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7MO SEMESTRE > OTORRINO PRIMER PARCIAL > Flashcards

OTORRINO PRIMER PARCIAL Flashcards

1
Q

Most common cancer of the external ear

A

Basal cell carcinoma

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2
Q

Congenital anomalies of the external ear

MICROTIA: características

A

Patients typically present at birth with obvious auricular malformations. The patient course with conductive hearing loss

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3
Q

Grade I microtia

A

-mild deformity
-All major structures of the external ear are present to some degree.
-slightly dysmorphic helix and antihelix
-low-set ears, lop ears, cupped ears

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4
Q

Grade II microtia

A

-atypical microtia
-auricular framework is present
-tissue deficiency and significant deformity exist
-mini-ear, conchal bowl, and cup ear deformities

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5
Q

Grade III microtia

A

-classic microtia or “peanut ear”
-few or no recognizable landmarks of the auricle

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6
Q

Grade IV microtia or anotia

A

-complete absence of the external ear

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7
Q

Associated symptoms of microtia

A

-OAV spectrum (Goldenhar)
-Branchio-oto-renal
-Treacher collins
-Townes-brocks
-Robinow

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8
Q

Treatment of microtia grade I

A

-only observation (auditory brainstem response, CT scan)

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9
Q

Treatment of microtia

A

-Observation
-Prosthetic management (best one)
-Single-stage reconstruction with implant
-Staged autologous costochondral reconstruction (4 stages or 6 stages)

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10
Q

Congenital anomalies of the EAC range from mild stenosis to complete atresia

A

-90% of patients within the microtia spectrum have conductive hearing loss on the affected side
- The typical pattern of hearing loss in atretic ears is a conductive hearing loss of 50 to 70 dB

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11
Q

Protruding ears (prominauris)

A

-Really big ears
-Helical rim to mastoid abnormality
-Protruding ears don’t cause any functional problems such as hearing loss

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12
Q

Protruding ears (prominauris) are due to ..

A
  • lack of antihelical fold –> most common.
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13
Q

Protruding ears treatment and complications

A

-Otoplasty (where we cut the conchal bowl)

**complications: Excessive overcorrection of the middle third of the ear should be avoided to prevent development of the “telephone ear” deformity

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14
Q

EMPIEZA: EXTERNAL EAR TRAUMA

Auricular hematoma

-ESSENTIALS OF DX

A

-accumulation of blood in the subperichondrial space, usually secondary to blunt trauma.

-History of auricular trauma.
-Edematous, fluctuant, and ecchymotic pinna with loss of normal cartilaginous landmarks.
- Early diagnosis and treatment is necessary to minimize cosmetic deformity.

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15
Q

Clinical findings in auricular hematoma

A

dematous, fluctuant, and ecchymotic pinna, with loss of the normal cartilaginous landmarks.

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16
Q

Complications of auricular hematoma

A

-if you don’t drain it it can lead to necrosis (this is a medical emergency)

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17
Q

Treatment of auricular hematoma

A

-Best way to treat this: incision and drain the blood using splints (cotton/ferula) to avoid the new formation of an hematoma and suture
-Quinolone (frequently suggested after evacuation of hematoma) (ciprofloxacin) VO

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18
Q

Auricular laceration management

A

-cleaned and debrided prior to repair
-expeditious repair
-prevention of infection (quinolone) ciprofloxacin
-second reconstruction (if resultant defects are not satisfactory)

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19
Q

Best option in auricular laceration

A

Microvascular replantation ( is considered the best option but is challenging due to the size of the vasculature)

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20
Q

Auricular burns can be classified in

A

-1st degree
-2nd degree
-3rd degree
-4th degree

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21
Q

1st degree auricular burns

A

SUPERFICIAL AURICULAR BURNS (superficial layer of epidermis)
-Erythema and pain (moderate)

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22
Q

2nd degree auricular burns

A

PARTIAL-THICKNESS BURNS (epidermis and extension to dermis)
→ VERY
PAINFUL

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23
Q

3rd degree auricular burns

A

FULL THICKNESS OF THERMIS (epidermis & dermis)
-painless gray/black and charred (tejido muerto)

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24
Q

4th degree auricular burns

A

Subcutaneous tissue, fat, muscle, tendon, cartilage, bone
-painless gray/black and charred (tejido muerto)

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25
Q

Treatment of 1st degree auricular burn

A
  • Moisturizing creams or Silver Sulfadiazine (antimicrobiano tópico para quemaduras)
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26
Q

Treatment of 2nd degree auricular burn

A

-Blister debridement and Antibiotic ointment
◆ Silver-based dressings, silicone coated nylon, and biosynthetic dressings → Better outcomes than silver sulfadiazine.

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27
Q

Mafenide acetate is another topical agent that helps:

A

reduce chondritis

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28
Q

Treatment of 3rd and 4th degree auricular burn

A
  • both topical and systemic cartilage­ penetrating antibiotics

Debridement and clouruse with skin grafts (injertos de piel) or vascularized tissue

Debridement: the removal of damaged tissue or foreign objects from a wound

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29
Q

Otitis externa is mostly caused by

A

pseudomona aeruginosa and secondly by staphylococcus aureus.

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30
Q

Otitis externa is suggested by the presence of:

A

-otalgia (dolor de oído)
-Otorrhea (secreción patológica)
-Pruritus
-Hearing loss
-History of water exposure or local trauma
-Oclussion of EAC (SEVERE CASES) edema occludes ear canal –> WICK

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31
Q

BEST ADVICE for otitis externa

A

AVOID CONTACT WITH WATER

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32
Q

Factors to have otitis externa

A

-Humidity
-Maceration
-Heat
-Absence of cerumen
-Alkaline pH (Loss of acidity has been shown to be proportionate to the degree of infection)
-Chronic > 3 moths (Incomplete resolution or persistent inflammation for more than 3 months refers to the chronic inflammatory stage)

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33
Q

Treatment of otitis externa

A

-Debridement of EAC with binocular microscopy
-Analgesia (nonsteroidal anti­ inflammatory drugs (NSAIDs), opioids, or topical steroid preparations)

***After cleansing is complete, otic drop preparations that are antiseptic, acidifying, or antibiotic (or any combination of these) should be used —> BEST TREATMENT PREGUNTA DE EXAMEN

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34
Q

VOLVER A PREGUNTA 13 (SIGUE SIENDO DEL TEMA “Congenital anomalies of the external ear”)

A

First branchial cleft anomalies

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35
Q

FIRST BRANCHIAL CLEFT ANOMALIES

A

Branchial cleft anomalies are relatively common neck masses, first branchial cleft anomalies alone involve the external ear.

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36
Q

FIRST BRANCHIAL CLEFT ANOMALIES ARE ASSOCIATED WITH:

A

infection and present with pain and swelling in the preauricular and cervical regions

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37
Q

What makes management challenging in FIRST BRANCHIAL CLEFT ANOMALIES?

A

Their intimate proximity to the facial nerve

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38
Q

Clinical findings in FIRST BRANCHIAL CLEFT ANOMALIES:

A

the patient may have a history of recurrent infection, swelling, or drainage (purulent discharge) from the ear or neck along the anterior border of the sternocleidomastoid

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39
Q

PATHOGENESIS OF FIRST BRANCHIAL CLEFT ANOMALIES:

A

Error in the fusion 1st and 2nd branchial arches, with
incomplete obliteration of first branchial cleft (BCA).

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40
Q

The Work classification system has been used to describe first branchial cleft cysts.

A

○ Type 1 anomaly duplicates the membranous EAC only and presents as a preauricular mass or sinus, lateral to the facial nerve, that parallels the EAC and terminates in the EAC or middle ear.
○ Type 2 anomaly is more common and duplicates both the membranous and cartilaginous EAC.

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41
Q

Tx of FIRST BRANCHIAL CLEFT ANOMALIES:

A

complete excision!!

Incomplete excision, or incision and drainage alone, predisposes the patient to recurrence and re­infection

We only take them to surgery if the infection is recurrent

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42
Q

VOLVER A PREGUNTA 33 Y SIGUE CON OTITIS EXTERNA

A

-

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43
Q

Incomplete resolution or persistent inflammation for more than____ refers to the chronic inflammatory stage.

A

3 MONTHS

44
Q

TRAGUS SIGN IN OTITIS EXTERNA:

A

We press the tragus and the patient has too much pain

45
Q

OTOMYCOSIS

A

-

46
Q

OTOMYCOSIS: ESSENTIALS OF DIAGNOSIS

A

-Pruritus, otalgia, otorrhea, fullness, hearing loss, and no response to topical antibiotics.
-Fungal elements on physical examination.
-Positive potassium hydroxide (KOH) preparation or fungal culture.

47
Q

OTOMYCOSIS

In 80% of cases, the etiologic agent is:

A

Aspergillus, whereas Candida is the next most frequently isolated pathogen

48
Q

Otomycosis has similar predisposing factors to bacterial otitis externa.

**Patients with _______ are particularly susceptible to otomycosis

A

diabetes mellitus or an immunocompromised state

**mastoid bowl after a canal wall­down procedure are also predisposed

AVOID WATER EXPOSURE

49
Q

OTOMYCOSIS

CLINICAL FINDINGS

A

pruritus, aural fullness (sensation of blockage in the ear), and otorrhea, and may also complain of otalgia and hearing loss.

50
Q

The hearing loss associated with otomycosis usually results from:

A

accumulation of mycotic debris

51
Q

Otoscopy often reveals ___, TO ESTABLISH TE DIAGNOSIS OF OTOMYCOSIS

A

mycelia

○ Erythema.
○ Fungal debris may appear withe, gray or black.

52
Q

TREATMENT OF OTOMYCOSIS

A

cleansing and debriding the EAC, acidifying the canal, and administering antifungal agents

*Nonspecific antifungal agents include thimerosal (eg, Merthiolate) and gentian violet

*specific antifungals include clotrimazole, nystatin (otic drops or powder), and ketoconazole ( EBERCONAZOL - únicas
gotas antifúngicas que hay en México. No se utiliza en membrana perforada por su
alta toxicidad.)

53
Q

Por qué no se utiliza el eberconazol en la membrana perforada?

A

por su alta toxicidad

54
Q

SKULL BASE OSTEOMYELITIS

A

MOE/NOE

“Malignant or Necrotizing Otitis Externa”

55
Q

SKULL BASE OSTEOMYELITIS
is caused by:

A

bacterial infection of the EAC and skull base

56
Q

SKULL BASE OSTEOMYELITIS

ESSENTIALS OF DIAGNOSIS

A

Immunosuppressed (mostly elderly diabetic) patients with intense otalgia, otorrhea, hearing loss, fullness, and pruritus.

57
Q

It begins as an ____ that progresses to involve the temporal bone, and may progress to fatal meningitis, sepsis, and death if unrecognized or untreated.

A

external otitis

58
Q

The most frequently isolated causative organism is____ (90% of cases)

A

P aeruginosa

high levels of antibiotic resistance

59
Q

SKULL BASE OSTEOMYELITIS

Signs and Symptoms

A

-intense long­standing otalgia, often worse at night,
-otorrhea (for months)
-aural fullness,
-pruritus, and
-hearing loss

*** As the disease advances to involve the temporal bone, granulation tissue is seen on the floor of the EAC at the osseocartilaginous junction and is pathognomonic.

60
Q

Pathogenesis of MOE

A

commonly begins in the soft tissues of the EAC and progresses to cellulitis, chondritis, osteitis, and, ultimately, osteomyelitis. NOE disseminates through Haversian canals, fissures of Santorini, foramina, and vascularized spaces of the skull base

61
Q

Pathognomonic in otoscopy:

A

granulation tissue

62
Q

what is found in advanced stages?

A

Edema and erythema of the EAC, granulation tissue at the bony­cartilaginous junction, cranial neuropathies –> facial palsy

63
Q

Diagnostic tests in MOE

A

-Erythrocyte sedimentation rate (ESR) or C­reactive protein (CRP) are commonly elevated.
-CT and MRI are useful in the initial evaluation to determine the extent of disease, with CT particularly useful for identifying bony changes, whereas MRI is more useful for identifying soft­tissue changes and intracranial abnormalities.
-Cultures and sensitivity for selecting antibiotics.

64
Q

Gallium scans are used to:

A

track the resolution, because they track leukocytes and show areas of inflammatory cell activity that resolve quickly with resolution of the infection (

65
Q

DIFERENCIAL DIAGNOSIS OF MOE

A

● Carcinoma of the EAC
● Chronic granulomatous disease
● Paget disease (in both the bones is affected).
● Fibrous dysplasia
● Nasopharyngeal carcinoma

66
Q

TX OF MOE, first line treatment:

A

Long­term parenteral antibiotics, often 6 weeks in duration

(Aminoglycosides (eg, tobramycin) and antipseudomonal β­lactam antibiotics, including piperacillin­tazobactam, cefepime, or ceftazidime, are often used)

  • cultures should be obtained to guide appropriate therapy
67
Q

Surgical debridement in MOE

A

To remove nonviable bone or to help abort rapidly progressive infection, but efficacy has not been critically evaluated.

68
Q

OTITIS MEDIA

A
  • Acute otitis media and chronic otitis media with effusion
69
Q

OM refers to an inflammatory process localized:

A

to the middle ear cleft

70
Q

AOM is characterized by a rapid onset of signs and symptoms, such as :

A

pyrexia and otalgia, secondary to inflammation of the middle ear

71
Q

OM is mainly considered a ____ medical problem

A

pediatric

72
Q

acute middle ear inflammation secondary to an infectious process.

A

AOM

73
Q

Recurrent AOM is defined as ≥ ___ episodes in a 6­month period or ≥ ___ episodes in a 12­month period with complete resolution of symptoms between episodes.

A

3

4

74
Q

inflammation of the middle ear space with the presence of effusion

A

OME

75
Q

acute symptoms of infection are absent

A

OME

76
Q

OME is the presence of effusion for ≥ ___ months.

A

3

77
Q

Eustachian tube dysfunction is the most important factor in development of ___

A

OM

78
Q

The most common bacterial pathogens that cause AOM are

A

streptococcus pneumonia, Haemophilus influenzae, and Moraxella catarrhalis.

79
Q

Pathogenesis of OM is multifactorial and depends on host factors including anatomy and intrinsic factors such as age, allergic tendency, or genetic predisposition; infectious factors; and environmental factors, true or false?

A

true

80
Q

the eustachian tube plays a role in mucociliary clearance of the middle ear space and protects the middle ear from entrance of nasopharyngeal contents, how is the eustachian tube in infants?

A

shorter, wider and more horizontal

81
Q

Risk factors for AOM and subsequent OME include:

A

family history of AOM, day care attendance, immunodeficiency, parental smoking, absence of breastfeeding, craniofacial anomalies, adenoid hypertrophy, and allergic rhinitis

82
Q

Manifestations of AOM:

A

otalgia, pyrexia, thickened or bulging tympanic membrane, hearing loss, otorrhea, decreased appetite, upper respiratory infection, and fatigue

83
Q

Manifestations of OME

A

persistent conductive hearing loss, dull or immobile tympanic membrane, and flat tympanogram

*

84
Q

Formal diagnosis of AOM or OME must include:

A

direct visualization of the tympanic membrane (TM) using an otoscope or pneumatic otoscope in conjunction with history.

Use the mnemonic “COMPLETES”

85
Q

history and physical exam are sufficient for AOM diagnosis, true or false

A

true

86
Q

Otoscopy in AOM classically demonstrates :

A

a thickened, hyperemic, immobile TM

87
Q

Patients with OME are often asymptomatic or may present with decreased hearing. Otoscopy classically demonstrates:

A

dull gray­tinged or yellow­tinged, immobile TM. If the TM is clear, bubbles or air fluid levels can be elucidated

88
Q

complementary diagnostic tools used in evaluating patients with OME:

A

Tympanometry and audiometry

89
Q

OME Tympanometry

A

Type B (indicating fluid in the middle ear space)

90
Q

OME often presents with varying degrees of hearing loss. An age­-appropriate hearing test should be performed if:

A

OME is present for ≥ 3 months or for at­risk children (eg, children with speech/language delay, developmental disability, trisomy 21, or craniofacial abnormalities).

91
Q

Conductive hearing loss is most often documented in children with OME and should be reevaluated in ___ intervals until the effusion and hearing loss have resolved.

A

3 month to 6 month

92
Q

Current recommendations are to initiate antibiotic therapy in patients ≥ 6 months with:

A

unilateral AOM and severe symptoms (ie, otorrhea, severe otalgia, or temperature ≥ 39°C), or for patients < 24 months with bilateral AOM regardless of symptom severity

93
Q

first­line antibiotic treatment for AOM.:

A

High­dose amoxicillin with additional coverage if the patient has received amoxicillin in the past 30 days or has concurrent purulent conjunctivitis.

● + Decongestants
● + Vasoconstrictors.
(not recommended in new guides)

94
Q

In nonsevere AOM, close observation is appropriate with initiation of antibiotics in ____ hours if the patient fails to improve or worsens

A

48 to 72

95
Q

There is little role for medical therapy in the treatment of OME. The most recent guidelines from the American Academy of Otolaryngology (2016) recommend :

A

AGAINST the use of antibiotics in the treatment of OME

96
Q

AOM largely resolves spontaneously or responds to medical management, true or false:

A

true

97
Q

tympanostomy tube placement is reserved in the acute setting for patients who:

A

develop complications of AOM.

98
Q

The mainstay of treatment for chronic OME is:

A

surgical intervention with tympanostomy tubes

99
Q

purpose of surgical intervention:

A

is to provide ventilation of the middle ear space and prevent onset of serious OME sequelae, including conductive hearing loss and delayed speech/language development in the pediatric population

100
Q

Surgery for OME is recommended for patients with:

A

persistent middle ear effusion for ≥ 3 months and hearing loss or in at­risk patients (ie, trisomy 21 or craniofacial abnormalities)

101
Q

Recommendation for adenoidectomy in management of OME:

A

adenoidectomy is not recommended for patients < 4 years old unless there is a distinct indication such as chronic adenoiditis or nasal obstruction from adenoid hypertrophy. In children ≥ 4 years old, options for surgical management include tympanostomy tubes alone, adenoidectomy alone, or both procedures concurrently

102
Q

COMPLICATIONS OF AOM

A

Acute mastoiditis is a severe manifestation of AOM defined as extension of the infection into the mastoid with bony destruction of the mastoid air cells

103
Q

most common complication of OME:

A

Hearing loss!

must be monitored to avoid delay of speech/language development

104
Q

Intracranial complications are a rare but severe consequence of AOM necessitating:

A

urgent surgical management

105
Q

ANOTAR TMBN DEL RESUMEN

A

-

7MO SEMESTRE (22 decks)

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