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Decay
Erosive process driven by bacteria and carbohydrates
Acid
Bacteria + Fermentable Carbs =
Dental plaque, acid exposure, acid strength, tooth susceptibility
Factors influencing dental damage
Decay in enamel → dentin → pulp
Stages of tooth decay
Fluoride varnish/gel applications
Professional primary prevention and control
Water fluoridation and fluoride toothpaste
Community and home care for dental plaque and caries
Smoking cessation and limiting alcohol
Lifestyle modification for dental plaque and caries
Mechanical cleansing
Brushing and flossing
Nursing responsibilities of dental plaque and caries
soft-bristled brushes > foam sticks or sponges
Gauze wipe w/antiseptic rinse
Water-soluble gel
Cariogenic alternatives
Dietary modifications for dental plaque and caries
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.
Cheilosis (Angular Stomatitis)
Erythema and fissuring (bleed or develop yellowish crust), maceration, crusting and bleeding
Vitamin B2 (Riboflavin), B12, Iron, or Folate
Nutritional deficiencies as causes of cheilosis
Ill-fitting dentures
Mechanical cause of cheilosis
Candida albicans (fungal) or Staph aureus (bacterial)
Infection fungal and bacterial causes of cheilosis
Intake of Vitamin B rich foods - leafy greens, lean meats, dairy
Dentist - for ill-fitting dentures
Nursing Considerations of cheilosis (angular stomatitis)
Actinic Cheilitis
irritation of lips associated with scaling, crusting, fissure
White hyperkeratosis
Considered premalignant squamous cell skin cancer
White hyperkeratosis
Overgrowth of horny layer of epidermis
Exposure to sun and chronic inflammatory lesion (leads to squamous cell cancer)
Causes of actinic cheilitis
Sun block lips
Periodic checkup
Nursing considerations of actinic cheilitis
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
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
comfort measures (saline rinses) and soft/bland diet
Antibiotics or corticosteroids
OTC benzocaine
Nursing considerations of aphthous stomatitis
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
Opportunistic infection, immunocompromised patients, recur w/menstruation, fever, or sun exposure
Causes of herpes simplex virus-1 (cold sore or fever blister)
acyclovir ointment
Analgesic agents
Avoid irritating foods
Nursing considerations of herpes simplex virus-1 (cold sore or fever blister)
Candidiasis (moniliasis/thrush)
cheesy white plaque that looks like milk curds
Erythematous and often bleeding base (when rubbed off)
Candida albicans (fungus)
Diabetes, antibiotic therapy, immunosuppression
Causes of candidiasis
Antifungal medications - nystatin or clotrimazole
Swish vigorously - 1 min and then swallow
Oral agents - fluconazole
Nursing considerations of candidiasis
Vincent’s Angina
trench mouth or acute necrotizing ulcerative gingivitis
Sudden onset, punched-out ulcers, grayish pseudomembrane
Halitosis
Fusospirochetal
Primary pathogens of vincent’s angina
Mixture of Borrelia vincentii and Fusobacterium
High emotional stress, poor oral hygiene and smoking, nutritional deficiencies
Risk factors of vincent’s angina
Periodontal destruction and noma (cancrum oris)
Complications of Vincent’s angina
Oral debridement, pain management, infection control, hygiene education, stress reduction
Nursing management of vincent’s angina
Saliadenitis
Inflammation of the salivary glands
Pain, swelling, purulent discharge
Dehydration, radiation therapy, stress, malnutrition, salivary gland calculi (stones, sialolithiasis), improper oral hygiene
Causes of sialadenitis
S. aureus (most common) and methicillin resistant S. aureus
Pathogens of sialadenitis
Massage, hydration, warm compress, sialagogues
Massage of sialadenitis
Chronic Sialadenitis
Due to decreased salivary flow
Sialendscopy; instillation of antibiotics, corticosteroids; irrigation
Management of chronic sialadenitis
Surgical drainage and excision of the gland and duct
For recurrent sialadenitis or refractory to antibiotics
Achalasia
Absent or ineffective peristalsis of the distal esophagus + failure of the esophageal sphincter (LES) to relax
Regurgitation, noncardiac chest/epigastric pain, pyrosis
Dysphagia
Hallmark sign of achalasia
X-ray studies
Barium swallow
CT scan of the chest
Endoscopy
Assessment and diagnostic of achalasia
Bird’s beak deformity
X-ray finding of achalasia
High resolution manometry
Confirmatory test of achalasia
Lifestyle
Botulinum Toxin (Botox) injection
Pneumatic Dilation
Heller myotomy
Per-oral endoscopic myotomy
Medical and surgical management of achalasia
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.
Incompetent lower esophageal sphincter
Pyloric stenosis or motility disorders
Hiatal hernia
Causes of excessive reflux
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
Ambulatory pH monitoring
Gold standard of GERD
Proton Pump Inhibitors Trial
To see if GERD symptoms resolve
Endoscopy/Barium Swallow
Evaluate mucosal damage, strictures, hernias for GERD
Nissen Fundoplication Surgery
Surgical intervention of GERD
Antacids
Neutralizes existing stomach acid
C. Difficile
Calcium carbonate, magnesium hydroxide, alginate
Examples of antacids
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
Famotidine, cimetidine
Key examples of H2 Receptor antagonists
Proton Pump Inhibitors (PPIs)
Decreases gastric acid production (First-line)
may increase risk of hip fractures. Interferes with Vitamin B12, Iron, Magnesium absorption
Pantoprazole, omeprazole, esomeprazole
Examples of proton pump inhibitors
Prokinetic agents
Accelerates gastric emptying
Tardive dyskinesia - involuntary movements
Short term us
Metclopramide
Example of prokinetic agents
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
Sucralfate
Examples of surface agent
Reflux inhibitors
stimulates the parasympathetic system
Do not use with GI obstruction or peptic ulcers
Urinary retention - primary use
Bethanechol chloride
Example of reflux inhibitors
TLESR inhibitors
Reduces transient LES relaxations
used primarily when PPI therapy fails. It is a GABA-B agonist
Baclofen
Example of TLESR inhibitors
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
Pharngoesophageal
Upper esophageal diverticulum
Midesophageal
Middle esophageal diverticulum
Epiphrenic
Lower esophageal diverticulum
Zenker Diverticulum
Most common type of esophageal diverticulum, located in the pharyngoesophageal area, pulsion diverticulum
Midesophageal diverticula
Uncommon
Symptoms are less acute
Condition does not require surgery
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
Intramural diverticulosis
Occurrence of numerous small diverticula associated with a stricture in the upper esophagus
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
Intramural diverticulosis
occurrence of numerous small diverticula associated with a stricture in the upper esophagus
Barium swallow, manometric studies, esophagoscopy
Assessment and diagnostic findings of esophageal diverticulum
Endoscopic septotomy, POEM, myotomy of cricopharyngeal muscle
Management of esophageal diverticulum
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
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
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
Paraesophageal hernia
All or part of the stomach pushes through the diaphragm next to the gastroesophageal junction
hemorrhage, obstruction, volvulus, strangulation
X-ray studies, barium swallow, esophagogastroduodenoscopy (EGD), esophageal manometry, chest CT scan
Assessment and diagnostic findings of hiatal hernias
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
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.
Upper endoscopy
Gold standard for esophageal varices and to directly visualize, grade, and treat dilated veins in the esophagus
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