NR 602 Midterm download to score A ,(Excellent Paper)
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Nr 602
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Chamberlain College Of Nursing
NR 602 Midterm download to score A ,(Excellent Paper)
Chalazion
Chalazion is a chronic sterile inflammation of the eyelid resulting from a lipogranuloma of the meibomian glands that line the posterior margins of the eyelids (see Fig. 29-7). It is deeper in the eyelid tissue than a hordeolum a...
NR 602 Midterm
NR 602 Midterm download to score A ,(Excellent Paper)
Chalazion
Chalazion is a chronic sterile inflammation of the eyelid resulting from a lipogranuloma of the meibomian
glands that line the posterior margins of the eyelids (see Fig. 29-7). It is deeper in the eyelid tissue than a
hordeolum and may result from an internal hordeolum or retained lipid granular secretions.
Clinical Findings
Initially, mild erythema and slight swelling of the involved eyelid are seen. After a few days the inflammation resolves, and a slow growing,
round, nonpigmented, painless (key finding) mass remains. It may persist for a long time and is a commonly acquired lid lesion seen in
children (see Fig. 29-7).
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Management
• Acute lesions are treated with hot compresses.
• Refer to an ophthalmologist for surgical incision or topical intralesional corticosteroid injections if the condition is unresolved or if
the lesion causes cosmetic concerns. A chalazion can distort vision by causing astigmatism as a result of pressure on the orbit.
Complications
Recurrence is common. Fragile, vascular granulation tissue called pyogenic granuloma that enlarges and bleeds rapidly can occur if a
chalazion breaks through the conjunctival surface.
Blepharitis
Blepharitis is an acute or chronic inflammation of the eyelash follicles or meibomian sebaceous glands of the eyelids (or both). It is usually
bilateral. There may be a history of contact lens wear or physical contact with another symptomatic person. It is commonly caused by
contaminated makeup or contact lens solution. Poor hygiene, tear deficiency, rosacea, and seborrheic dermatitis of the scalp and face are also
possible etiologic factors. The ulcerative form of blepharitis is usually caused by S. aureus. Nonulcerative blepharitis is occasionally seen in
children with psoriasis, seborrhea, eczema, allergies, lice infestation, or in children with trisomy 21.
Clinical Findings
• Swelling and erythema of the eyelid margins and palpebral conjunctiva
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• Flaky, scaly debris over eyelid margins on awakening; presence of lice
• Gritty, burning feeling in eyes
• Mild bulbar conjunctival injection
• Ulcerative form: Hard scales at the base of the lashes (if the crust is removed, ulceration is seen at the hair follicles, the lashes fall out,
and an associated conjunctivitis is present)
Differential Diagnosis
Pediculosis of the eyelashes.
Management
Explain to the patient that this may be chronic or relapsing. Instructions for the patient include:
• Scrub the eyelashes and eyelids with a cotton-tipped applicator containing a weak (50%) solution of no-tears shampoo to maintain
proper hygiene and debride the scales.
• Use warm compresses for 5 to 10 minutes at a time two to four times a day and wipe away lid debris.
• At times antistaphylococcal antibiotic (e.g., erythromycin 0.5% ophthalmic ointment) is used until symptoms subside and for at least 1
week thereafter. Ointment is preferable to eye drops because of increased duration of contact with the ocular tissue. Azithromycin 1%
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ophthalmic solution for 4 weeks may also be used (Shtein, 2014).
• Treat associated seborrhea, psoriasis, eczema, or allergies as indicated.
• Remove contact lenses and wear eyeglasses for the duration of the treatment period. Sterilize or clean lenses before reinserting.
• Purchase new eye makeup; minimize use of mascara and eyeliner.
• Use artificial tears for patients with inadequate tear pools.
Chronic staphylococcal blepharitis and meibomian keratoconjunctivitis respond to oral erythromycin. Doxycycline, tetracycline, or
minocycline can be used chronically in children older than 8 years old.
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Acute Otitis Media
AOM is an acute infection of the middle ear (Fig. 30-4). The AAP Clinical Practice Guideline requires the
presence of the following three components to diagnose AOM (Lieberthal et al, 2013):
• Recent, abrupt onset of signs and symptoms of middle ear inflammation and effusion (ear pain, irritability,
otorrhea, and/or fever)
• MEE as confirmed by bulging TM, limited or absent mobility by pneumatic otoscopy, air-fluid level behind
TM, and/or otorrhea
• Signs and symptoms of middle ear inflammation as confirmed by distinct erythema of the TM or onset of ear
pain (holding, tugging, rubbing of the ear in a nonverbal manner)
Characteristics of different types of AOM are defined in Table 30-4. AOM often follows eustachian tube dys-
function (ETD). Common causes of ETD include upper respiratory infections, allergies, and ETS. ETD leads
to 746functional eustachian tube obstruction and inflammation that decreases the protective ciliary action in
the eustachian tube. When the eustachian tube is obstructed, negative pressure develops as air is absorbed in
the middle ear (see Fig. 30-4). The negative pressure pulls fluid from the mucosal lining and causes an
accumulation of sterile fluid. Bacteria pulled in from the eustachian tube lead to the accumulation of purulent
fluid. Young children have shorter, more horizontal and more flaccid eustachian tubes that are easily disrupted
by viruses, which predisposes them to AOM. Respiratory syncytial virus and influenza are two of the viruses
most responsible for the increase in the incidence of AOM seen from January to April. Other risk factors
associated with AOM are listed in Boxes 30-1 and 30-2.
S. pneumoniae, nontypeable Haemophilus influenzae, Moraxella catarrhalis, and S. pyogenes (group A
streptococci) are the most common infecting organisms in AOM (Conover, 2013). S. pneumoniaecontinues to
be the most common bacteria responsible for AOM. The strains of S. pneumoniae in the heptavalent
pneumococcal conjugate vaccine (PCV7) have virtually disappeared from the middle ear fluid of children with
AOM (Lieberthal et al, 2013). With the introduction of the 13-valent S. pneumoniae vaccine, the bacteriology of
the middle ear is likely to continue to evolve. Bullous myringitis is almost always caused by S. pneumonia.
Nontypeable H. influenza remains a common cause of AOM. It is the most common cause of bilateral otitis
media, severe inflammation of the TM, and otitis-conjunctivitis syndrome. M. catarrhalis obtained from the
nasopharynx has become increasingly more beta-lactamase positive, but the high rate of clinical resolution in
children with AOM from M. catarrhalis makes amoxicillin a good choice for initial therapy (Lieberthal et al,
2013). M. catarrhalis rarely causes invasive disease. S. pyogenes is responsible for AOM in older children, is
responsible for more TM ruptures, and is more likely to cause mastoiditis.
Although a virus is usually the initial causative factor in AOM, strict diagnostic criteria, careful specimen
handling, and sensitive microbiologic techniques have shown that the majority of AOM is caused by bacteria or
bacteria and virus together (Lieberthal et al, 2013).
Clinical Findings
History
Rapid onset of signs and symptoms:
• Ear pain with possible ear pulling in the infant; may interfere with activity and/or sleep
• Irritability in an infant or toddler
• Otorrhea
• Fever
Other key factors or symptoms:
• Prematurity
• Craniofacial anomalies or congenital syndromes associated with craniofacial anomalies
• Exposure to risk factors
• Disrupted sleep or inability to sleep
• Lethargy, dizziness, tinnitus, and unsteady gait
• Diarrhea and vomiting
• Sudden hearing loss
• Stuffy nose, rhinorrhea, and sneezing
• Rare facial palsy and ataxia
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Physical Examination
• Presence of MEE, confirmed by pneumatic otoscopy, tympanometry, or acoustic reflectometry, as evidenced by:
• Bulging TM (see Fig. 30-4)
• Decreased translucency of TM
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