gi.org/physicians/guidelines/ManagementofHpylori.pdf
</li></ul><ul><li>http:// www.cdc.gov/ncidod/dbmd/diseaseinfo/hpylori_t.htm
</li></ul><ul><li>http://courses.ahc.umn.edu/pharmacy/5880/LectureSlides/Peptic%20Ulcer%20Disease%
20(PUD)_files/frame.htm </li></ul><ul><li>http:// www.cdc.gov/ulcer/history.htm
</li></ul><ul><li>http://www.drugdigest.org/DD/Comparison/NewComparison/0,10621,550540-21,00.html
</li></ul>
. 56. References cont’d <ul><li>Fendrick M, Forsch R etal. Peptic Ulcer Disease Guidleines for Clinical Care.
University of Michigan Health System May 2005 </li></ul><ul><li>American Gastroenterological Association
medical position statement: evaluation of dyspepsia. Gastroenterology 1998;114:579-81.
</li></ul><ul><li>Krogfelt K, Lehours P, Mégraud F. Diagnosis of Helicobacter pylori Infection . Helicobacter
2005 10:s1 5 </li></ul><ul><li>Meurer L, Bower D. Management of Helicobacter pylori Infection . American
Family Physician Vol 65, No. 7, 2002 pp 1327-1336 </li></ul><ul><li>Standards of Practice Committee of the
American Society for Gastrointestinal Endoscopy; The role of endoscopy in dyspepsia . Gastrointestinal
Endoscopy Vol 54, No. 6, 2001 pp 815-817 </li></ul><ul><li>Vaira D, Gatta L, Ricci C, et al . Peptic ulcer and
Helicobacter pylori: update on testing and treatment. Postgrad Med 2005;117(6):17-22, 46 </li></ul>
bnormalities of the GIT • Dysphagia: – Difficulty swallowing, caused by obstruction of the esophagus – Obstruction may
be caused by • tumors, congenital narrowing • Neurologic disorders such as brain injury stroke or Parkinson’s disease
may affect voluntary swallowing or peristalsis of the esophagus • Dyspepsia – Epigastric fullness, discomfort,
indigestion • Odynophagia – Painful swallowing usually associated with dysphagia • Heartburn – Burning sensation
retrosternally associated with reflux
4. Abnormalities of the GIT • Anorexia – Loss of appetite • Haematemesis – Vomiting blood (could be red or altered
“coffee ground”) • Melaena – Passing of black tarry, offensive stool (usually due to upper GI bleeding) • Haematochezia
– Passing blood through rectum (PR bleeding) • Gastritis – Inflammation of the gastric mucosa – Acute gastritis –
Chronic gastritis
5. Abnormalities of the GIT • Peptic ulcers A peptic ulcer is an abnormal area of mucosa that has been damaged by the
pepsin and hydrochloric acid of gastric juice, with consequent inflammation of the underlying and surrounding tissue.
Erosion may subsequently occur into the lamina propria and submucosa to cause bleeding. – Most of peptic ulcer occur
either in the duodenum, or in the stomach – Ulcer may also occur in the lower oesophagus due to reflexing of gastric
content – Rarely in certain areas of the small intestine
6. Epidemiology • Peptic ulcers are common and it has been estimated that up to 10% of the population has an ulcer
and annual incidence of symptomatic peptic ulcer about 0.3%. • Duodenal ulcers are four times as common as gastric
ulcers and occur mainly in the duodenal cap. • Gastric ulcers occurs mostly in the lesser curvature of the stomach.
These are benign, some time develop as a tumors (5%). • Gastric malignancy is common in Japan, Chile, Finland and
Iceland than other world countries (because of environmental and diet factor).
7. Aetology Aetology of peptic ulcer disease is multifactorial. • Infection with the bacteria Helicobacter pylori occurs in
80 to 95% of patients with peptic ulcer disease. • H. pylori infection impairs the protective mechanisms of the G.I. tract
against low pH and digestive enzymes and leads to ulceration of the mucosa. • Stress — Emotional, trauma, surgical. •
Injury or death of mucus-producing cells. • Chronic use of NSAIDs • Smocking • Alcohol and diet • Hypercalcemia
(↑gastric secretion)
8. Aetology • Excess acid production in the stomach. The old hypothesis that ulceration is caused simply by
hyperacidity is not tenable. About 70% of gastric ulcers and 50% of duodenal ulcers are not associated with abnormally
high acid production. • Genetic factor: The lifetime prevalence of developing ulcer disease in first-degree relatives of
ulcer patients is about three times greater than the general population. 20-50% of duodenal ulcer reported a positive
family history. • Ulcers are also more common in blood group O subjects and in those who do not secrete blood group
antibodies into gastric secretions.
9. Classification of peptic ulcer • Peptic ulcers classified based on region or location of illness – – – – Stomach (called
gastric ulcer) Duodenum (called duodenal ulcer) Esophagus (called Esophageal ulcer) Meckel's Diverticulum (called
Meckel's Diverticulum ulcer) Modified Johnson Classification of peptic ulcers Type I: Ulcer along the lesser curve of
stomach Type II: Two ulcers present - one gastric, one duodenal/prepyloric Type III: Prepyloric ulcer Type IV: Proximal
gastroesophageal ulcer Type V: Anywhere (associated with chronic NSAID use)
10. Sites of peptic ulcer • Duodenum: First portion, Anterior wall • Stomach: usually antrum, lesser curvature (common),
anterior and posterior wall, greater curvature (less common) • Meckel’s diverticulum In the margins of a
gastroenterostomy (stomal ulcer) • In the duodenum, stomach or jejunum of patients with Zollinger- Ellison syndrome. •
Within or adjacent to a Meckel’s diverticulum. ZES
11. Symptoms of peptic ulcer Symptoms of peptic ulcer very with location of the ulcer and the patient age. • Abdominal
discomfort • Pain or nausea (pain is located in the epogastrium; not radiate) Waterbrash • Waterbrash • Loss of appetite
and weight loss • Hematemesis (vomiting of blood) Rarely, ulcer lead to a gastric or duodenal perforation.
Hematemesis
12. Manifestations of peptic ulcer disease • Episodes of remission and exacerbation • Pain that for duodenal ulcers is
often relieved by eating or antacids • G.I. bleeding and possible hemorrhage (20 to 25% of patients) • Perforation of
ulcers with significant mortality • Obstruction of G.I. tract
13. Complications of peptic ulcer • Gastrointestinal bleeding. (Sudden large bleeding can be life threatening) • Cancer
(Helicobacter pylori as the etiological factor making it 3-6 times likely to develop stomach cancer) • Perforation (hole in
the wall) • Penetration.
14. Diagnosis of peptic ulcer
15. Diagnosis of peptic ulcer • Radiological Diagnosis: Barium x-ray or upper GI series is a widely used for diagnosis.
Barium x-ray is difficult to analysis and less sensitive and accurate. • Laboratory test: – Noninvasive urea breath test. –
Patient with refractory or recurrent peptic ulcer may have underlying H. pylori infection, histopathology investigation
may req. – Serologic test for detecting H. pylori (levels of IgG and IgA ELISA test) – Stool antigen test for non-invasive
detecting the presence of H. pylori. • Endoscopic diagnosis
16. Drugs for Treatment of Peptic Ulcer Disease • Antibiotics for eradication of H. pylori, if present (amoxicillin,
clarithromycin) • Antacids (magnesium hydroxide, aluminum hydroxide) • H2 receptor antagonists (ranitidine,
cimetidine) • Proton-pump inhibitors (omeprazole) • Mucosal protective agents (bismuth, sucralfate)
17. Management of peptic ulcer The objectives of management are to: • relieve pain and discomfort • accelerate
healing • prevent recurrence and complications
18. Thank you
19. Helicobacter pylori & Ulcer • H. pylori -- causes chronic and indolent inflammation by damaging the mucosal
defense system by reducing the thickness of the mucus gel layer, diminishing mucosal blood flow, and interacting with
the gastric epithelium throughout all stages of the infection. • H. pylori infection can also increase gastric acid secretion
by producing various antigens, virulence factors, and soluble mediators
20. Helicobacter pylori & Ulcer
21. Zollinger–Ellison syndrome • Tumors of the gastrinsecreting endocrine cells of the pancreas or, less frequently, the
duodenal wall. • Leads to excessive acid production by the G.I. tract. • Development of serious and aggressive peptic
ulcers. • Complications can include perforation, hemorrhage and obstruction. • Treatment may include resection of
tumor, administration of H2 receptor antagonists, anticholinergics and antacids.
CROHN’S DISEASE IS A CHRONIC,RELAPSING AND REMITTING DISEASE THAT INVOLVES TRANSMURAL

INFLAMMATION OF THE INTESTINE. USUALLY CONFINED TO DISTAL SMALL INTESTINE AND COLON.
THE DISEASE REFLECTS A FAILURE TO DOWN- REGULATE INFLAMMATORY RESPONSES TO NORMAL
COMMENSAL MICROBIOTA.
3. IN GENETICALLY SUSCEPTIBLE INDIVIDUALS, MUTATIONS IN GENES CONTROLLING INNATE IMMUNE

RESPONSE REGULATORS OF ACQUIRED IMMUNITY APPEARS TO PREDISPOSE TO DISEASE WHEN
INDIVIDUALS ARE EXPOSED TO APPROPRIATE ENVIRONMENTAL FACTORS,
4. The pattern recognition receptors(PRRs) May be intracellular, such as the NOD protein One of the NOD protein
the NOD-2 encoding gene may undergo mutation which leads to crohn’s disease
5. NOD -2 protein
6. The mainstay of treatment remains high- dose corticosteroids to suppress inflammation nonspecifically. Surgery
may be required to treat strictures, fistulas and abscesses. Probiotics therapeutic microorganisms can be used to
maintain healthy microbiota The cascade is selectively implicated in individuals patients with different genetic
backgrounds .
7. probiotics corticosteroids The end

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Peptic Ulcer • An Ulcer is … Erosion in the lining of the stomach or the first part of the small

5. Peptic UlcerPeptic Ulcer

6. • The gastroduodenal mucosal integrity is determined by protective (defensive) & damaging

7. Mucosal damage erosions & ulcerations

15. Complication of ulcer • Bleeding. • Perforation. • Narrowing and obstruction.

4. The gastroduodenal mucosal integrity isdetermined by protective (defensive) &damaging

5. • Bicarbonate • Helicobacter pylori• Mucus layer • NSAIDs• Prostaglandins • Pepsins• Mucosal

11. Life Style Change.Medical.Surgical.

12. Discontinue NSAIDsSmoking cessation. Alcohol cessation. Stress reduction.

20. Gastrointestinal continuity is restored bygastroduodenal (Billroth 1) anastomosisOR gastrojejunal

21. Dehiscence. Stenosis of anastomosis. Bleeding. Injury to neighbour tissues. Dumping

22. HemorrhagePerforation peptic ulcerGastric outlet obstruction

32. Helicobacter pylori Spiral shaped, flagellated, Gram negative bacterium

33. Helicobacter pylori on gastric mucus- secreting epithelial cells

SYMPTOMS <ul><li>Burning abdominal pain </li></ul><ul><li>Haematemesis

13. DIAGNOSIS <ul><li>Endoscopy: </li></ul><ul><li>Flexible tube fitted with camera is threaded

15. LIFE-STYLE MODIFICATION IN PUD <ul><li>Doubtful efficacy </li></ul><ul><ul><li>REST

16. ANTI ULCER DRUGS <ul><li>REDUCTION OF GASTRIC ACID SECRETION </li></ul><ul><li>Histamine

17. ANTIULCER DRUGS <ul><li>Neutralization of gastric acid(antacids) Systemic : Sodium bicarbonate,

18. HISTAMINE ANTAGONIST <ul><li>Cimetidine </li></ul><ul><li>.Histamine antagonists inhibit the

21. PROTON PUMP INHIBITORS <ul><li>OMEPRAZOLE </li></ul><ul><li>Omeprazole is inactive at

22. ACETYL CHOLINE ANTAGONIST <ul><li>PIRENZEPINE </li></ul><ul><li>MECHANISM:

23. AGENTS THAT ENHANCE MUCOSAL DEFENSE <ul><li>Prostaglandin Analogs:

24. MISOPROSTOL <ul><li>MECHANISM: </li></ul><ul><li>Misoprostol acts upon gastric parietal cells ,

25. ULCER PROTECTIVES <ul><li>SUCRALFATE </li></ul><ul><li>MECHANISM:

. Depth till submucosa </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>In any part of GI tract exposed

6. Nerves of GI tract<br />

10. Stomach<br /><ul><li>Function:

12. Chief cells secrete Pepsinogen pepsin

18. Small intestine<br />

25. UGI exam<br />

27. Colonoscopy<br />

33. GERD<br />

47. Peptic Ulcers<br />

55. Perforated ulcer<br />

66. GI bleeding<br />

70. Billroth 1<br />

74. Pernicious anemia<br />

81. Colorectal Cancer<br />

86. Colostomy<br />

91. Intestinal obstruction<br />

100. Ulcerative Colitis<br />

102. Crohn’s Disease<br />Garrard<br />Crohn's story<br />

6. Nerves of GI tract<br />

10. Stomach<br /><ul><li>Function:

12. Chief cells secrete Pepsinogen pepsin

18. Small intestine<br />

25. UGI exam<br />

27. Colonoscopy<br />

33. GERD<br />

47. Peptic Ulcers<br />

55. Perforated ulcer<br />

66. GI bleeding<br />

70. Billroth 1<br />

74. Pernicious anemia<br />

81. Colorectal Cancer<br />

86. Colostomy<br />

91. Intestinal obstruction<br />

100. Ulcerative Colitis<br />

102. Crohn’s Disease<br />Garrard<br />Crohn's story<br />

14. Diagnosis of peptic ulcer

18. Thank you

20. Helicobacter pylori & Ulcer

CROHN’S DISEASE IS A CHRONIC,RELAPSING AND REMITTING DISEASE THAT INVOLVES TRANSMURAL