DISORDERS OF THE MOUTH Common disorders of the mouth and esophagus that interfere with adequate nutrition include poor dental hygiene, infections, & inflammation

DISORDERS OF THE MOUTH

Common disorders of the mouth and esophagus that interfere with adequate nutrition include poor dental hygiene, infections, & inflammation (stomatitis).

DO YOU BRUSH AND FLOSS?

POOR DENTAL CARE

DISORDERS OF THE MOUTH

Dental plaque and cariesEtiology/pathophysiologyErosive process that results from the action of bacteria on carbohydrates in the mouth, which in turn produces acids that dissolve tooth enamel

FACTORS THAT CAUSE TOOTH DECAYThe presence of dental plaque; a thin film

on the teeth made of mucin and colloidal material found in saliva and often secondarily invaded by bacteria.

The strength of acids and the ability of the saliva to neutralize them.

The length of time the acids are in contact with the teeth.

Susceptibility of the teeth to decay.

MEDICAL MANAGEMENT

INTERVENTIONS INCLUDE: 1. Treatment of dental caries by

removal of affected areas of the tooth and replacement with some form of dental material.

2. Treatment of periodontal disease centers on removal of plaque from the teeth.

3. If the disease has advanced, then surgical interventions of the gingivae and alveolar bone may be necessary.

DENTAL PLAQUES AND TARTAR

ALVEOLAR BONE

NURSING INTERVENTIONS

1. Emphasize the importance and the NECESSITY to brush and floss twice a day. The pt. should give a return demonstration for the proper technique for brushing and flossing.

2. Plaque forms continuously and must be removed periodically through regular visits to the dentist.

3. Prevention plays a key role through routine dental care.

PREVENTION

NURSING INTERVENTIONS, CONT.4. Carbohydrates create an environment in

which caries develop and plaques accumulate more easily. Proper nutrition is included in pt. teaching. So the pt. needs to be aware of what food groups he eats for appropriate dental care.

5. The cleansing mechanism of the mouth is impaired when a person is ill.

6. Illnesses, drugs, and irradiation of the mouth all interfered with the normal action of saliva.

7. If the pt. can’t manage oral hygiene, then the nurse or someone who knows how must take on this responsibility.

PROGNOSIS

The prevention and elimination of dental caries and plaque is directly related to oral hygiene, dental care, nutrition, and heredity.

All of the above are controllable factors, except heredity.

Factors that can foster good dental health: Regularly brush, floss, and visit the dentist; eat a low-CHO diet; drink fluoridated water.

CANDIDIASIS

Etiology/Pathophysiology: 1. This condition is any infection caused

by a species of Candida, usually C. albicans. Candida is a fungal organism normally present in the mucous membranes of the mouth, intestine, vagina, and the skin of healthy people.

2. Also known as thrush and moniliasis. 3. More common in the newborn

(becomes infected while passing through the birth canal).

4. In older people, it occurs in those who are immunosuppressed, those with DM, leukemia, alcoholism, taking steroids, on chemotherapy, or living with AIDS.

THRUSH

CLINICAL MANIFESTATIONS

It appears as pearly, bluish white “milk-curd” membranous lesions on the mucous membranes of the mouth, tongue, and larynx. Some of the lesions may be on the mucosa. If you remove the plaque or patch, it will be painful and will bleed.

PATCHES OF THRUSH IN THE ESOPHAGUS

MEDICAL MANAGEMENT

1. 1-4 mL of nystatin dropped in the infant’s mouth several times/day.

2. For the adult, nystatin or Amphotericin B (oral suspension) or buccal tablets and half-strength hydrogen peroxide/saline mouth rinses may provide some relief

3. Adult vaginal infection: insert vaginal tablets (100,000 units) into the vagina twice a day.

4. Also Ketoconazole is effective.

MEDICINES


1. Use thorough handwashing.2. Handwashing, care of feeding

equipment, and cleanliness of the mother’s nipples are important to prevent spread of the infection.

3. The nurse should clean the infant’s mouth of any foreign material; rinsing the mouth and lubricating the lips.

4. Inspect the mouth by using a flashlight and a tongue blade.

NURSING INTERVENTIONS, CONT.5. For adults, instruct the pt. to use a

soft-bristled toothbrush.

6. Have the adults administer a topical anesthetic (Lidocaine or Benzocaine) one hour before meals.

7. Give soft or pureed foods and avoid hot, cold, spicy, fried, or citrus foods.

PUREED FOODS

LEUKOPLAKIA

1. Leukoplakia is a white, firmly attached patch on the mouth or tongue mucosa. This may appear on the lips and buccal mucosa. These nonsloughing lesions cannot be rubbed off by simple mechanical force.

2. They can be benign or malignant.3. Some can develop into squamous cell

carcinomas. A bx. is recommended if the lesions persist for > 2 weeks. They occur most frequently between the 50-70 y.o. They appear more commonly in men.

LEUKOPLAKIA

ESOPHAGEAL VARICES

“Varicose veins” of the esophagusDilated and tortuous veins in the submucosa of the esophagus

Bleeding varices is an emergency

The goals of treatment are to control bleeding, prevent complications, and prevent the reoccurrence of bleeding.

NURSING MANAGEMENT

HOB ↑ 30°

VS, including orthostatic hypotension

Monitor lung sounds

NPO

Prepare for NG tube insertion

Administer O2 as ordered

Instruct the client to avoid activities that will initiate vasovagal responses!

SURGICAL MANAGEMENT

Endoscopic injection (Sclerotherapy)

Endoscopic variceal ligationSurgical shunt proceduresSplenorenalPortacavalMesocavalTransjugular intrahepatic portal-systemic

DISORDERS OF THE ESOPHAGUS: GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Etiology/Pathophysiology: 1. GERD is a backward flow of stomach

acid up into the esophagus. 2. Sx. are usually burning and pressure

behind the sternum. 3. Most cases are attributed to the

inappropriate relaxation of the lower esophageal sphincter in response to an unknown stimulus.

GERD, CONT.

4. Reflux allows gastric contents to move back into the distal esophagus.

5. Sx. of GERD develop when the lower esophageal sphincter (LES) is weak or experiences prolonged or frequent transient relaxation, conditions that allow acids and enzymes to flow into the esophagus.

6. GERD is more common in the post-prandial state; more than 60% suffer delayed gastric emptying.

7. GERD occurs in all ages.

GERD

GERD


1. The sx. vary in severity.2. The irritation of chronic reflux produces

the primary sx., pyrosis, which is heartburn. The pain is described as a substernal or retrosternal burning sensation that tends to radiate upward and may involve the neck , jaw or back.

3. The pain typically occurs 20 minutes to 2 hours after eating.

4. An atypical pain pattern that mimics angina may also occur and needs to be differentiated from true cardiac disease.

HEARTBURN

CLINICAL MANIFESTATIONS, CONT.5. The second major sx. of GERD is regurgitation.

The pt. experiences a feeling of warm fluid moving up the throat. If it reaches the pharynx, a sour taste is perceived. Water brash, a reflux salivary hyersecretion that does not have a bitter taste, occurs less commonly.

6. In severe cases, GERD can produce dysphagia or painful swallowing.

7. Eructation or flatulence are other sx.8. Nocturnal cough, wheezing, or hoarseness may

occur with GERD.9. It is estimated that > 80% of asthmatics may

have reflux.

FLATULENCE

ASSESSMENT

SUBJECTIVE: 1. Heartburn, substernal or retrosternal

burning sensation that may radiate to the back, or jaw (the pain may mimic angina).

2. Regurgitation (not associated with nausea or eructation) in which a sour or bitter taste is perceived in the pharynx.

3. Frequent eructation, flatulence, and dysphagia or trouble swallowing (usually occurs in severe cases)

OBJECTIVE: Sx. may include nocturnal cough,

wheezing, and hoarseness

DIAGNOSTIC TESTS

1. The gold standard is the 24-hour pH monitoring, which accurately records the number, duration, and severity of reflux episodes and is considered to be 85% sensitive.

2. Mild cases are diagnosed from the sx.3. The esophageal motility and Bernstein

tests can be performed in conjunction with pH monitoring to evaluate LES competence and the response of the esophagus to acid infusion.

4. Barium swallow with fluoroscopy is used to document the presence of a hiatal hernia.

5. Endoscopy is also used to observe for esophagitis, and to rule out any malignancy.

MEDICAL MANAGEMENT

1. In its simplest form, only mild sx. are produced. In these cases, avoid problem foods or beverages, stop smoking, or lose weight, if necessary.

2. Use antacids or acid-blocking meds. called H2 receptor inhibitors, such as Tagamet, Zantac, Pepcid, or Axid.

3. More severe and frequent episodes cause asthma attacks, cause severe chest pain, result in bleeding, or promote a narrowing or chronic irritation of the esophagus. In these cases, proton pump inhibitors may be prescribed.

4. Some proton pump inhibitors are: Prilosec, Nexium, Protonix, Aciphex, and Prevacid.

5. Reglan is used in moderate to severe cases of GERD. It is an example of a class of drugs called promotility agents

that increase peristalsis without stimulating secretions .

6. If nothing else works, a surgical procedure, called a fundoplication is performed to strengthen the sphincter.

FUNDOPLICATION

7. If GERD is left untreated, pathologic changes (precancerous) in the esophageal lining can occur; a condition called Barrrett’s esophagus. In Barrett’s esophagus, there is replacement of the normal squamous epithelium of the esophagus with columnar epithelium. Pts. with Barrett’s are at higher risk for adenocarcinoma, so they need to be monitored on a regular basis, (every 1-3 years), by endoscopy and bx.

BARRETT’S ESOPHAGUS


1. Educate the pt. about diet and lifestyle modifications that may alleviate the s/s of GERD.

2. What are the diet recommendations?

3. What are the lifestyle changes?

ACHALASIA

Etiology/Pathophysiology: This is also called cardiospasm. It is an

abnormal condition in which a muscle cannot relax, particularly the cardiac sphincter of the stomach.

The cause is unknown. Factors that can contribute are: nerve degeneration, esophageal dilation, and hypertrophy. These factors disrupt the normal neuromuscular activity of the esophagus. This results in decreased motility of the lower esophagus, absence of peristalsis, and dilation of the lower portion.

ACHALASIA, CONT.

So little or no food can enter the stomach. Sometimes, the dilated esophagus can hold as much as a liter or more of fluid.

This disease can occur with any age, but is more prevalent in ages 20-50 y.o.

ACHALASIA


The primary sx. is dysphagia.

As the condition progresses, the pt. complains of regurgitation of food, which relieves prolonged distention of the esophagus.

There may be some occurrence of substernal chest pain.

ASSESSMENT

The nurse observes for weight loss, poor skin turgor, and weakness.

DIAGNOSTIC TESTS

X-rays show esophageal dilation above the narrowing of the cardioesophageal junction.

The dx. is confirmed by manometry which shows the absence of primary peristalsis.

Esophagoscopy is also used.

ESOPHAGEAL MANOMETRY

MEDICAL MANAGEMENT

1. Drug therapy: anticholinergics, nitrates, and calcium channel blockers reduce pressure in the LES.

2. Forceful dilation of the narrowed of the esophagus. This is done by first emptying the esophagus. Then a dilator is passed down to the sphincter. The balloon is inflated and remains so for one minute; it may be needed to be reinflated once or twice.

BALLOON DILATION

MEDICAL MANAGEMENT, CONT.3. A cardiomyotomy is the preferred

surgical approach. In this procedure, the muscular layer is incised the long way down to the mucosa, but not through it. 2/3 of the incision is in the esophagus, and the remaining 1/3 is in the stomach. This allows the mucosa to expand so that food can pass easily into the stomach.

DIAGNOSES

1. Imbalanced nutrition; less than body requirements related to difficulty swallowing both liquids and solids.

a. Encourage fluids with meals to increase LES pressure and push food into the stomach.

b. Monitor liquid diet for 24 hours after dilation procedure.

DIAGNOSES, CONT.

2. Anxiety, related to continuous dilation process with threat of complications

a. Monitor for s/s of esophageal perforation (chest pain, shock, dyspnea, fever) after dilation.

b. Provide calm, relaxed environment (NO STRESS!!!).

c. Reinforce the PCP’s explanation of the disease process.

d. Encourage verbalization of fears; assist the pt. with identifying stressors and positive coping behaviors.

PATIENT & FAMILY TEACHING1. Explain the need for high-calorie, high-protein

diet, and provide printed material describing the same.

2. The pt. should elevate the head while sleeping, and should avoid bending and stooping.

3. Discuss the meds if prescribed; name, dosage, time of administration, purpose and side effects.

4. Discuss the methods of avoiding constipation by using high fiber foods and natural laxatives.

5. Stress follow-up care.6. Discuss the sx. of recurrence or progression

of the disease. Report to the PCP.

DISORDERS OF THE ESOPHAGUS

AchalasiaEtiology/pathophysiology

Cardiac sphincter of the stomach cannot relaxPossible causes: nerve degeneration, esophageal dilation, and hypertrophy

Clinical manifestations/assessmentDysphagiaRegurgitation of foodSubsternal chest painLoss of weight; weaknessPoor skin turgor


Achalasia (continued)Diagnostic tests

Radiologic studies; esophagoscopyMedical management/nursing interventions

Medications: anticholinergics, nitrates, and calcium channel blockers

Dilation of cardiac sphincterSurgery

Cardiomyectomy


Gastroesophageal reflux diseaseEtiology/pathophysiology

Backward flow of stomach acid into the esophagus

Clinical manifestations/assessmentHeartburn (pyrosis) 20 min – 2 hrs after eatingRegurgitationDysphagia or odynophagiaEructation


Gastroesophageal reflux disease (continued)Diagnostic tests

Esophageal motility and Bernstein testsBarium swallowEndoscopy

Medical management/nursing interventionsAntacids or acid-blocking medicationsDiet: 4-6 small meals/day, low fat, adequate protein, remain upright for 1-2 hours after eating

Lifestyle: eliminate smoking, avoid constrictive clothing, HOB up at least 6-8 inches for sleep


Gastroesophageal reflux diseaseEtiology/pathophysiology

Backward flow of stomach acid into the esophagus

Clinical manifestations/assessmentHeartburn (pyrosis) 20 min – 2 hrs after eatingRegurgitationDysphagia or odynophagiaEructation

DISORDERS OF THE STOMACH

Acute gastritisEtiology/pathophysiology

Inflammation of the lining of the stomachMay be associated with alcoholism, smoking, and stressful physical problems

Clinical manifestations/assessmentFever; headacheEpigastric pain; nausea and vomitingCoating of the tongueLoss of appetite


Acute gastritis (continued) Diagnostic tests

Stool for occult blood; WBC Serum electrolytes Elevated Hct r/t dehydration

Medical management/nursing interventions Antiemetics Antacids Antibiotics IV fluids NG tube and administration of blood, if bleeding NPO until signs and symptoms subside


Gastric ulcers and duodenal ulcers Ulcerations of the mucous membrane or deeper structures of the GI tract Most commonly occur in the stomach and duodenum Result of acid and pepsin imbalances H. pylori

Bacterium found in 70% of patients with gastric ulcers and 95% of patients with duodenal ulcers


Gastric ulcers (continued)Etiology/pathophysiologyGastric mucosa are damaged, acid is secreted, mucosa erosion occurs, and an ulcer develops

Duodenal ulcers (continued)Etiology/pathophysiologyExcessive production or release of gastrin, increased sensitivity to gastrin, or decreased ability to buffer the acid secretions


Gastric and duodenal ulcers (continued) Clinical manifestations/assessment

Pain: Dull, burning, boring, or gnawing, epigastric Dyspepsia Hematemesis Melena

Diagnostic tests Esophagogastroduodenoscopy (EGD) Breath test for H. pylori

FIGURE 5-5

Fiberoptic endoscopy of the stomach.

(From Phipps, W.J., Monahan, F.D., Sands, J.K., Marek, J.F., Neighbors, M. [2003]. Medical-surgical nursing: health and illness perspectives. [7th ed.]. St. Louis: Mosby.)


Gastric and duodenal ulcers (continued)Medical management/nursing interventions

AntacidsHistamine H2 receptor blockers Proton pump inhibitorMucosal healing agentsAntibioticsDiet: high in fat and carbohydrates; low in protein and milk products; small frequent meals; limit coffee, tobacco, alcohol, and aspirin use


Gastric and duodenal ulcers (continued) Medical management/nursing interventions

Surgery

AntrectomyGastrodudodenostomy (Billroth I)Gastrojejunostomy (Billroth II)Total gastrectomyVagotomyPyloroplasty

FIGURE 5-6

Types of gastric resections with anastomoses.

A, Billroth I. B, Billroth II.


Gastric and duodenal ulcers (continued)Complications after gastric surgery

Dumping syndromePernicious anemiaIron deficiency anemia

GASTROINTESTINAL MEDICATIONS

Antacids and Mucosal Protective Medications

Histamine H2-Receptor Antagonists

Proton Pump Inhibitors

Gastrointestinal stimulants

Antiemetics

ANTACIDS & MUCOSAL PROTECTIVES

Pepto-Bismol, Tums, Aluminum Carbonate

DescriptionReact w/ gastric to produce neutral, low acidic salts

Inactivates pepsin & enhances mucosal protection but does not coat the ulcer

Used for PUD & GERD

SUCRALFATE

CarafateCreates a protective barrier against acid and pepsin

Take on an empty stomachMay cause constipationMay impede absorption of coumadin, dilantin, digoxin and some abx, give at least 2 hours apart

MISOPROSTOL

CytotecThe only drug used to prevent gastric ulcers caused by long-term NSAID use

Suppresses secretion of gastric acidGive w/ mealsABSOLUTELY CONTRAINDICATED in pregnancy

MAGNESIUM HYDROXIDE

Rapid acting

MOM

Often causes diarrhea

Contraindicated in clients w/ intestinal obstruction, appendicitis

ALUMINUM HYDROXIDE

Slow-acting

Has considerable amounts of sodium

Use w/ caution in patients w/ hypertension and heart failure

Can reduce the effects of tetracyclines, coumadin and digoxin

CALCIUM CARBONATE

TumsRapid actingMay cause constipationDon’t give w/ milk or supplements high in Vitamin D

SODIUM BICARBONATE

NaHCO3

Rapid onset

Liberates carbon dioxide, increases intra-abdominal pressure and promotes flatulence

Use w/ caution in HTN and heart failure

HISTAMINE H2-RECEPTOR ANTAGONISTSSuppresses secretions of gastric acid

Alleviate symptoms of heartburn and assist in preventing complications of PUD

Prevent stress ulcers and reduce the recurrence of all ulcers

Promotes healing in GERD

Cimetidine (Tagamet), Ranitidine (Zantac) Famotidine (Pepcid) & Nizatidine (Axid)

PROTON PUMP INHIBITORS

Suppress gastric acid secretionUsed w/ active ulcer disease, erosive

esophagitis and pathological hypersecretory conditions

NexiumPrevacidPrilosecProtonixAciphex

GI STIMULANTS

Urecholine, Duvoid, Reglan, Ilopan, Prostigmin

Stimulates motility of the UGI tract and increases rate of gastric emptying without stimulating gastric, biliary, or pancreatic secretions

Used for GERD

Reglan can cause parkinsonian reactions

ANTIEMETICS

Vomit control!

Choice of antiemetic is determined by the cause of N/V.

Documents

DISORDERS OF THE MOUTH Common disorders of the mouth and esophagus that interfere with adequate nutrition include poor dental hygiene, infections, & inflammation