Week 1 (Exam 1): Chapter 55 Flashcards Preview

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Inflammation of gastric mucosa (stomach lining).



Causing ulcers


Acid autodigestion

A process where prostaglandins provide a protective mucosal barrier that prevents the stomach from digesting itself.


What protects the stomach mucosa from autodigestion?



Acute Gastritis

- Damage by local irritants
- Inflammation of the gastric mucosa or submucosa after exposure to local irritants or other causes.


Chronic Gastritis

- Appears as a patchy, diffuse (spread out) inflammation of the mucosal lining of the stomach.
- Associated with an increased risk for gastric cancer.
- May be categorized as type A, type B, or atrophic
- Chronic local irritation and toxic effects caused by alcohol ingestion, radiation therapy, and smoking have been linked.


Chronic Atrophic gastritis

- Old age- mostly work related (exposure to lead, nickel and all) or H. pylori infection, or related to autoimmune factors.
- Diffuse inflammation and destruction of deeply located glands accompany the condition
- Affects all layers of the stomach, thus decreasing number of cells
- Characterized by total loss of fundal glands, minimal inflammation, thinning of the gastric mucosa, and intestinal metaplasia (abnormal tissue development).


Type A (nonerosive) chronic gastritis

Refers to an inflammation of the glands and the fungus and body of the stomach.


Type B Chronic Gastritis

Usually affects the glands of the antrum but may involve the entire stomach.


Etiology of gastritis

- H. Pylori (gram-negative bacterium that penetrates the mucosal gel layer of the gastric epithelium).
- Long-term NSAID, high risk for acute gastritis. Inhibit prostaglandin production in mucosal barrier.
- Use of alcohol, coffee, caffeine, and corticosteroids.
- Local irritation from radiation therapy
- Accidental or intentional ingestion of corrosive materials (acids or alkalis ex: lye and drain cleaners).
- Autoimmune causes


What can atrophic gastritis lead to?

- Gastric cancer
- Gastric mucosa-associated lymphoid tissue (MALT) lymphoma


Health Promotion and Maintenance

- Balanced diet (limiting caffeine, chocolate, mustard, pepper, and other strong or hot spices)
- Regular exercise (helps prevent gastric contents from irritating the gastric mucosa)
- Stress-reduction techniques (aerobic exercise, meditation, reading, and/or yoga)
- Limit foods and spices that cause gastric distress
- Avoid tobacco (causes vasoconstriction), alcohol
- Avoid excessive use of aspiring, NSAIDs (ibuprofen), and corticosteroids.
- Protect yourself against exposure to toxic substances in the workplace (lead and nickel).


Assessment: Noticing

Acute Gastritis

- Rapid onset of epigastric pain or discomfort
- N/V
- Hematemesis (vomiting blood)
- Gastric hemorrhage
- Dyspepsia (heartburn)
- Anorexia


What are some diagnostic assessments for gastritis?

- EGD with biopsy
- Cytologic examination
- Rapid urease testing


What may the patient report with gastritis?

Epigastric alteration in comfort or pain, anorexia, cramping, and N/V.


What should you assess with gastritis?

Assess for abd. tenderness and bloating, hematemesis (vomiting blood), or melena (dark, sticky feces, as evidence of blood in the stool).


What may result from Aspirin/NSAID-related gastritis?

Dyspepsia (heartburn)


What can often occur with ingestion of contaminated food? Time?

Severe N/V often occur within 5 hours of ingestion of the contaminated food.
In some cases gastric hemorrhage is the presenting sx, which is a life-threatening emergency.


Assessment: Noticing

Chronic Gastritis

- Vague report of epigastric pain that is relieved by food
- Anorexia
- N/V
- Intolerance of fatty and spicy foods
- Pernicious anemia
- Periodic epigastric pain may occur after a meal
- Radiation therapy. Smoking and alcohol use are known to be associated with the development of chronic gastritis


Interventions: Responding

- Acute gastritis treated with supportive care
- Chronic gastritis treated based on causative agents
- Pharmacological Management: H2-receptor antagonists (famotidine (Pepcid)), sucralfate (Carafate, Sulcrate), antacids (maalox and mylanta), antisecretory agents/PPI (Prilosec), prostaglandin analogs, and animicrobials


Treatment for acute gastritis

- If bleeding severe, a blood transfusion may be necessary
- Fluid replacement is prescribed with severe fluid loss
- Surgery, such as partial gastrectomy, pyloroplasty, and/or vagotomy, may be needed for patients with major bleeding or ulceration.
- Primary health care provider prescribes drugs that block and buffer gastric acid secretions to relieve pain.


Treatment for chronic gastritis

- Includes the elimination of causative agents, treatment of any underlying disease (Uremia, Crohn’s disease), avoidance of toxic substances (alcohol, tobacco), and health teaching.
- Primary treatment is eliminating the causative factors, such as H. pylori infection if present.
- Drugs and nutritional therapy


H2 Antagonists (Blockers)

- Block gastric secretions
- Decrease gastric acid secretions
- Give single dose at bedtime for tx of GI ulcers, heartburn, and PUD
-Ex: famotidine (Pepcid), nizatidine (Axid), and ranitidine (Zantac)


Mucosal Barrier Fortifiers

- Protect stomach mucosa
- Ex: sucralfate (Carafate, Sulcrate)- Give 1 hr before and 2 hr after meals and at bedtime (food may interfere with drug’s adherence to mucosa). Do not give within 30 min of giving antacids or other drugs.
- Ex: Bismuth subsalicylate (Pepto-Bismol)- Remind pt to refrain from taking aspirin while on this drug (aspirin is a salicylic acid and can lead to OD).



- Increase pH of gastric contents by deactivating pepsin
- Do not give other drugs writhing 1-2 hrs of antacids.
- Ex: Magnesium hydroxide with aluminum hydroxide- Give 2 hr after meals and at bedtime. Use liquid rather than tablets. Assess pt for hx of renal disease and HF. Observe pt for SE of diarrhea.
- Ex: aluminum hydroxide (Gaviscon, Alugel)- Give 1 hr after meals and at bedtime. Use liquid rather than tablets. Observe pt for SE of constipation. Use for pts with renal failure


Proton Pump Inhibitors

- An antisecretory agent which suppresses gastric acid secretion
- Ex: omeprazole (Prilosec, Losec, Olex)- take whole, do not crush. Give 30 min before main meal of the day (activated by presence of food).
- Ex: Lansoprazole (Prevacid)- Give 30 min before the main meal of the day.
- Ex: Rabeprazole (Aciphex, Pariet)- Take after morning meal. Do not crush capsule.
- Ex: pantoprazole (protonix, pantoloc, tecta)- Do not crush, IV for must be given on a pump with a filter and in separate line.
- Ex: esomeprazole (Nexium)- Assess for hepatic impairment


Prostaglandin Analogs

- Stimulate mucosal protection and decreased gastric acid secretion
- Vasodilate nearby blood vessels (more blood flow)
- Ex: misoprostol (Cytotec)- Avoid magnesium-containing antacids. Do not administer to pregnant women.



- Treats H. pylori infection
- Ex: clarithromycin (Biaxin)- Give with caution to pts with renal impairment; motor renal function lab values (can increase BUN lvls and should be monitored).
- Ex: amoxicillin (Amoxil, Novamoxin)- Teach pts to take drug with food or immediately after meal
Ex: tetracycline- Teach to take at least 1 hr before meals or 2 hrs after meals. No dairy. Teach to avoid direct sunlight and wear sunscreen when outdoors.
- Ex: metronidazole (flagyl, nidagel, novo-nidazol)- Take with food. Avoid alcohol during drug therapy and for at least 3 days after therapy is completed.


Peptic Ulcer Disease (PUD)

- Mucosal lesion of stomach or duodenum
- Results when mucosal defenses become impaired and no longer protect the epithelium from the effects of acid and pepsin


What are the 3 types of PUD?

Stress (less common)


How is H. pylori transmitted?

Not certain how but believed to be spread through contaminated food or water.


Gastric Ulcers
May result from?

- Are deep and penetrating, and occur on the lesser curvature of the stomach, near the pyloric sphincter (at the end).
- May result from back-diffusion of acid or dysfunction of the pyloric sphincter. W/o normal functioning of the pyloric sphincter, bile reflexes (backs up) into the stomach. This reflux of bile acids may break the integrity of the mucosal barrier, which leads to mucosal inflammation and compromise in immunity.


Duodenal Ulcer

- Most occur in the upper portion of the duodenum.
- They are deep, sharply demarcated lesions that penetrate through the mucosa and submucosa into the muscularis propria (muscle layer).
- Main feature of a duodenal ulcer is high gastric acid secretion
- pH lvls are low (excess acid) in the duodenum for long periods


What can stimulate acid secretion?

Protein-rich meals, calcium, and vagus nerve excitation


Stress Ulcer

- Acute gastric mucosal lesions occurring after an acute medical crisis or trauma, such as sepsis or head injury. Ulcer is secondary
- Bleeding caused by gastric erosion is the main manifestation of acute stress ulcers.
- Multifocal lesions associated with stress ulcers occur in the stomach and proximal duodenum.
- Most pts with major trauma or surgery receive IV drug therapy (ex. PPI) to prevent stress ulcer development.
- Extensive burns (Curling’s ulcer)
- Sepsis (ischemic ulcer)
- Increased intracranial pressure (Cushing’s ulcer)


Complications of Ulcers

- Hemorrhage, most serious complication (Blood lose from ruptured blood vessel). More often in pts with gastric ulcers and in older adults.
- Perforation (Hole), surgical emergency
- Pyloric obstruction (Gastric outlet blockage)
- Intractable disease - hard to control or deal with



- Vomit that is bright red or coffee-ground blood.
- Usually indicated bleeding at or above the duodenojejunal junction (upper GI bleeding).


Signs and Sx of upper GI bleeding (Chart 55-4, pg. 1108)

- Bright red or coffee-ground vomitus (hematemesis)
- Melena (tarry or dark, sticky) stools
- Decreased BP
- Increased HR
- Weak peripheral pulses
- Acute confusion (in older adults)
- Vertigo
- Dizziness or light-headedness
- Syncope (loss of consciousness)
- Decreased hemoglobin and hematocrit


Herbs that are commonly used by patients with gastritis and PUD:

- Powders of slippery elm
- Marshmallow root
- Quercetin
- Licorice



- Abd is tender, rigid, and boardlike (peritonitis)
- Pt assumes a “fetal” position to decrease tension on abd. muscle.
- Bacterial septicemia and hypovolemic shock follow
- Pain that radiates to the back or upper quadrant
- Accompanied w/ rebound tenderness and pain


Pyloric Obstruction
- Manifested by?
- Where does it occur?
- What do you do?
- What can happen?

- Vomiting caused by stasis and gastric dilation
- Occurs at pylorus (gastric outlet)
- If pt. reports sudden muscle weakness, request an ECG.
- Pyloric stenosis can lead to hypokalemia (causes muscle weakness). Potassium imbalances can lead to cardiac dysrhythmias


Etiology and Genetic Risk of PUD

- H. pylori
- NSAIDs (Ibuprofen, Aspirin)
- Corticosteroids(Prednisone)
- Caffeine
- Radiation therapy


Sign and Sx for Upper GI bleeding

- Bright red or coffee-ground vomitus (hematemesis)
- Melena (tarry or dark, sticky) stools
- Decrease BP
- Increase HR
- Weak peripheral pulse
- Acute confusion (older adults)
- Vertigo
- Decrease hemoglobin and hematocrit
- Syncope (loss of consciousness, fainting)
- Dizziness/Light-headedness


Physical Assessment for PUD

- Epigastric tenderness (located at the midline between the umbilicus and xiphoid process, upper abd.)
- Dyspepsia (Indigestion)
- Rigid, boardlike abd. w/rebound tenderness and pain= perforation into peritoneal cavity. They will need emergency surgery.
- Gastric versus duodenal ulcer pain
- Assess for fluid volume deficit


Gastric ulcer pain

Upper epigastric with localization to the left of the midline and is aggravated by food


Peptic ulcer pain

Duodenal ulcer pain is usually located to the right of or below the epigastrium. The pain associated with a duodenal ulcer occurs 90 min to 3 hours after eating and often awakens the pts at night


Dyspepsia signs and sx

-Most common sx w/ PUD
- Sharp, burning, or gnawing pain
- Some perceive discomfort as a sensation of abd pressure or of fullness/hunger


Dx for PUD
Lab value to detect venous bleeding?

- Testing for H. pylori
- EGD (scope to the stomach, can biopsy) (may be repeated 4-6 weeks)
- Chest, abd x-ray (if perforation suspected)
- Nuclear medicine test (if GI suspected)
- Urea breath test (swallows a capsule, liquid, or pudding that contains urea with a special carbon atom. After a few min the pt exhales; and if special carbon atom is found, the bacterium is present

-If pt has venous bleeding from a PUD, may have decrease hemoglobin and hematocrit values