What is Peptic Ulcer Disease?

PUD
 is ulcer formation in the lining of the upper GI tract that affects mainly the mucosal lining of the
stomach, duodenum or esophagus, depending on its location
 an excavation that forms in the mucosa of the esophagus, stomach, in the pylorus, duodenum or
in the jejunum (if jejunum is anastomosed to the stomach)
 an erosion may from in the in the mucosa and may extend deeply in the muscle layers and
peritoneum (thin membrane that lines the inside of the abdominal wall.

Three Types of Peptic Ulcers:

Gastric Ulcers
 located inside the stomach
 chronic gastric ulcer tend to occur in the lesser curvature of the stomach
 20 percent of peptic
Duodenum Ulcer
 located inside the duodenum which is the first part of the small intestine
 Peptic ulcers are more likely to occur in the duodenum than in the stomach
 80 percent
Esophageal Ulcer
 located inside the lower part of the esophagus
 it occurs as a result of the backflow of hydrochloric acid from the stomach into the esophagus
associated with GERD.

Anatomy of Stomach
 Role of the stomach is to liquefies the food by churning it and release acids and enzyme such as
HCL (hydrochloric acid) and pepsin to break down food.

Layers of the Stomach

1. Mucosa
 top layer of the mucosa that releases mucous rich in bicarbonate that protects the lining from the
stomach acid. It also contains gastric pits that contain the parietal, chief cells, and g-cells.
 Parietal cells: release hydrochloric acid along with intrinsic factor
 Chief cells: release pepsinogen which mixes with hydrochloric acid and becomes PEPSIN
 G-cells: release gastrin

2. Submucosa
 made up of connective tissue, nerves, vessels
3. Muscularis externa
 (has 3 smooth muscle layers) : function is to perform peristalsis which pushes food down through
the GI tract
4. Serosa
 outer layer that has connective tissue that connects to surrounding organs

Pylorus
 opening from the stomach to the first part of the small intestine
 It is a muscular like structure that allows food to flow into the small intestine.
 Pyloric sphincter: main function is to prevent intestinal contents from re-entering
the stomach when the small intestine contracts and to limit the passage of large food particles or
undigested material into the intestine through the aids of
Duodenum
 first part of the small intestine that is responsible for the continuous breaking-down process.
 After foods mix with stomach acid, they move into the duodenum, where they mix with bile
(Bile is a fluid that is made and released by the liver and stored in the gallbladder. That breaks
down fats into fatty acids, which can be taken into the body by the digestive tract) from the
gallbladder and digestive juices from the pancreas. (These enzymes include trypsin and
chymotrypsin to digest proteins; amylase for the digestion of carbohydrates; and lipase to break
down fats.)

Jejunum and ileum

 are mainly responsible for absorption of nutrients into the bloodstream.

Key Players in Peptic Ulcer Disease:

 The body tries to keep a fine balance between the amounts of stomach acid and defense
mechanisms that protect the stomach from ulcer formation. To function normally and prevent
ulcers, the stomach has to have the good with the ugly because although they don’t really get
along they need each other to perform digestion.
 I like to break the key players into two teams. The GOOD team which is the defense system and
the UGLY team which is the toxic system.

Good:
 the defense system of the stomach. The defense system protects the stomach lining so food can be
digested. It takes a lot of effort to digest food so it can go through the lower GI tract.
 a. Bicarbonate (HCO3): coats the gastric layer and protects the cells from acids
 b. Prostaglandins: regulates perfusion to stomach, causes stomach cells to release mucous rich in
bicarb, controls acid amounts via the parietal cells
 Anything that affects these “key players” increases the chances of ulcer formation…see the
villains below.
Ugly:
 the toxic system of the stomach.
 Hydrochloric acid via parietal cells, Pepsin via chief cells
 It does the ugly/dirty work by breaking down the food…if the “good”/defense wasn’t in place,
the stomach in a sense would digest itself.,

Who are at risk?

 Both sexes are equally affected to develop PUD
 Older adults or 65 years and above have increased the cases of PUD associated with NSAIDs
used and H.Pylori infection in older adult populations (Anand, 2015)

PATHOPHYSIOLOGY
 Peptic ulcers mainly occurs in the gastroduodenal mucosa because this tissue cannot
withstand or tolerate the digestive action of hydrochloric acid and pepsin.
 The hydrochloric acid and pepsin in the stomach that normally works to digest food starts to
erode the mucosal lining because the defense mechanisms of the stomach are disrupted or the
amount of acid is excessive. In a sense, the stomach starts to digest itself.
 The combination of hydrochloric acid and pepsin serves as aggressor to the GI mucosa. Increased
secretion of HCl and pepsin maybe caused by stress and stimulants that contributes in the
formation of PUD. (Udan, 2017)
  So, what happens when acid penetrates the mucosa of the stomach? When the mucosal lining is
damaged, histamine is released it signals the parietal cells to release more HCL…so you get
even more toxic acid in the stomach which continues to erode the damaged area.
 A damage mucosa cannot secrete enough mucus (protector of the GI tract) to act as a barrier
against normal digestive juices. Exposure of the mucosa to gastric acid, pepsin and other irritating
agents (NSAIDS or H. Pylori) leads to inflammation, injury and erosion of the mucosa
 The mucus secretion of the GI tract serves as protector. Decreased secretion of mucus maybe
caused by decreased blood flow and presence of irritants are factors that damage the mucous
membrane of the GI track. Increased action of the aggressor or decreased action of the protector
may lead to PUD. (Udan, 2017)
 Patients with duodenal ulcers secrete more acid than normal, where as patients with gastric ulcer
tend to secrete normal or decreased level of acid.
 When the mucosal barrier is impaired, even normal or decrease levels of HCl may result to
formation of peptic ulcers.

Causes of Peptic Ulcers

1. Bacterial infection due to Helicobacter pylori (H. pylori)
 Most PUD results from infection a gram negative bacteria H. Pylori which maybe acquired
through ingestion of food (eating raw or improperly cook meat) and water
 Per CDC.gov: 90% of duodenal ulcers and up to 80% of gastric ulcers are caused by h.
pylori (Helicobacter Pylori: Fact Sheet For Health Care Providers 1).
 May be transmitted from person to person of the bacteria, also occurs through close contact and
exposure to vomitus; It is most likely spread from consuming something contaminated with h.
pylori via fecal to oral or oral to oral.
 These bacteria are spiral-shaped which helps them invade the GI mucosa.
 How can h. pylori live in the acidic conditions of the stomach? Because it secretes urease and
this breakdown UREA which produces ammonia to neutralize the acid. In addition, the
ammonia causes more damage to the mucosal lining.

2. NSAIDs (long term usage)

 NSAIDs usage such as ibuprofen and Aspirin (Ulcerogenic drugs) is a major risk factor for Peptic
ulcer.
 Think of how NSAIDS work: they work to decrease the production of prostaglandins or inhibit
prostaglandin synthesis which is associated with a disruption of the normal protective mucosal
barrier.
 Prostaglandins cause us to feel pain, inflammation, fever etc.
 the stomach uses prostaglandins to keep the stomach protected by promoting the stomach cells to
release mucous rich in bicarb, regulates acid amount via parietal cells, and perfusion to stomach.
NSAIDs inhibit them from working.
 Therefore, if a patient takes NSAIDs for a long period of time the defense system of the stomach
is broken down….hence risk for ulcer formation.

3. Zollinger-Ellison Syndrome
 Benign or malignant tumor formation in the pancreas or duodenum that causes increased release
of gastrin which increases stomach acid production or extreme hyperacidity and cause PUD
(Anand, 2015, NIDDK, 2014)
 ZES is unknown cause, 25% of cases are link to inherited, genetic condition called Multiple
endocrine Neoplasia, Type I (Epelboy and Mazeh,2014)

4. Smoking
  nicotine stimulates increased HCl secretion and causes vasoconstriction which results to
irritation and damage of GI mucosa
 decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increase
acidity of the duodenum. It is also associated with delayed healing of peptic ulcer (Li et al, 2014)
5. Stress
 Initially, in response to stress, the SNS is triggered. However if stress is prolonged, SNS is
exhausted and the PNS is activated. PNS activation causes hypersecretion of hydrochloric acid.

6. Alcohol consumption
 irritates GI mucosa, causes vasoconstriction and increases gastric acid secretion

7. Caffeine
 stimulates increased HCl secretion
 It also causes vasoconstriction, decreased blood flow to the GI mucosa causes decreased mucous
secretion

8. Genetics/ Familial tendency

 may be a significant predisposing factor. There are individuals who have higher parietal cells
mass than other individuals.

9. Type O Blood
 are more susceptible to the development of PUD than are those with blood type of A, B, AB.
Type O individuals have higher pepsinogen levels. Pepsinogen is activated into pepsin. Pepsin in
combination with HCl acts as aggressor to the GI mucosa.
10. Gastritis
 This leads to increased HCl secretion and mucous ulceration

11. Type A personality (Udan, 2018)

 Stress personality. This personality is characterized by over-conscientiousness, perfectionism,
workaholic, inability to concentrate in one task, very punctual. The individual has increased
gastric motility and HCl secretion

12. Stress Ulcer

 Acute mucosal ulceration of the duodenum or gastric area that occurs due to physiological
stressful events such as burns, shock, sepsis, and multiple organ dysfunction syndrome (Clark et
al, 2015). Diseases such as COPD, cirrhosis and CKD have association to PUD (Anand, 2015)
 Most common in patients who are ventilator dependent after trauma or surgery
 Fiberoptic endoscopy within 24 hours of trauma or surgery reveals shallow erosions of the
stomach wall, by 72 hours, multiple gastric erosions are observed. When the patient recovers, the
lesions are reverse. This pattern is typical of stress ulceration.
 Types of Stress Ulcers as a results of stressful conditions: Curling and Cushing
 Curling ulcer- frequently observed about 72 hours after extensive burn injuries and often involves
the antrum of the stomach or duodenum (Anand, 2015)
 Cushing ulcer-common in patients with Traumatic brain injury, stroke, brain tumor or intracranial
surgery. This ulcer is cause by increase ICP resulting to overstimulation of the vagal nerve and
increased secretion of HCl (Grossman and Porth, 2014)

NOTE: Stress and certain foods do not cause ulcers but can irritate them and prolong their healing. There
is no evidence that ingestion of milk, caffeinated beverages and spicy foods are associated with
development of peptic ulcers (Anand, 2015, NIDDK, 2014)
 13. Irregular, Hurried meal (Udan, 2017)
 This is stressful and leads to increased HCl secretion and gastric motility

14. Fatty, spicy, highly acidic foods (Udan, 2017)

 These are irritants to GI mucosa

Signs and Symptoms of PUD

Mainly: Indigestion and Epigastric pain….described as burning, dull, or gnawing pain

Gastric Ulcers Duodenal Ulcers

 Also called “Poor Man’s” or  Also called “executive”
“Laborer’s” Ulcer because the ulcer because it is
stomach is usually empty. primarily stress-related.
Incidence  20% Incidence 80% incidence
At risk  Commonly affects who are 50  Commonly affects those who
yrs old and above. Older people are 25-50 yrs of age. The
usually lost their interest in food years of struggles or stressful
 If affects malnourished in life
 Usually well-nourished
Pathophysiology  There is increased back  There is increased HCl
diffusion of HCl in the gastric secretion.
mucosa
 Both types of PUD are characterized by dull, aching, gnawing(worrying/bothering) epigastric
pain
Signs and  Pain radiates to the left side of  Pain radiates to the right side
symptoms the abdomen (Stomach is of the abdomen (Duodenum
located in the left side of the is located in the right side of
abdomen the abdomen)
 Awake in middle of night
with pain
 Pain is not relieved by food  Pain is relieved by food.
intake. Food may worsen the Food in the stomach delays
pain when it comes in contact emptying of gastric acid into
with ulcer the duodenum. Food makes
it BETTER
 Pain ½ -2 hours minutes after  Pain 2-3 or 3-4 hours after
eating). When food comes in eating. The time when the
contact with exposed nerve acidic chyme from the
endings in ulcers, pain occurs stomach empties into the
duodenum. The exposed
nerve ending in the
duodenum are irritated by
the acidic chyme
 Weight loss  Weight normal
 Severe: vomit blood more  Severe: tarry, dark stool from
common (hematemesis) GI bleeding (Melena)
because the blood is acted
upon by gastric acid
Complications  Hemorrhage, perforation,  Obstruction, Hemorrhage,
 peritonitis perforation, peritonitis

Diagnostic Findings
For ulcers from H. Pylori:
 Blood or stool antigen test and urea breath test
 UREA breath test: patient will ingest a urea tablet and if h. pylori is present it will break down
urea into ammonia and carbon dioxide. Breath samples will be analyzed for abnormally high
carbon dioxide levels.
Scope of the stomach (EGD)/ Upper endoscopy
 Allows direct visualization of inflammatory changes ulcers and lesions and its size and location
Upper GI series:
 patient will drink barium which will coat the stomach and x-rays will be taken to assess for
ulcers
CBC
 to determine the extent of blood loss ad whether or not blood transfusion is advisable
Gastric secretory studies
 are valuable in diagnosing ZES and achlorhydria (lack of HCl) and hypochlordria (low HCl
levels) and hyperchlorhydria ( high levels of HCl)

Assessment
 Inspect for bloating or abdominal distention,
 Auscultate Bowel sounds: hypoactive or absent due to perforation of ulcers
 Palpation for tenderness, assess vital signs
 Ask patient when do you experience stomach pain? Its pattern and whether or not occurs
predictably (after meal, during the night)
 Does eating help it or make it worst? Do you awake with pain in the middle of the night?
 Note the characteristics of vomiting. Bright red, coffee ground, or ask patient if he noted any
bloody or tarry stools.
 Assess medical history: taking what medications? NSAIDS, salicylates, corticosteroids,
anticoagulant…make ulcer worst), any history of being diagnosed with h. pylori or any one in
your family have it,
 Smoking ( Do they smoke cigarettes? How many?
 Drinking alcohol (Does the patient ingest alcohol? If yes; How much and how often)
 Caffeine products (prevents ulcer from healing and can exacerbate ulcers)
 Ask the patient to List the usual food intake for 72 hours

Nursing Diagnosis
 Fluid volume deficit r/t hemorrhage
 Pain r/t epigastric distress secondary to hypersecretion of acid, mucosal erosion or perforation
 Altered Nutrition Less than body requirement r/t disease process

Potential Complications
 Hemorrhage
 Perforation
 Penetration
 Gastric Outlet Obstruction
Planning
 The goal for the patient may include relief of pain, reduce anxiety, maintenance of nutritional
requirements and absence of complications

Nursing Interventions for Peptic Ulcer Disease

Pain Relief
 Assess the level of pain
 Provide small frequent feedings to prevent gastric distention (if not NPO)
 Encourage Relaxation techniques it helps to manage stress and pain.
 Avoid gastric irritating food and drugs (Aspirin and NSAIDS, alcohol)
 Administer medications as prescribed. Ex (antacid)

Avoiding Fluid Volume Deficit

 Monitor intake and output, to determine fluid volume status
 Monitor stools for blood and emesis
 Monitor hemoglobin, hematocrit and electrolytes
 Monitor VS- increase PR and decrease BP indicates shock
 Administer IV fluids and blood replacement as prescribed
 Insert NGT as prescribed and monitor the tube for drainage
 Administer medications via NGT to neutralize acidity
 Saline lavage as ordered

Achieving Adequate nutrition

 DAT when asymptomatic
 Diet: High calorie, high protein diet
 High calorie Peanut butter, Whole milk, yogurt, mayonnaise, and sour cream, Granola cereal
with fruit and granola bars, Muffins, pancakes, waffles, and other breads, Milkshakes, puddings,
and custard
 High CHON- meat, fish, dairy products, beans and legumes, eggs, and vegetables such as
asparagus and spinach
 Small frequent meals, to prevent gastric distention if not on NPO

Reduce anxiety
 Assess the patient’s level of anxiety. (mild anxiety, moderate anxiety, severe anxiety and
panic level anxiety)
 Provide emotional support.
 Explain that the test and medications as scheduled help reduce anxiety
 Interact with patient in a relax manner and help identify stressor
 Relaxation methods such as meditation
Panic level anxiety
 characterized by frequent, recurring and unexpected panic attacks.
 A panic attack can include symptoms such as Rapid onset of extreme fear, Heart palpitations,
Rapid breathing, Nausea or dizziness Fear of death
 Panic attacks usually last around 10 minutes. The triggers for panic attacks vary from person to
person, and the cause of an attack may be familiar to a person or unknown.
Managing Potential Complications
Hemorrhage
 The most life-threatening complication, blood loss of 20% (1000ml) is fatal leading to shock.
 Manifested by hematemesis fresh bright red or melena (black tarry because of digested or
oxidated hemoglobin to metheglobin) or coffee ground (due to acids)

Nursing Interventions
 Monitor VS and watch signs of hypovolemia or shock
 Monitor hemoglobin, hematocrit
 Record urine output to detect anuria or oliguria
 NGT insertion to distinguish fresh blood to coffee ground and to remove clots via saline lavage,
through nausea and vomiting through suction decompression of gastric content
 IV fluids resuscitation and blood transfusion
 Endoscopic interventions, administer epinephrine or cauterizing the site or clipping the ulcer to
stop the bleeding
 Gastric resection such as gastrectomy, vagotomy, pyloroplasty

Perforation
 Is the erosion of the ulcer through the gastric mucosa into the peritoneal cavity
 This is emergency and requires immediate open surgery to suture the perforation and to prevent
peritonitis
 Signs includes
 Sudden and severe abdominal pain (persisting and increasing in intensity), radiating to right
shoulder due to irritation of the phrenic nerve in the diaphragm
 Vomiting, fainting (collapse) extremely tender and rigid (boardlike) abdomen
 Hypotension, tachycardia indicating shock
Management
 Surgery
Penetration
 Is the erosion of the gastric ulcer through gastric serosa into adjacent structures such as pancreas,
biliary tract
 It requires surgery
 Signs includes back and epigastric pain unrelieved by medications

Peritonitis
 The inflammation of the peritoneum which affects the serous membrane lining of the
abdominal cavity and covering of the viscera due to perforation
 It is the result of bacterial infection but may occur secondary to a fungal or mycobacterial
infection
 The most common bacteria: E. Coli, Klebsiella, Proteus, Pseudomonas. Streptococcus species

Early manifestations
 Pain- diffuse then becomes constant. Localized and more intense over the site of the pathologic
process (site of maximal peritoneal irritation) aggravated by movement
 Abdominal tenderness and distension, Muscles becomes rigid
 Nausea Anorexia, vomiting, Diminished peristalsis followed by Paralytic ileus
 Fever 37.8 to 38.3 above and Increase PR
Late Signs
  Hypotension, Signs of sepsis and Septic Shock

NURSING MANAGEMENT

 The nursing management is based on secondary peritonitis

 If septic shock occurs, intensive care is needed
 Monitor level of pain
 Monitor VS
 Monitor electrolytes hemoglobin and hematocrit
 Administer fluids such as colloid and isotonic solutions as prescribe to prevent hypovolemia.
Massive fluid and electrolytes moves from the interstitial lumen into the peritoneal cavity and
deplete the fluids in the vascular space.
 Administer anti emetics as ordered to prevent or reduce nausea and vomiting
 Administer antibiotics as prescribed usually broad expectrum in order to treat the secondary
peritonitis
 Increase fluid and food intake gradually and reduce parenteral IV fluids

Medical Management
 Fluid, colloid, and electrolyte replacement is the major focus of the management
 Isotonic solution as prescribed- hypovolemia occurs due to massive fluid and electrolytes
moves from the interstitial lumen into the peritoneal cavity and deplete the fluids in the
vascular space.
 Analgesics as prescribe for pain
 Anti emetic for nausea and vomiting
 Intestinal intubation and suction to relieve abdominal distension and to promote intestinal
function. Fluid in the abdominal cavity can cause pressure that restricts expansion of the lungs
and causes respiratory distress
 Oxygen therapy by nasal cannula promote adequate oxygenation due to shock
 Antibiotic therapy initiated early in the treatment of peritonitis usually broad expectrum in
order to treat the secondary peritonitis

Treatment for PUD:

Pharmacologic Therapy

DRUG REGIMEN FOR PUD

Indications Drug Regimen Nursing Consideration
Ulcer healing H2 Receptor Antagonist (ends Should be used for 6-8 weeks for
with “dine) complete peptic ulcer healing
 Ranitidine Pt who are at high risk require
 Cimetidine maintenance dose for 1 year
 Famotidine
 Nizatidine
PPI ends with ‘zole” Should be used for 4-8 weeks for
 Omeprazole complete peptic ulcer healing
  Lansoprazole
 Rabeprazole
 Pantoprazole
 Esomeprazole
H.Pylori infection Triple therapy: Efficacy of therapy is
 PPI BID, Clarithromycin approximately 85 % qid dosing
500mg BID, Plus may decrease adherence to the
Amoxicillin 1000mg BID regimen
or (Metronidazole 500 mg
BID) for 10-14 days
Quadruple Therapy
 Bismuth salicylate 525
mg QID, tetracycline
500mg QID,
Metronidazole 250 mg
QID, PPI daily 10-14
days
Prophylactic therapy for PPI above Prevents recurrent ulceration in
NSAID’s Ulcers Misoprostol 100 mg-200mcg qid approximately 80-90% of patients

Medications
 Antacids
 Histamine-receptor blockers
 Proton-pump inhibitors
 Bismuth Subsalicylates
 Mucosal healing
 Prostaglandin analogue
 Anticholinergic
 Antibiotics

Antacids: neutralizes the stomach acid

 Best administer 1-2 hours after eating. This is the time peak of HCl secretion
 Magnesium Hydroxide, Calcium Carbonate…these are chewed thoroughly and then swallowed
 Interferes with MANY drugs: antibiotics, mucosal healing, H2 blockers so always give alone and
allow for 1-2 hours before administering other medications

Histamine-receptor blockers
 H2 blockers “Ranitidine HCL “Zantac” or Famotidine “Pepcid”
 End in “tidine”
 How do they work? They block histamine. When histamine is released it causes the parietal cells
to release HCL but this response will be blocked so gastric acid secretion will be decreased.
Decreased HCl secretion.
 Avoid giving at the same time with antacids or Carafate. Instead give 30-45 minutes apart.
 Best taken in the morning and at bedtime. Food may delay the absorption of the medications
 SE: diarrhea, abdominal cramps, confusion, dizziness and weakness

Bismuth Subsalicylates
 Pepto-Bismol….used for h.pylori infections by covering the site of the ulcer and keeps the
stomach acid away.
 suppresses H. Pylori in the gastric mucosa and assist in healing of ulcers
  should be taken on an empty stomach.
 May given with antibiotics to eradicate the H Pylori
 It is used with antibiotics, PPIs, or H2 blockers for treatment.

Mucosal healing/ Cytoprotective drugs

 lines the stomach and adheres to the ulcer site and protects it from acids and enzymes.
 Coat the ulcers, and enhances prostaglandin synthesis
 EX: Sucralfate “Carafate”
 Take on empty stomach…hour before eating….
 SE: Constipation, diarrhea, nausea, vomiting, upset stomach, itching, rash; dizziness,
drowsiness; sleep problems (insomnia);headache; or, back pain.
 don’t give at same time as antacids or H2 blockers. Adminster at least 60 minutes apart

Prostaglandin Analogue
 replaces gastric prostaglandin and it suppresses secretion of the gastric acid
 Ex: Cytotec (Misoprostol)
 Administer with meals
 It causes diarrhea and abdominal pain
 It is abortifacient, therefore it is contraindicated to pregnancy

Proton-pump Inhibitors (PPIs)

 decreases stomach acid and help the protect stomach lining
 used with h.pylori infection along with antibiotic
 Types: “Omeprazole “Prilosec” or Pantoprazole “Protonix”…drugs
 How do they work? Attaches to the “proton pump” on the parietal cells which is the
hydrogen/potassium (H+, K+) ATPase enzyme and blocks the release of hydrogen ions. These
ions would mixed with the chloride ions and form gastric acid but this is blocked so there is
decrease in gastric acid
 Common side effects: headache, diarrhea, nausea, and vomiting.

Anti-Cholinergic Drugs
 Reduce gastric motility and hydrochloric acid secretion
 Ex. Atropine sulfate, Bentyl (diclomine), Robinul, (Glypyrrolate), levsin (Hyoscyamine)
 CSE: dry mouth, blurry vision, constipation.

Antibiotics
 used if h. pylori is causing the ulcer formation: various regime ordered by physician. They are
used with PPIs or bismuth subsalicylate or H2 blockers
 used to treat h. pylori infections
 Types: Clarithromycin (Biaxin), Metronidazole (Flagyl), Tetracycline, Amoxicillin (Amoxil)

Metronidazole (Flagyl),
 Antibacterial & anti protozoal that assist in eradicating H. Pylori in gastric mucosa
 NC: Give with meals
 Avoid alcohol to prevent disulfiram manifestations
 drug that causes an adverse reaction to alcohol leading to nausea, vomiting, flushing, dizziness,
throbbing headache, chest and abdominal discomfort, hypotension, tachycardia, palpitation,
dyspnea, respiratory collapse, convulsion
Tetracycline
 MA: Eradicated H pylori bacteria in gastric mucosa
 NC: May cause photosensitivity reaction,
 Advise the patient to use sunscreen
 May cause GI upset
 Caution in renal or hepatic impairment
 Avoid intake of milk and dairy products
 Avoid alcohol while taking this drug if may result to disulfiram manifestations
 CSE: Discoloration of teeth and enamel hypoplasia (young children),Diarrhea, Nausea,
Photosensitivity, Stomach upset, Loss of appetite, White patches or sores inside your mouth or
on your lips, Swollen tongue.

DIET for Ulcers

 Avoid spicy, acidic foods (tomato/citric juices/fruits), foods with caffeine (including
decaffeinated coffee, chocolate, soft drinks , fried foods, alcohol -as these stimulates acid
secretion
 Consume a low-fiber diet that is bland and eat to digest, eat white rice, bananas etc.
 Eat 3 regular meals a day to neutralize acid
 DAT when asymptomatic
 Diet: High calorie, high protein diet
 High calorie Peanut butter, Whole milk, yogurt, mayonnaise, and sour cream, Granola cereal
with fruit and granola bars, Muffins, pancakes, waffles, and other breads, Milkshakes, puddings,
and custard
 High CHON- meat, fish, dairy products, beans and legumes, eggs, and vegetables such as

Health Education/Teachings
 Report the signs and symptoms of bleeding and notify the PHCP
 Promote a healthy lifestyle changes like Enhance coping through stress therapy
AVOIDANCE
 Alcohol – gastric irritant and also cause vasoconstriction, increase HCl
 Smoking- nicotine stimulate the incrase of HCl secretion and cause vasoconstriction
 Fatty foods, coffee, tea, chocolate, colas, spices, red and black pepper these are gastric irritants
 Large quantities of milk-milk is alkaline, thus it stimulate the stomach to increase HCl secretion
to neutralize it, it cause rebound acidity. May take 400 ml (2 glasses) per/day
 Bedtime snack- to prevent reflux
 Binge eating- to prevent gastric stimulation
 Enhance coping through stress therapy- regular exercise, develop recreation and hobbies, stress
reduction at home and work

Surgical Management

 Usually recommended for patients with intractable ulcers( failing to heal after 12 to 16 weeks of
medical treatment, life threatening hemorrhage, perforation or obstruction and for those with ZES
that is unresponsive to medications (Anand, 2015)
 Severe cases due to chronic ulcer formation: Gastric resection: (various types) removal of the
diseased parts of the stomach
 Surgeries includes vagotomy, (with or without pyloroplasty), antrectomy (Billroth I and Billroth
II)
  May be perform in two ways: traditional open abdominal surgery (requires abdominal incision) or
via abdominal laparoscopy.
Operation Description
Vagotomy (with or without  cutting parts of the vagus
pyloroplasty)
 severing the vagus nerve to
Truncal vagotomy
Selective vagotomy
Pyloroplasty
ANTRECTOMIES
 Surgical resection of
50% of the distal part of
the stomach followed by
anastomosis with the
Adverse effects
 Feeling of fullness,
nerve to prevent it from  Dumping syndrome
stimulating the gut to  Diarrhea
produce hydrochloric acid  Gastritis
decrease the gastric by
diminishing cholinergic
stimulation to the parietal
cells making less responsive
to gastrin.
 Cuts the right and left vagus  Feeling of fullness,
nerves as they enter the  Dumping syndrome
stomach at the distal part of  Diarrhea or
the esophagus constipation
 Most commonly used to
decrease the acid secretions
 Cuts the vagal innervation to  Fewer adverse
the stomach but maintains effects than truncal
the innervation (nerve
supply) to the rest of the
abdominal organs
 Longitudinal incision is  See the adverse
made into the pylorus and effects of truncal
transversely sutured close to and selective
enlarge the outlet and relax vagotomy
the muscle
 Usually accompanies truncal
and selective vagotomies
 performed when there is
scarring to the pylorus
(specifically from chronic
duodenal ulcers) that can
cause an obstruction in the
opening of the duodenum
from the stomach so GI
contents can NOT flow into
the small intestine.
 removal of the lower portion Feeling of fullness
of the antrum of the stomach Dumping syndrome
(which contain cells that Diarrhea
secrete gastrin) as well as
small portion of the pylorus
 duodenum and jejunum with anastomosis (surgical
Billruth I/ connection) to the duodenum
Gastroduodenostomy
- Indicated in gastric
ulcer
Billruth II/ Gastrojejunostomy  removal of the lower portion Dumping syndrome
- indicated in duodenal of the stomach with Anemia
ulcer anastomosis to jejunum Weight loss
Malabsorption

Nursing Interventions for the Patient Undergoing Gastric Surgery

Pre- Operative care

 Provide psychosocial support. Anxiety is the most common reaction to therapy
 Teach the patient DBCT with incentive spirometer (Deep breathing, Coughing, and Turning)
exercises to prevent respiratory complications. Due to abdominal incision near the diaphragm,
the patient is at risk to develop respiratory complications such as atelectasis, hypostatic
pneumonia (infection developing in the dependent portions of the lungs due to decreased
ventilation of those areas, with resulting failure to drain bronchial secretions.)
 Provide nutritional support (TPN) as ordered. To enhance the patient’s ability to withstand the
stress of surgery.

Post Operative care

Priority is to promote patent airway and ventilation. To prevent atelectasis and hypostatic pneumonia due
to immobilization
 Place patient in Semi- Fowlers position
 Reinforce DBCT exercises and incentive spirometry
 Administer analgesics as ordered
 Splint incision when patient’ cough. To prevent Dehiscence is secondary to technical failure of
sutures, shear forces from tension, or fascial necrosis from infection and/or ischemia and
Evisceration( the uncontrolled exteriorization of intraabdominal contents through the dehisced
surgical wound outside of the abdominal cavity.)
 Encourage early ambulation. To improve blood flow which aids in faster wound healing

Promote adequate nutrition

 NPO until peristalsis returns. Presence of bowels sounds (5-40/min) and passing out of flatus
indicate the return of peristalsis
 Diet: Provide clear, soft, full diet (Progressive diet)
 Provide small frequent feedings
 Monitor the weight regularly. Weight is the best indicator of nutritional status

Complications of Gastric Resection

 Dumping Syndrome- common after gastric surgery

What is Dumping syndrome?

 A complex reaction or group of unpleasant vasomotor and GI symptoms because of rapid
emptying of gastric content into the jenunum.
 Stomach is not able to regulate the movement of food due to the removal of sections of the
stomach (usually the pyloric valve and duodenum) so it enters into the small intestine too fast
 before the stomach can finish digesting it. The food will act hypertonically and cause water from
the blood to enter jejunum
Early dumping
 (happens 5-30 minutes after eating)
 fluid shifts and this causes small bowel distention and increased bowel motility.
 Signs: nausea, bloating, and diarrhea.
 In addition, from the quick shifting of fluid the heart tries to compensate so the patient may
experience hypotension, syncope, dizzy.

Late dumping
 (2-3 hours after eating):
 the food that has entered into the small intestine is high in carbs/sugars (body was unable to break
it down because it entered into the small intestine too early) resulting to HYPERGLYCEMIA.
This will cause the pancreas to release insulin. The patient will experience signs and symptoms
of hypoglycemia like sweating, weak, dizzy.

Note: patients can have both or just one type of dumping

Patient education on how to decrease signs and symptoms:

 Should eat in lying/ recumbent position
 Place the patient on the left side after meal (jejunum is on the right side) as this prevent rapid
emptying of the stomach by gravity
 Eat many small meals rather than 3 large ones
 Instruct the client to take fluid after meals or in between meals; not with meals.
 Avoid sugary food and drinks (milk, chocolate), or no simple sugars,. These foods empty the
stomach rapidly
 Eat food high in protein, and low-carbs. These foods empties the stomach slowly (34 hours after
eating.
 Teach to avoid very hot and cold foods and beverages. These are stimulants and may cause rapid
emptying of the stomach
 Administer

APPENDICITIS
 is an inflammation and obstruction of the appendix
 Can affect any age group, most common in males 10-30 years old (Lippincot and Williams, 2001)
CAUSES
 A blockage in the lining of the appendix by a fecalith (hardened mass stools), lymphoid
hyperplasia, foreign bodies and tumors or infection
 H. Pylori bacteria multiply rapidly, causing the appendix to become inflamed, swollen and filled
with pus.
 TRAUMA/Injury
 Other causes: Low fiber diet and high intake of refined carbohydrates, kinking of appendix and
swelling of the bowel wall.

PATHOPHYSIOLOGY
  appendicitis due to a blockage of some kind that is blocking the lumen of the appendix (which is
the inside of the appendix) that causes major INCREASE PRESSURE inside the appendix.
 What is causing the increased pressure? Inside the appendix is mucosal lining, which is
continuously secreting mucus and fluids. There are also bacteria that normally live in the
appendix that start to increase in production due to the blockage. All this “material” (mucous,
fluids, bacteria) continue to grow and it can NOT move anywhere due to the blockage. This
causes major pressure in the lumen of appendix that can lead to perforation (rupture) of the
appendix.
 Note: if appendicitis is not treated within 48-72 hours there is a risk for rupture which will lead to
abscess and peritonitis.
 What happens as the pressure continues to build? It leads to major venous obstruction of the
veins of the appendix. Therefore, there is occlusion of blood flow and the stagnant blood can’t go
anywhere.
 What happens when blood stays stagnant? It coagulates, hence leads to the development of a
clot formation. This further complicates everything and leads to ISCHEMIA. Therefore, the
appendix will start to slowly die.
 As the appendix dies, the walls of the appendix break down and start to leak all of its contents
(bacteria etc.) into the abdominal cavity. This leads to an abscess forming at the site of rupture
and PERITONITIS, which is life-threatening.

Summary: The appendix becomes inflamed and edematous as a result of occluded fecalith (hardened
stools) lymphoid hyperplasia, foreign bodies and tumors.. The inflammatory process increases
intraluminal pressure causing edema and obstruction of the orifice. The appendix become ischemic due to
obstruction and bacterial overgrowth occurs leading to perforation within 6-24 hours

Clinical Manifestations
Abdominal pain/ Acute Epigastric or peri-umbilical pain (will be dull at first with pain at or around the
belly button that radiates to the right lower quadrant and it will localize at this spot)

 Rebound tenderness/ Blumberg’s sign or the production of Deep palpation of the viscera over
the suspected inflamed appendix and intense pain is felt when pressure is released.
 ROVSING’S sign may be elicited by palpating the left lower quadrant; this usually causes pain
to be felt at the right lower quadrant.
 Psoas sign. Right lower quadrant pain is produced when the patient extending the hip due to
inflammation of the peritoneum overlying the psoas muscle. Straightening out the leg causes the
pain because it stretches the muscle and flexing the hip into the fetal position relieves the pain.
This is due to retrocecal inflammation of appendix
 Obturator sign- pain is massive internal and external rotation of the FLEX RIGHT THIGH
 Dunphy’s Sign- increased pain when coughing
Point of McBurney’s will have the most pain (found one-third distance between the belly button and
anterior superior iliac spine)
  Local tenderness at McBurney’s point when pressure is applied. McBurney's point is over the
right side of the abdomen that is one-third of the distance from the anterior superior iliac spine to
the umbilicus (navel). This point roughly corresponds to the most common location of the base
of the appendix where it is attached to the cecum. Pain with pressure over McBurney point, or
two-thirds the distance between the umbilicus and anterior superior iliac spine, is the
physical exam finding in the vast majority of patients (91%) and corresponds with an inflamed
appendix lying within the typical location in the right lower quadrant
Poor appetite
Elevated temperature: Temperature of 38 to 38.5 C
Nausea/vomiting, Anorexia, due to vagal stimulation
Desire to be in the fetal position to relieve pain (side lying with knees bent)
Increased WBC, inability to pass gas or have a bowel movement
 leukocytosis., WBC level is above 10,000/cu.mm due to inflammatory response of the body. If
WBC level is 20,000cu/mm, this indicates peritonitis due to rupture of appendix
eXperiences rebound tenderness (when pressure is applied to the right lower quadrant it hurts but
it HURTS MORE when the pressure is released) and abdominal rigidity on palpation (involuntary
stiffening of the abdominal muscle when abdomen palpated).

 Rigid guarding abdomen. A protective mechanism to relieve the pain

 If the appendix has ruptured, the pains becomes consistent with Peritonitis
 Abdominal distension, and as a result of paralytic ileus or rupture appendix
 Decrease or absent bowel sound and constipation, inflammation in the area reduces
peristalsis
 NOTE: DON’T give LAXATIVE: it may result to perforation of appendix

Assessment
 Assess the Onset, Duration, Quality and characteristics, Severity, pattern and distribution of
referred pain and its location, and Precipitating factors, Relieving factors
Diagnostics
 Physical exam- consistent clinical manifestations
 WBC/ leukocytosis with an elevated neutrophils
 Imaging test/ Abdominal X-ray- can visualize fecalith in the appendix or perforation
 UTZ- confirmatory diagnosis that shows enlarge appendix,
 if female, PT test then transvaginal UTZ to role out ectopic pregnancy
 Abdominal CT scan- may reveal RLQ density or localized distention of the bowel, enlarged
appendix by at least 6mm
 U/A- to rule out UTI or renal caliculi

COMPLICATIONS OF APPENDICITIS
 Gangrene and Rupture or perforation of appendix (95% in all cases) which can lead to
 peritonitis, Perforation generally occurs within 6 to 24 hours after the onset of pain and lead to
peritonitis (Craig, 2015, Saccomano & Ferrara, 2013)
  abscess formation may located in the pelvis, diaphragm, or in the liver causing fever, high PR and
WBC

NURSING DIAGNOSIS
 Acute pain related to inflammation of appendix
 Hyperthermia related to disease process secondary to rupture of appendix
 Risk for infection related to perforation
Planning
 Relieving of pain, preventing fluid volume deficit, prevent surgical site infection
MEDICAL MANAGEMENT
• Immediate Surgery (Appendectomy- removal of appendix) is indicated if appendicitis is
diagnosed and should be performed as soon as possible to decrease risk of perforation.
• Antibiotics and Intravenous fluids during and after surgery to prevent dehydration and
risk of infection or sepsis. For complicated appendicitis it is treated antibiotics 3-5 days post
operatively
• Analgesic agents can be given after diagnosis is made.
SURGICAL TREATMENT
Open Appendectomy
 Surgical removal of the appendix to decrease the risk of perforation
 A cut or incision about 2 to 4 inches long is made in the lower right-hand side of your belly or
abdomen.
 The appendix is taken out through the incision.
 It is typically performed using general anesthesia

Laparoscopic Appendectomy
 This method is less invasive with or without perforation
 it’s done without a large incision. Instead, from 1 to 3 tiny cuts are made.
 A long, thin tube called a laparoscope is put into one of the incisions. It has a tiny video camera
and surgical tools.
 The surgeon looks at a TV monitor to see inside your abdomen and guide the tools. The
appendix is removed through one of the incisions.
 The recovery is quick

Plan: The goal is to relieve pain, preventing fluid volume deficit, preventing infections and reduce
anxiety

Pre Op Nursing Interventions

 Assess the level of pain, intensity, and location
 Monitor VS
 Place in comfortable position
 Signs the appendix may have rupture (perforated) : patient’s pain is suddenly relieved which
will be followed by intense abdominal pain
 Bedrest. To reduce peristalsis and prevent rupture of appendicitis
  NPO. To observe pattern of abdominal pain accurately and preparation for emergency
appendectomy
 Cold application over the abdomen to relieve pain
 IV infusion to replace fluid loss and promote adequate renal
 Antibiotic administration to prevent infection and analgesics for pain
 Consent
 DON’TS: Never give enema, laxative or cathartics and warm or hot compresses. It can lead to
PERFORATION

Post-Op Nursing Interventions

 High Fowlers- this reduces the tension on the incision site and abdominal organs, it help to reduce
pain. It also promotes thoracic expansion to decreased atelectasis.
 If the client received SPINAL ANESTHESIA, during immediate POST op is FLAT on bed for 6-
8 hours to prevent spinal headache
 Monitor for the return of sensation in the lower exrtremities. This indicates recovery from the
spinal anesthesia
 Spirometry used once patient is awake every 2 hours. It also promotes thoracic expansion to
decreased atelectasis.
 Auscultate bowel sounds.
 Maintain NPO until peristalsis returns. Return of bowel sounds and passing out of flatus indicates
return of persitalsis
 Monitor Urine output- to ensure hydration is adequate and to check urinary retention
 Encourage to ambulate the day of surgery to reduce the risk of atelectasis and VTE formation
 Oral fluids as Diet and as tolerated
 DAT when bowels sounds are present- ask the patient for passing of flatus and auscultate the
bowel sounds
 Morphine- IV opioids to relieve pain to switch to oral agent
 To prevent infection, cleanse the insertion site of penrose drain and the skin around separately

Health teachings
 Instruct the patient to make an appointment to have surgeon to remove sutures and check the
wound 1-2 weeks after surgery
 First incision care should be done by the surgeon
 Avoid lifting heavy objects to prevent evisceration
 Normal activity can be resume within 2-4 weeks
 Teach the family members how to care for the incision and perform change dressings and
irrigations as prescribed.
 Monitor for complications and wound healing

NURSING ALERT
 Patient with gangrenous or perforated appendix are at greater risk for infection and peritonitis.
They may be kept in the hospital for several days
 Secondary abscesses may form in the pelvis, under the diagphram or in the liver causing elevated
temperature, PR and WBC count

PERITONITIS
  The inflammation of the peritoneum which affects the serous membrane lining of the abdominal
cavity and covering of the viscera
 It is the result of bacterial infection but may occur secondary to a fungal or mycobacterial
infection
 The most common bacteria: E. Coli, Klebsiella, Proteus, Pseudomonas. Streptococcus species
 Can also result abdominal surgery or trauma (gunshot and stab wounds) or inflammation that
extends from an organ outside the peritoneal area (such as kidney, or from peritoneal dialysis.
CATEGORY OF PERITONITIS (ACCORDING TO DADLEY 2015)
Primary Peritonitis
 AKA Spontaneous Bacterial Peritonitis (SBA)
 Occurs as spontaneous bacterial infections of ascitic fluid.
 This occurs most commonly in adult patients with liver failure.
Secondary Peritonitis
 Occurs secondary to perforation of abdominal organs with spillage that infects the serous
peritoneum
 The most common causes include Perforated Appendix, Perforated Peptic Ulcer, Perforated
sigmoid colon cause by diverticulitis and strangulation of small intestine
Tertiary Peritonitis
 Occurs as a result of suprainfection in a patient who is immunocompromised
 Tuberculous peritonitis in a patient with AIDS is an example of tertiary peritonitis
 Rare causes of peritonitis
PATHOPHYSIOLOGY
Secondary peritonitis is caused by leakage of contents from the abdominal organs into the abdominal
cavity as a result of inflammation, infection, ischemia, trauma, or tumor perforation. Bacterial
proliferation occurs. Edema of the tissue results and exudation of fluids develops in a short time. Fluid in
the peritoneal cavity becomes turbid with increasing amount of protein, WBC, cellular debris and blood.
The immediate response of the intestinal tract is hypermotility followed by paralytic ileus with
accumulation of air and fluid in the bowel
CLINICAL MANIFESTATIONS
Early manifestations
 Abdominal Pain and tenderness - diffuse then becomes constant. Localized and more intense over
the site of the pathologic process (site of maximal peritoneal irritation) aggravated by movement
 Abdominal distension due to accumulation of gas and fluid in the abdomen
 Abdominal guarding rigidity. An attempt to protect the painful area
 Nausea Anorexia, vomiting due to vagal stimulation
 Diminished peristalsis followed by Paralytic ileus
 Fever 37.8 to 38.3 above due to inflammatory process
Late Signs
 Hypotension
  Signs of sepsis and Shock- restlessness, tachycardia, tachypnea, weakness, pallor diaphoresis,
oliguria
Sepsis
 a life-threatening illness caused by your body’s response to an infection. Your immune system
protects you from many illnesses and infections, but it’s also possible for it to go into overdrive in
response to an infection.
 chemicals the immune system releases into the bloodstream to fight an infection cause
inflammation throughout the entire body instead
Symptoms of sepsis include:
 High a fever above 101ºF (38ºC) or a temperature below 96.8ºF (36ºC), tachypnea
 probable or confirmed infection
 patches of discolored skin
 decreased urination
 changes in mental ability
 low platelet (blood clotting cells) count
 problems breathing
 abnormal heart functions
 chills due to fall in body temperature
 Unconsciousness
 extreme weakness

Septic shock
 Symptoms of septic shock include the symptoms of severe sepsis, plus a very low blood pressure

The serious effects of sepsis

 Formation of blood clots throughout your body. These clots block the flow of blood and oxygen
to vital organs and other parts of your body. This increases the risk of organ failure and tissue
death (gangrene).

DIAGNOSTIC TEST
 WBC- elevated with increase immature neutrophils consistent with bacterial infection
 Hemoglobin and hematocrit- low if blood loss occurs
 Electrolytes may reveal altered levels of K, Na, and chloride
 Abdominal X-ray- show air and fluids levels as distended bowel loops
 Abdominal UTZ may reveal abscess (collection of purulent material surrounded by inflamed
tissues)
 CT scan- shows abscesses formation
 Peritoneal aspiration- aspirated fluid may reveal infection and identify the pathogen via C and S
 MRI- to diagnose intra-abdominal abscess
MEDICAL MANAGEMENT
  Fluid, colloid, and electrolyte replacement is the major focus of the management
 Isotonic solution as prescribed- hypovolemia occurs due to massive fluid and electrolytes
moves from the interstitial lumen into the peritoneal cavity and deplete the fluids in the vascular
space.
 Analgesics as prescribe for pain
 Anti emetic for nausea and vomiting
 Peritoneal lavage/ Intestinal intubation and suction to relieve abdominal distension and relieve
exudate and to promote intestinal function. Fluid in the abdominal cavity can cause pressure
that restricts expansion of the lungs and causes respiratory distress
 Insertion of drainage tubes (penrose drain, hemovac, Jackson Pratt) to drain exudate from the
area
 Oxygen therapy by nasal cannula promote adequate oxygenation
 Antibiotic therapy initiated early in the treatment of peritonitis usually broad expectrum in
order to treat the secondary peritonitis
 Administration of TPN as ordered. To support nutritional requirement of the client
NURSING MANAGEMENT
 The nursing management is based on secondary peritonitis upon the patient’s primary diagnosis
and treatment.
 If septic shock occurs, intensive care is needed
 Monitor level of pain
 Monitor VS, I and O to assess fluid balance
 Monitor electrolytes hemoglobin and hematocrit
 NGT insertion to relieve abdominal distension
 Bed rest in Semi fowlers- to localize the inflammatory process
 Administer fluids such as colloid and isotonic solutions as prescribe
 Administer anti emetics as ordered
 Administer antibiotics as prescribed
 Signs of peritonitis subsides like temperature, pulse rate, softening of the abdomen, return
peristaltic movement, passing of flatus and bowel movement
 Increase fluid and food intake gradually and reduce parenteral IV fluid
What is Celiac Disease? An autoimmune, GI disorder where when gluten is ingested, which is found
in wheat barley, grains, and rye products, it causes damage to the small intestine, specifically
the intestinal villi.

Key Points about Celiac Disease

 Wheat is a problem for patients with Celiac Disease. There are several proteins in wheat
and one of them is called GLUTEN.
 Gluten itself is constructed of a group of proteins called gliadin and glutenin. Gliadin is
the problem with Celiac Disease.
 Celiac Disease tends to be genetic and occurs in both children and adults.
 Celiac Disease is different from a wheat allergy or gluten sensitivity in that it can cause
similar signs and symptoms BUT there isn’t the same extensive damage to the small
intestine as in Celiac Disease.
 Celiac disease causes damage to the small intestine due to an autoimmune response. The
body sees the protein Gliadin as a foreign invader because it can NOT be broken down
correctly
Key Players in Celiac Disease

Gliadin and the amino acids that make up the protein:

Gliadin is a wheat prolamin which is a plant storage protein that is high in the amino acids, particularly
proline and glutamine.

What do amino acids do? They help store and transport nutrients and give the protein its structure. The
body can’t break down the amino acids correctly. Therefore, it crosses the gut cells and causes an
immune response.

What does the body do NORMALLY with proteins? Normally, the body will take proteins, which start
out as long amino acid chains, and break them down into single amino acids. The GI cells will then use
them appropriately. However, the amino acids (proline and glutamine) of Gliadin can NOT be broken
down into a single amino acid but stay as a small collection of amino acids called peptides (this is what
causes the immune response).

The enterocytes which are found in the villi allows them to cross and the immune system doesn’t like this
and views it as a bacteria or virus and attacks.

Immune System: sends immune cells to kill the Gliadin. The Gliadin reacts with TTG (Tissue
Transglutaminase) enzyme and antibodies are formed by the immune cells to fight the gliadin because
the body thinks it is bad. The antibodies formed are:

 Tissue Transglutaminase Antibodies (tTg)

 Antibody IgA
 Endomysial antibody (EMAs)
NOTE: in the process of doing this “warfare” between the immune system and glidian the VILLI of the
small intestine are damaged.
Intestinal Villi: found in the small intestine and normally look like little finger-like projections that aid in
the absorption of the nutrients by increasing the surface area for absorption. They are surrounded by are
a network of blood vessels that easily take the nutrient collected from the food and allows it in the blood
stream. Each villus contain cells called enterocytes which help absorb nutrients and aid in digestion.

From recurrent immune system overdrive from fighting the gluten entering the body, the villi LOSES its
finger-like like projections and become FLAT (see the top picture in the image above). This LEADS TO
DECREASE SURFACE AREA FOR ABSORPTION. Hence, the patient is going to experience
malnutrition.

**All of this tends to occur in the jejunum of the small intestine

Signs and Symptoms of Celiac Disease

“MALNOURISHED” this is the whole reason why pts with CD get sicks due to malabsorption of
nutrients needed by the body

Mouth ulcers
Anemia- due to malabsorption of minerals and vitamins B12, iron
Lactose intolerance (can’t break down lactose),
Nausea/vomiting
Osteo change (thinning, fractures)-due to malabsorption of calcium
Unexplained slow growth, delay puberty (children) and weight loss
Rashes (very itchy dermatitis herpetiformis…elbows, backside, and knees)
Irregular periods, irritable (depression) (loss of nutrients)
Stools: greasy and odorous
Hair loss
Enamel changes to the teeth (yellow or brown spot and deformity)
Diarrhea

Diagnosing Celiac Disease

Blood tests are used to check for antibodies:

 Tissue Transglutaminase Antibodies (tTG-IgA)

 IgA serum
 IgA Endomysial antibody (EMA)

Endoscopy: a biopsy will look at the villi for abnormalities

Complications of Celiac Disease

 Malnourishment (bone, skin, teeth, health mental, growth, reproductive problems)

 Cancer (lymphoma)
 Villi take time to heal BUT sometimes the villi never heal back (condition called refractory celiac
disease) and the patient suffers from constant malnourishment and will need IV supplementation.
Nursing Interventions for Celiac Disease
 Assess the Signs and symptoms of Celiac Disease by asking patient when they notice the
most oblivious signs and symptoms and to list what foods they eat on a regular basis…( do they
have bloating abdomen, diarrhea/constipation, irritable, depression, or mental fog after eating
foods with gluten?)
 Patient needs to keep a food dairy along with the signs and symptoms and the nurse should
assess the diet log (look for foods that contain gluten)
 Skin, teeth, weight (normal vs abnormal)
 Family history
 Ability to read food labels and the patient’s or families’ knowledge about gluten
 Educate: AVOID ALL FOOD CONTAINING GLUTEN (watch foods with hidden gluten) and
substitute with foods that do not contain gluten

More than ever grocery chains and restaurants are carrying more and more gluten free foods to help
people enjoy foods they normally couldn’t and food labels will say GLUTEN FREE- like this:

Foods Without Gluten

 Plain Meats (fish, beef, chicken, turkey etc.)

 Grains: Rice, Corn, Soy, Millet, Quinoa, Tapioca, Chia, Buckwheat (most of these are used as
substitutes for baking as in cakes, breading on meats, pasta etc.)
 Vegetables and Fruits
 Nuts, Beans, Legumes
 Dairy (not malt)….however watch dairy because many patients with Celiac Disease may be
lactose intolerant
Foods with GLUTEN TO AVOID

 Wheat (anything that says wheat expect buckwheat)

 Barley,Malt, Beer, Pasta Noodles, Rye,Seasonings, soups
 Anything with breading that doesn’t say GF
 Anything that looks like bread: croutons, crackers, breads, dough, cookies, most cereals, oats
unless they say GF
 most processed foods have gluten

Other Interventions:

Implementing the GF diet and making sure food trays are GF and that patient and family understand the
importance of following the gluten-free diet

Administering per MD order supplements to help with any vitamin deficiencies

References:

1. “Celiac Disease | NIDDK”. National Institute of Diabetes and Digestive and Kidney
Diseases. Web. 11 Apr. 2017.
2. “‘Gluten-Free’ Now Means What It Says”. Fda.gov. Web. 10 Apr. 2017.
 3. “Gluten Sensitivity | Gluten Intolerance | Medlineplus”. Medlineplus.gov. Web. 10 Apr.
2017.

Disturbances in Digestion
Gastrointestinal bleeding
 A bleeding symptom either in upper of lower GI
 Maybe obvious in emesis or stool or occult or hidden

TYPES OF GI BLEEDING (LOCATION)

Upper GI bleeding
• bleeding in the upper gastrointestinal tract arising from the esophagus, stomach or
duodenum.
• Coffee ground or black
Lower GI Bleeding
 Bleeding occurs in the colon, rectum, or anus
 presents hematochezia or melena

Pathophysiology and Etiology

 Trauma in the GI tract
 Erosions or ulcers
 Ruptured of an enlarged vein such as varicosity (esophageal or gastric varices
 Inflammation such as esophagitis (cause by acid), gastritis,
 Inflammatory bowel disease (ulcerative colitis and Crohn’s
 Alcohol and drugs ( aspirin, NSAIDS and cortecosteroids)
 Diverticular disease
 Hemorrhoids or fissures

Clinical Manifestations
Characteristic of blood
 Bright red: vomited from high esophagus (hematemesis), rectum or distal colon
 Mixed with dark red: higher up in colon and small intestine, mixed with stool
 Coffee Ground: esophagus, stomach, and duodenum
 Melena (black tarry stool) excessive blood in the stomach

Signs and Symptoms of Bleeding

Massive bleeding
 Acute, bright red hematemesis or large amount of black tarry stool
 Rapid pulse, hypotension, hypovolemia and shock
Subacute bleeding
  Intermittent/alternate melena or coffee ground emesis
 Weakness, dizziness
Chronic Bleeding
 Intermittent appearance of blood
 Increased weakness, paleness or SOB
 Occult blood

Diagnostic Evaluation/test/Assessment
History
 Change in bowel pattern,
 Presence of pain or tenderness
 Recent intake of food and what kind(red beef),
 Alcohol consumption and medications taken (aspirin or steroids, NSAIDS)
CBC
 Low hemoglobin, high hematocrit, low platelet
 High PT( 10-12 sec )and aPTT( 30-45sec); NV
Endoscopy and MRI or CT
 Identifies the source and cause of bleeding
Stool test- for occult blood

Nursing Diagnosis
 Fluid volume deficit related to blood loss
 Altered Nutrition: Less than body requirement related to nausea, vomiting and diarrhea

EMERGENCY INTERVENTION
 Patient remains on NPO
 IV lines and oxygen therapy
 Administer vasopressin and blood replacement because severe bleeding is life threatening and to
treat shock
 Intra arterial vasopressin- to slow or stop bleeding from diverticulum
 Surgical if indicated.

Nasogastric tube Intubation

 An NG tube should be in place for most patients with acute or upper GI bleeding
 2-3 L of tap water lavage and if the aspirate continues to be bloody, this indicate that the patient
is in active bleeding that requires emergent intervention

Nursing Interventions
Attaining Normal Fluid Volume
 Maintain NG tube and NPO status to rest GI tract and evaluate bleeding
 Monitor I and O to evaluate fluid status and hydration
 Monitor VS
 Administer IV fluids,
 Assess signs of shock such as hypotension, tachycardia, tachypnea (increase RR), decrease urine
output, change in mental status.

Attaining Balance Nutritional Status

 Weigh daily to monitor caloric status’
 TPN, to promote hydration and nutrition while on NPO restriction
 Begin liquids if patient is no longer on NPO, then DAT. DAT should be high in calorie, high
CHON. Frequent small feedings if indicated.,
Patient Education
 Instruct the patient to report signs of GI bleeding such as melena, emesis that is bright red or
coffee ground color, rectal bleeding, weakness, fatigue and SOB
Evaluation
 Fluid volume is maintained, hypovolemic shock is prevented
 Patient verbalized no signs of bleeding
 Nutritional and body weight status is maintained

Complications
 Hemorrhage, Shock, Death

GASTRITIS
 Inflammation of the gastric or stomach mucosa
 It affects both sexes but more common in older adults

TYPES OF GASTRITIS
ACUTE
 lasting several hours to few days

Causes
 severe form of acute gastritis is caused by ingestion of strong acid or alkali that may cause the
mucosa to become gangrene or possible for perforation. Scarring can occur which results to
Pyloric stenosis (narrowing or tightening) or obstruction
 AG maybe develop in acute illnesses or major traumatic injuries (Burns, severe infection,
hepatic,kidney or respiratory failure and major surgery also known as Stress Related Gastritis

CLASSIFICATION OF ACUTE GASTRITIS

Based on pathologic manifestations present in the gastric mucosa (Wehbi, et al.,2104)

Erosive Acute Gastritis

 most often cause by local irritants such as aspirin and other NSAIDS (Naproxen, Voltaren,
Ibuprofen), alcohol consumption and gastric radiation therapy (Grossman, & Porth, 2014, Wehbi,
et al.,2104NIDDK, 2015)

Non-Erosive Acute Gastritis

 most often caused by an infection with Helicobacter Pylori (H. Pylori) (Wehbi, et al.,2104)
 70% of individauls in US and other industrialized countries are infected with H. Pylori (CDC,
2016)

CHRONIC
 results from repeated exposure to irritating agents or recurrent episodes of acute gastritis

Causes
 H. Pylori infection is the most common cause (Marcus and Greenwald, 2014). Chronic H. Pylori
gastritis is implicated in the development ofPUD, gastric adeno carcinoma, and gastric mucosa
associated with lymphoid tissue lymphoma (Chin, et al.,2015)
 Chemical gastric injury (Gastropathy)- long term use of NSAIDS and aspirin
 Autoimmune disease- Hashimoto thyroiditis, Addison’s disease, Grave’s disease are also be
associated with Chronic Gastritis (Grossman and Porth, 2014; Marcus and Greenwald, 2014)
PATHOPHYSIOLOGY
 Gastritis is characterized by Disruption of the mucosal barrier that normally protects the
stomach from digestive juices (Hcl and pepsin) are irritating agents (Aspirin, NSAID and H.
Pylori) comes in contact with the gastric mucosa that resulted to inflammation.
 In Acute gastritis, the inflammation is usually transient and self-limiting in nature. Inflammation
causes the gastric mucosa to become edematous and hyperemic (congested with fluid and blood)
and to undergo superficial erosion which will result to hemorrhage.
 In chronic gastritis, persistent and repeated insults lead to chronic inflammation that leads to
atrophy or thinning of the gastric tissue. (Grossman and Porth, 2014)

Clinical Manifestations
Acute Gastritis- rapid onset of symptoms that last from a few hours to a few days
 Hiccups
 Anorexia
 Epigastric pain (rapid onset
 Dyspepsia (Indigestion)
 Nausea and vomiting
 Melena (black, tarry stools,) hematemesis (blood in vomitus), hematochezia (bright red, bloody
stools)- Erosive gastritis (NIDDK, 2015.; Wehbi etal.; 2014)
 Possible sign of shock

Chronic Gastritis
 Belching
 Early satiety Anorexia
 Intolerance to fatty and spicy foods
 Nausea and vomiting
 Pyrosis/heartburn (Burning sensation in the stomach and esophagus that moves up into the mouth
after eating
 Sour taste in mouth
 Epigastric pain relieves by eating
 Systemic: Fatigue and anemia

Diagnostic Test
 Upper Endoscopy and histologic examination confirms the diagnosis. This visualized
inflammatory changes lesions or erosion and can determine H.Pylori by biopsy
 Other non invasive test that can detect H. Pylori is through serologic testing for antibodies against
H Pylori antigen, stool antigen test , Urea breath test
 CBC- to assess anemia as a result of hemorrhage

NURSING INTERVENTIONS
Independent
Promoting Optimal Nutrition
 No foods of fluids by mouth for a few days- until acute symptoms subside to allow gastric
mucosa to heal. (Erosive)
 Monitor I and O and electrolytes (Na, K, Chloride) if in IVF every 24 hrs. to detect any
imbalances and signs of DHN (minimum oral fluid intake of 1.5 L/day
 Assess for signs of hemorrhagic gastritis such as hematemesis, tachycardia and hypotension. All
stools should examine for the presence of occult bleeding.
 Monitor VS and notify the primary provider or the attending physician.

Dependent Nursing Interventions

Diet
 Ice chips followed by clear liquids after symptoms subsides then solid foods as ordered.
 Advise Non-irritating food. high-fiber foods, such as whole grains, fruits, vegetables, and beans.
low-fat foods, such as fish, lean meats, and vegetables. Foods with low acidity, including
vegetables and beans.
 IV fluids if symptom persist just to maintain hydration if bleeding persist. If IV 3L/day
 NG tube intubation
 Administer antacids. H2 receptors blockers, PPI, Antibiotics

Pharmacological Therapy
ANTACIDS
 Neutralized gastric acid by increasing the in pH the GI tract. Provide symptomatic relief but do
not heal esophageal lesions.
 Ex: Aluminum hydroxide (Amphogel), Aluminum hydroxide and Magnesium hydroxide
(Maalox); Milk of magnesia
 Antacids containing both aluminum and magnesium hydroxide balance the constipating effects of
ALUMINUM with the LAXATIVE effects of MAGNESIUM

Nursing Responsibilities
 shake the suspension or chewable tablets chew them thoroughly and drink half glass of water to
promote passage to the stomach
 Give antacids at least 1 hour from enteric coated tablets

Histamine 2 receptor antagonist/H2 blockers

 Inhibit or decrease acid production by blocking action of histamine on histamine receptors of
parietal cells of the stomach
 Ex: Cimetidine (Tagamet), Famotidine (Pepcid), Ranitidine (Zantac)

PROTON PUMP INHIBITORS

 Block gastric acid secretions by inhibiting acid pump in gastric parietal cells
 Treat erosive esophagitis and GERD
 Doudenal ulcer, Active gastric ulcer
 Eradicate H. Pylori infection
 Ex: Esomeprazole (Nexium), Lanzoprazole, Omeprazole, Pantoprazole, Rabeprazole

NURSING RESPONSIBILITY
  Swallow the capsules whole and not to chew or crush them
 Administer 1 hour before meal
 Avoid gastric irritants like alcohol, smoking, aspirin, caffeine, NSAIDS

For CHRONIC GASTRITIS

 Modify the diet. Avoid carbonated and caffeine, irritating foods
 Rest
 Reduce stress
 Avoid NSAIDS and alcohol
 Antacids, H2 blockers, PPI (NIDDK, 2015)
 Antibiotics- Metronidazole (Flagyl), Amoxixillin, Clarithromicin, Tetracycline
 Bismuth salts (rare)

Metronidazole (Flagyl)
 MA: Antibacterial & anti protozoal that assist in eradicating H. Pylori in gastric mucosa. It may
cause anorexia and metallic taste
 NC: Give with meals to decrease GI upset. Avoid alcohol, it increases blood thinning effects of
warfarin

Amoxixillin,
 MA: Eradicated H pylori bacteria in gastric mucosa
 NC: Should not be used in patients with hypersensitivity to penicillin

Clarithromicin,
 MA: Eradicated H pylori bacteria in gastric mucosa
 NC: may cause GI upset, headache and altered taste, Can cause drug-drug interaction

Tetracycline
 MA: Eradicated H pylori bacteria in gastric mucosa
 NC: may cause photosensitivity reaction, advise the patient to use sunscreen
 May cause GI upset
 Caution in renal or hepatic impairment
 Avoid intake of milk and dairy products that reduce effectiveness
 Do not take iron supplements, multivitamins, calcium supplements, antacids, or laxatives within
2 hours before or after taking tetracycline. These products can make tetracycline less effective
in treating your infection.

Bismuth salts (rare)

 MA: suppresses H. Pylori in the gastric mucosa and assist in healing of ulcers
 NC: should be taken on an empty stomach. And maygiven with antibiotics to eradicate the H
Pylori

RELIEVES PAIN
 Assess the level of pain
 Analgesics as ordered.
Heath Teachings
 Avoid taking NSAIDS and Aspirin
 Avoid or refrain from alcohol and food until symptoms subside
 Avoid carbonated and caffeine drinks. Caffeine is a CNS stimulant that increase gastric activity
and pepsin secretion
 Avoid smoking because nicotine reduces secretion of pancreatic bicarbonate which inhibits
neutralization of gastric acid in the duodenum (Lu et al., 2014)
 Enforce to the patient the importance of completing medication regimen as prescribed to
eradicate H. Pylori infection
 Teach family members to how to administer vitamin B 12 injection or make arrangement to the
primary provider in order to receive injection . In gastritis or PUD, there is malabsorption of
Vitamin B 12
 Emphasized the follow up appointments with primary provider.