GI oral and esophagus disorders

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Last updated 12:45 PM on 4/12/26
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89 Terms

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Decay

Erosive process driven by bacteria and carbohydrates

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Acid

Bacteria + Fermentable Carbs =

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Dental plaque, acid exposure, acid strength, tooth susceptibility

Factors influencing dental damage

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Decay in enamel → dentin → pulp

Stages of tooth decay

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Fluoride varnish/gel applications

Professional primary prevention and control

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Water fluoridation and fluoride toothpaste

Community and home care for dental plaque and caries

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Smoking cessation and limiting alcohol

Lifestyle modification for dental plaque and caries

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Mechanical cleansing

Brushing and flossing

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Nursing responsibilities of dental plaque and caries

  • soft-bristled brushes > foam sticks or sponges

  • Gauze wipe w/antiseptic rinse

  • Water-soluble gel

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Cariogenic alternatives

Dietary modifications for dental plaque and caries

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Pit and fissure sealants

Coating is applied to seal deep grooves of primary and permanent molars that are prone to decay, last 36 to 48 months.

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Cheilosis (Angular Stomatitis)

Erythema and fissuring (bleed or develop yellowish crust), maceration, crusting and bleeding

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Vitamin B2 (Riboflavin), B12, Iron, or Folate

Nutritional deficiencies as causes of cheilosis

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Ill-fitting dentures

Mechanical cause of cheilosis

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Candida albicans (fungal) or Staph aureus (bacterial)

Infection fungal and bacterial causes of cheilosis

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Intake of Vitamin B rich foods - leafy greens, lean meats, dairy

Dentist - for ill-fitting dentures

Nursing Considerations of cheilosis (angular stomatitis)

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Actinic Cheilitis

  • irritation of lips associated with scaling, crusting, fissure

  • White hyperkeratosis

  • Considered premalignant squamous cell skin cancer

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White hyperkeratosis

Overgrowth of horny layer of epidermis

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Exposure to sun and chronic inflammatory lesion (leads to squamous cell cancer)

Causes of actinic cheilitis

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  • Sun block lips

  • Periodic checkup

Nursing considerations of actinic cheilitis

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Aphthous Stomatitis (canker sore)

  • shallow ulcer with a white or yellow center and typically a well-defined red border

  • Inner side of the lip, cheek, tongue

  • Burning or tingling sensation and slight swelling and painful

  • Lasts 7-10 days (minor) and heals without a scar

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  • HIV infection - immune-mediated inflammatory disorder

  • Emotional or mental stress, fatigue, hormonal factors, minor trauma (biting), allergies, acidic foods/juices, and dietary deficiencies

  • May recur

Causes of Aphthous stomatitis

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  • comfort measures (saline rinses) and soft/bland diet

  • Antibiotics or corticosteroids

  • OTC benzocaine

Nursing considerations of aphthous stomatitis

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Herpes Simplex virus-1 (cold sore or fever blister)

  • Symptoms may be delayed up to 20 days after exposure

  • Singular or clustered, irregular, painful vesicles throughout the oral cavity and lips that may rupture

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Opportunistic infection, immunocompromised patients, recur w/menstruation, fever, or sun exposure

Causes of herpes simplex virus-1 (cold sore or fever blister)

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  • acyclovir ointment

  • Analgesic agents

  • Avoid irritating foods

Nursing considerations of herpes simplex virus-1 (cold sore or fever blister)

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Candidiasis (moniliasis/thrush)

  • cheesy white plaque that looks like milk curds

  • Erythematous and often bleeding base (when rubbed off)

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  • Candida albicans (fungus)

  • Diabetes, antibiotic therapy, immunosuppression

Causes of candidiasis

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Antifungal medications - nystatin or clotrimazole

Swish vigorously - 1 min and then swallow

Oral agents - fluconazole

Nursing considerations of candidiasis

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Vincent’s Angina

  • trench mouth or acute necrotizing ulcerative gingivitis

  • Sudden onset, punched-out ulcers, grayish pseudomembrane

  • Halitosis

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Fusospirochetal

Primary pathogens of vincent’s angina

Mixture of Borrelia vincentii and Fusobacterium

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High emotional stress, poor oral hygiene and smoking, nutritional deficiencies

Risk factors of vincent’s angina

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Periodontal destruction and noma (cancrum oris)

Complications of Vincent’s angina

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Oral debridement, pain management, infection control, hygiene education, stress reduction

Nursing management of vincent’s angina

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Saliadenitis

Inflammation of the salivary glands

Pain, swelling, purulent discharge

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Dehydration, radiation therapy, stress, malnutrition, salivary gland calculi (stones, sialolithiasis), improper oral hygiene

Causes of sialadenitis

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S. aureus (most common) and methicillin resistant S. aureus

Pathogens of sialadenitis

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Massage, hydration, warm compress, sialagogues

Massage of sialadenitis

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Chronic Sialadenitis

Due to decreased salivary flow

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Sialendscopy; instillation of antibiotics, corticosteroids; irrigation

Management of chronic sialadenitis

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Surgical drainage and excision of the gland and duct

For recurrent sialadenitis or refractory to antibiotics

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Achalasia

Absent or ineffective peristalsis of the distal esophagus + failure of the esophageal sphincter (LES) to relax

Regurgitation, noncardiac chest/epigastric pain, pyrosis

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Dysphagia

Hallmark sign of achalasia

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  • X-ray studies

  • Barium swallow

  • CT scan of the chest

  • Endoscopy

Assessment and diagnostic of achalasia

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Bird’s beak deformity

X-ray finding of achalasia

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High resolution manometry

Confirmatory test of achalasia

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Lifestyle

Botulinum Toxin (Botox) injection

Pneumatic Dilation

Heller myotomy

Per-oral endoscopic myotomy

Medical and surgical management of achalasia

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Gastroesophageal Reflux Disease

a common disorder marked by the backflow (reflux) of gastric or duodenal contents into the esophagus

  • Pyrosis (heartburn), regurgitation, dyspepsia, dysphagia, odynophagia, hypersalivation.

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  • Incompetent lower esophageal sphincter

  • Pyloric stenosis or motility disorders

  • Hiatal hernia

Causes of excessive reflux

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  • Incidence increases with aging.

  • Linked to tobacco use, coffee drinking, alcohol

consumption, and H. pylori infection.

  • IBS and obstructive

airway disorders (Asthma, COPD, Cystic

Fibrosis)

Associations and risk factors

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Ambulatory pH monitoring

Gold standard of GERD

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Proton Pump Inhibitors Trial

To see if GERD symptoms resolve

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Endoscopy/Barium Swallow

Evaluate mucosal damage, strictures, hernias for GERD

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Nissen Fundoplication Surgery

Surgical intervention of GERD

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Antacids

Neutralizes existing stomach acid

  • C. Difficile

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Calcium carbonate, magnesium hydroxide, alginate

Examples of antacids

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H2 Receptor Antagonists

Decreases gastric acid production

  • Monitor for QT-prolongation in patients with kidney injury. Dilute IV doses and administer over at least 2 mins

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Famotidine, cimetidine

Key examples of H2 Receptor antagonists

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Proton Pump Inhibitors (PPIs)

Decreases gastric acid production (First-line)

  • may increase risk of hip fractures. Interferes with Vitamin B12, Iron, Magnesium absorption

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Pantoprazole, omeprazole, esomeprazole

Examples of proton pump inhibitors

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Prokinetic agents

Accelerates gastric emptying

  • Tardive dyskinesia - involuntary movements

  • Short term us

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Metclopramide

Example of prokinetic agents

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Surface agents

Preserves and protects the mucosal barrier

  • give on an empty stomach (1 hr before or 2 hrs after meals).

  • Separate from antacids by 30 mins

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Sucralfate

Examples of surface agent

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Reflux inhibitors

  • stimulates the parasympathetic system

  • Do not use with GI obstruction or peptic ulcers

  • Urinary retention - primary use

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Bethanechol chloride

Example of reflux inhibitors

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TLESR inhibitors

Reduces transient LES relaxations

  • used primarily when PPI therapy fails. It is a GABA-B agonist

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Baclofen

Example of TLESR inhibitors

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Esophageal Diverticulum

Out-pouching of mucosa and submucosa that protrudes through a weak portion of the musculature of the esophagus

  • dysphagia, fullness in neck, belching, regurgitation of undigested food, gurgling noises after eating, halitosis

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Pharngoesophageal

Upper esophageal diverticulum

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Midesophageal

Middle esophageal diverticulum

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Epiphrenic

Lower esophageal diverticulum

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Zenker Diverticulum

Most common type of esophageal diverticulum, located in the pharyngoesophageal area, pulsion diverticulum

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Midesophageal diverticula

  • Uncommon

  • Symptoms are less acute

  • Condition does not require surgery

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Epiphrenic diverticula

  • Larger diverticula in the lower esophagus just above the diaphragm

  • Related to improper functioning of the lower esophageal sphincter or to motor disorders of the esophagus

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Intramural diverticulosis

Occurrence of numerous small diverticula associated with a stricture in the upper esophagus

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Epiphrenic diverticula

  • Larger diverticula in the lower esophagus just above the diaphragm

  • Related to improper functioning of the lower esophageal sphincter or to motor disorders of the esophagus

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Intramural diverticulosis

  • occurrence of numerous small diverticula associated with a stricture in the upper esophagus

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Barium swallow, manometric studies, esophagoscopy

Assessment and diagnostic findings of esophageal diverticulum

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Endoscopic septotomy, POEM, myotomy of cricopharyngeal muscle

Management of esophageal diverticulum

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Evidence of leakage from esophagus and developing fistula, foods/fluids withheld until x-ray studies show no leakage at the surgical site, begin with liquid and progress as tolerated

Nursing management of esophageal diverticulum

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Hiatal Hernia

  • opening in the diaphragm through which the esophagus passes becomes enlarged, and part of the upper stomach moves up into the lower portion of the thorax

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Sliding esophageal hernia

The upper stomach and gastroesophageal junction have moved upward and slide in and out of the thorax

  • pyrosis, regurgitation, dysphagia, intermittent epigastric pain or fullness after eating, large hiatal hernias: associated with GERD

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Paraesophageal hernia

All or part of the stomach pushes through the diaphragm next to the gastroesophageal junction

  • hemorrhage, obstruction, volvulus, strangulation

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X-ray studies, barium swallow, esophagogastroduodenoscopy (EGD), esophageal manometry, chest CT scan

Assessment and diagnostic findings of hiatal hernias

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Small frequent feedings, patient advised not to recline after 1 hour after eating, elevate head of bed on 4- to 8- inch (10-20 cm)

  • manage nausea and vomiting

  • Diet starts liquids to solids

  • Tracking nutritional intake

  • Monitor weight

  • WOF: bleching, vomiting, gagging, abdominal distention, epigastric chest pain

Management of hiatal hernias

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Esophageal Varices

Result from portal hypertension, typically due to liver cirrhosis, where obstruction of blood flow through the liver causes pressure to build in the portal venous system.

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Upper endoscopy

Gold standard for esophageal varices and to directly visualize, grade, and treat dilated veins in the esophagus

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  • Acute bleeding management: IV fluids, blood transfusion, IV octreotide, endoscopic variceal band ligation, prophylactic antibiotics (Ceftriaxone), TIPSS Procedure

  • Prophylaxis - non selective beta blockers (nadolol or propranolol)

Management of esophageal varices