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Head & Neck Surgery Flashcards

1
Q

What is anosmia?

A

Inability to smell

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2
Q

What is otorrhea?

A

Fluid discharge from ear

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3
Q

What is dysphagia?

A

Difficulty swallowing

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4
Q

What is odynophagia?

A

Painful swallowing

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5
Q

What is globus?

A

Sensation of a lump in the throat

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6
Q

What is otalgia?

A

Ear pain (often referred from throat)

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7
Q

What is trismus?

A

Difficulty opening mouth

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8
Q

What is CN I and its motor/sensory actions?

A

Olfactory nerve.

Smell.

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9
Q

What is CN II and its motor/sensory actions?

A

Optic nerve.

Sight (sensory pupil reaction).

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10
Q

What is CN III and its motor/sensory actions?

A

Oculomotor nerve.

Eyeball movement, pupil sphincter, ciliary muscle (motor pupil reaction).

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11
Q

What is CN IV and its motor/sensory actions?

A

Trochlear nerve.

Superior oblique muscle movement.

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12
Q

What is CN V and its motor/sensory actions?

A

Trigeminal nerve.
Motor: chewing (massester).
Sensory: face, teeth, sinuses, cornea.

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13
Q

What is CN VI and its motor/sensory actions?

A

Abducens nerve.

Lateral rectus muscle (lateral gaze).

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14
Q

What is CN VII and its motor/sensory actions?

A

Facial nerve.
Motor: facial muscles, lacrimal/sublingual/submandibular glands.
Sensory: anterior tongue/soft palate, taste.

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15
Q

What is CN VIII and its motor/sensory actions?

A

Vestibulocochlear nerve.

Hearing, positioning.

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16
Q

What is CN IX and its motor/sensory actions?

A

Glossopharyngeal nerve.
Motor: stylopharyngeus, parotid, pharynx.
Sensory: posterior tongue, pharynx, middle ear.

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17
Q

What is CN X and its motor/sensory actions?

A

Vagus nerve.
Motor: vocal cords, heart, bronchus, GI tract.
Sensory: bronchus, heart, GI tract, larynx, ear.

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18
Q

What is CN XI and its motor/sensory actions?

A

Accessory nerve.

Motor: trapezius, SCM muscles.

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19
Q

What is CN XII and its motor/sensory actions?

A

Hypoglossal nerve.

Motor: tongue, strap muscles (ansa cervicalis branch)

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20
Q

What are the 3 divisions of the trigeminal nerve?

A
  1. Ophthalmic
  2. Maxillary
  3. Mandibular
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21
Q

What happens when the hypoglossal nerve is cut?

A

When the patient sticks out the tongue, it deviates to the same side as the injury

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22
Q

What is the duct of the submandibular gland called?

A

Wharton’s duct

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23
Q

What is the duct of the parotid gland called?

A

Stensen’s duct

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24
Q

What is the source of blood supply to the nose?

A
  1. Internal carotid artery (anterior and posterior ethmoidal arteries via ophthalmic artery)
  2. External carotid artery (superior labial artery via facial artery, and sphenopalatine artery via internal maxillary artery)
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25
Q

What are the 3 bones that make up the posterior nasal septum?

A
  1. Ethmoid (perpendicular plate)
  2. Vomer
  3. Palatine
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26
Q

What are the 7 bones of the bony eyeball orbit?

A
  1. Frontal
  2. Zygoma
  3. Maxillary
  4. Lacrimal
  5. Ethmoid
  6. Palatine
  7. Sphenoid
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27
Q

What are the 4 strap muscles?

A
  1. Thyrohyoid
  2. Omohyoid
  3. Sternothyroid
  4. Sternohyoid
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28
Q

Which muscle crosses the external and internal carotid arteries?

A

Digastric muscle

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29
Q

In a neck incision, what is the first muscle incised?

A

Platysma

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30
Q

Which nerve supplies the strap muscle?

A

Ansa cervicalis (XII)

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31
Q

What are the anterior and posterior neck triangles?

A

Two regions of the neck, divided by the SCM

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32
Q

Which nerve runs with the carotid in the carotid sheath?

A

Vagus

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33
Q

Which nerve crosses the internal carotid artery at approximately 1-2 cm above the bifurcation?

A

Hypoglossal nerve

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34
Q

What are the 3 auditory ossicle bones?

A
  1. Malleus
  2. Incus
  3. Stapes
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35
Q

What comprises the middle ear?

A

Eustachian tube, ossicle bones, tympanic membrane, mastoid air cell

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36
Q

What comprises the inner ear?

A

Cochlea, semicircular canals, internal auditory canal

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37
Q

What is otitis externa?

A

Swimmer’s ear:

Generalized infection involving the external ear canal and often the tympanic membrane.

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38
Q

What is the usual cause of otitis externa?

A

Prolonged water exposure and damaged squamous epithelium of the ear canal

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39
Q

What are the typical pathogens in otitis externa?

A

Pseudomonas, Proteus, Staphylococcus.

Occasionally, E. coli, fungi (Asperigillus, Candida), or virus (HSV).

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40
Q

What are the signs and symptoms of otitis externa?

A

Otalgia; swelling of external ear, ear canal or both; erythema; pain on manipulation of the auricle; debris in canal; otorrhea

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41
Q

What is the treatment for otitis externa?

A

Keep the ear dry.
Mild infections respond to cleaning and dilute acetic acid drops.
Most infections require complete removal of all debris and topical antibiotics +/- hydrocortisone.

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42
Q

What is malignant otitis externa?

A

Fulminant bacterial otitis externa

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43
Q

Who is affected by malignant otitis externa?

A

Elderly patient, poorly controlled diabetes

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44
Q

What are the causative organisms in malignant otitis externa?

A

Pseudomonas

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45
Q

What is the classic feature of malignant otitis externa?

A

Nub of granulation tissue on the floor of the external ear canal at the bony-cartilaginous junction

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46
Q

What are the signs and symptoms of malignant otitis externa?

A

Severe ear pain, excessive purulent discharge, usually exposed bone, nub of granulation tissue on the floor of the external ear canal at the bony-cartilaginous junction

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47
Q

What are the diagnostic tests for malignant otitis externa?

A
  1. CT (erosion of bone, inflammation)
  2. Technetium-99 scan (temporal bone inflammatory process)
  3. Gallium-tagged white blood cell scan
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48
Q

What are the complications of malignant otitis externa?

A

Invasion of surrounding structures to produce a cellulitis, osteomyelitis of temporal bone, mastoiditis.
Later, facial nerve palsy, meningitis, brain abscess.

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49
Q

What is the treatment for malignant otitis externa?

A

Control of diabetes, meticulous local care with extensive debridement, hospitalization and IV antibiotics

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50
Q

What are the most common types of tumors of the external ear?

A

Squamous cell carcinoma

Also, basal cell and melanoma

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51
Q

From what location do tumors of the external ear typically arise?

A

Auricle

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52
Q

What is the associated risk factor for external ear tumors?

A

Excessive sun exposure

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53
Q

What is the treatment for cancers of the auricle?

A

Usually wedge excision

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54
Q

What is the treatment for external ear tumors extending into the ear canal?

A

May require excision of the external ear canal or partial temporal bone excision

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55
Q

What is the treatment for external ear tumors with middle ear involvement?

A

En bloc temporal bone resection and lymph node dissection

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56
Q

What is the etiology of a tympanic membrane perforation?

A

Usually result of trauma (direct or indirect) or secondary to middle ear infection.
Often occurs secondary to slap to the side of the head (compression injury), explosions.

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57
Q

What are the symptoms of a tympanic membrane perforation?

A

Pain, bleeding from the ear, conductive hearing loss, tinnitus

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58
Q

What are the signs of a tympanic membrane perforation?

A

Clot in the meatus, visible tear in the TM

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59
Q

What is the treatment for a tympanic membrane perforation?

A

Keep dry.

Use systemic antibiotics if there is evidence of infection or contamination.

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60
Q

What is the prognosis for a tympanic membrane perforation?

A

Most (90%) heal spontaneously, though larger perforations may require surgery (fat plug, temporalis fascia tympanoplasty)

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61
Q

What is a cholesteatoma?

A

An epidermal inclusion cyst of the middle ear or mastoid, containing desquamated keratin debris.
May be acquired or congenital.

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62
Q

What are the causes of cholesteatoma?

A

Negative middle ear pressure from eustachian tube dysfunction (primary acquired) or direct growth of epithelium through a TM perforation (secondary acquired)

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63
Q

What other condition is cholesteatoma often associated with?

A

Chronic middle ear infection

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64
Q

What is the usual history of cholesteatoma?

A

Chronic ear infection with chronic, malodorous drainage

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65
Q

What is the appearance of cholesteatoma?

A

Grayish-white, shiny keratinous mass behind or involving the TM; often described as a “pearly” lesion

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66
Q

What are the associated problems with cholesteatoma?

A

Ossicular erosion, producing conductive hearing loss.
Also, local invasion resulting in: vertigo, sensorineural hearing loss, facial paresis/paralysis, CNS dysfunction or infection.

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67
Q

What is the treatment for cholesteatoma?

A

Surgery (tympanoplasty/mastoidectomy) aimed at eradication of disease and reconstruction of the ossicular chain

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68
Q

What is bullous myringitis?

A

Vesicular infection of the TM and adjacent deep canal

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69
Q

What are the causative agents of bullous myringitis?

A

Unknown.

Viral should be suspected because of frequent association with viral URI.

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70
Q

What are the symptoms of bullous myringitis?

A

Acute severe ear pain, low-grade fever, bloody drainage

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71
Q

What are the findings on otoscopic examination of bullous myringitis?

A

Large, reddish blebs on the TM, wall of the meatus, or both

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72
Q

Is hearing affected in bullous myringitis?

A

Rarely, with occasional reversible sensorineural loss

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73
Q

What is the treatment for bullous myringitis?

A 
Oral antibiotics (erythromycin if Mycoplasma is suspected).
Topical analgesics may be used, with resolution of symptoms usually occurring in 36 hours.
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74
Q

What is acute suppurative otitis media?

A

Bacterial infection of the middle ear, often following a viral URI.
May be associated with a middle ear effusion.

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75
Q

What is the cause of acute suppurative otitis media?

A

Dysfunction of the eustachian tube that allows bacterial entry from nasopharynx.
Often associated with an occluded eustachian tube, although it is uncertain whether this is a cause or a result of the infection.

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76
Q

What are the predisposing factors for acute suppurative otitis media?

A

Young age, male gender, bottle feeding, crowded living conditions, cleft palate, Down syndrome, CF

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77
Q

What are the causative agents of acute suppurative otitis media?

A

Strep pneumo, H. flu, Moraxella, Staph, Beta-hemolytic Strep, Pseudomonas, Viral

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78
Q

What are the causative agents of acute suppurative otitis media in infants younger than 6 months?

A

Staph aureus, E. coli, Klebsiella

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79
Q

What are the symptoms of acute suppurative otitis media?

A

Otalgia, fever, decreased hearing, infant pulls on ear, increased irritability.
As many as 25% of patients are asymptomatic.

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80
Q

What are the signs of acute suppurative otitis media?

A

First, redness of the TM, later TM bulging with loss of the normal landmarks, then impaired TM mobility on pneumatic otoscopy

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81
Q

If pain disappears instantly in acute suppurative otitis media, what may have happened?

A

TM perforation

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82
Q

What are the complications of acute suppurative otitis media?

A

TM perforation, acute mastoiditis, meningitis, brain abscess, extradural abscess, labyrinthitis.
If recurrent or chronic, may have adverse effects on speech and cognitive development due to decreased hearing.

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83
Q

What is the treatment for acute suppurative otitis media?

A

10-day course of antibiotics (amoxicillin, Bactrim, or erythromycin)

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84
Q

What is the usual course of acute suppurative otitis media?

A

Symptoms usually resolve in 24-36 hours

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85
Q

What are the indications for myringotomy and PE tube placement in acute suppurative otitis media?

A
  1. Persistent middle ear effusion over 3 months
  2. Debilitated or immunocompromised patient
  3. 4+ episodes over 6 months
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86
Q

What is a PE tube?

A

Pneumatic Equalization tube, placed across tympanic membrane

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87
Q

What is a Bezold’s abscess?

A

Abscess behind the superior attachment of the SCM muscle resulting from extension of a mastoid infection

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88
Q

What are the causes of chronic otitis media?

A

Mixed, Staph aureus, Pseudomonas

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89
Q

What are the signs and symptoms of chronic otitis media?

A

Otorrhea and hearing loss

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90
Q

What is otosclerosis?

A

Genetic disease characterized by abnormal spongy and sclerotic bone formation in the temporal bone around the footplate of the stapes, thus preventing its normal movement

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91
Q

What is the inheritance pattern of otosclerosis?

A

AD with incomplete penetrance (33%)

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92
Q

What are the symptoms of otosclerosis?

A

Painless, progressive hearing loss (may be unilateral or bilateral), tinnitus

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93
Q

What is the usual age of onset for otosclerosis?

A

2nd-4th decade

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94
Q

How is the diagnosis of otosclerosis made?

A

Normal TM with conductive hearing loss and no middle-ear effusion (though may be mixed or even sensorineural if bone of cochlea is affected)

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95
Q

What is Schwartze’s sign?

A

Erythema around the stapes from hypervascularity of new bone formation

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96
Q

What is the treatment for otosclerosis?

A 
Frequently surgical (stapedectomy with placement of prosthesis), hearing aid, or observation.
Sodium fluoride may be used if a sensorineural component is present or for preoperative stabilization.
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97
Q

How is facial nerve paralysis localized?

A
  1. Supranuclear: Paralysis of lower face only, forehead muscles are spared because of bilateral corticobulbar supply.
  2. Intratemporal bone: Paralysis of upper and lower face, decreased tearing, altered taste, absent stapedius reflex.
  3. Distal to stylomastoid foramen: Paralysis of facial muscles only.
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98
Q

What are the causes of facial nerve paralysis?

A

Bell’s palsy, trauma, cholesteatoma, tumor (carcinoma, glomus jugulare), herpes zoster inflammation of geniculate ganglion, peripheral lesions are usually parotid gland tumors

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99
Q

What is the most common cause of bilateral facial nerve palsy?

A

Lyme disease

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100
Q

What is Bell’s palsy?

A

Sudden onset, unilateral facial weakness or paralysis in absence of CNS, ear, or cerebellopontine angle disease

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101
Q

What is the clinical course of Bell’s palsy?

A

Acute onset, with greatest muscle weakness reached within 3 weeks

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102
Q

What is the incidence of Bell’s palsy?

A

Most common cause of unilateral facial weakness/paralysis

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103
Q

What is the pathogenesis of Bell’s palsy?

A

Unknown.
Most widely accepted hypothesis is viral etiology (HSV).
Ischemic and immunologic factors are also implicated.

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104
Q

What is the common preceding event in Bell’s palsy?

A

URI

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105
Q

What are the signs and symptoms of Bell’s palsy?

A

Pathology is related to swelling of the facial nerve.
May present with total facial paralysis, altered lacrimation, increased tearing on affected side, change in taste if region above chorda tympani is affected, dry mouth, and hyperacusis.

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106
Q

What is the treatment for Bell’s palsy?

A

Usually none is required, as most cases resolve spontaneously in 1 month.
Protect eye with drops and tape closed as needed.
Most otolaryngologists advocate steroids and acyclovir.
Surgical decompression of CN VII is indicated if paralysis progresses or tests indicate deterioration.

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107
Q

What is the prognosis for Bell’s palsy?

A

Overall, 90% of patients recover completely

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108
Q

What is sensorineural hearing loss?

A

Hearing loss from a lesion occurring in the cochlea or acoustic nerve, rather than the external or middle ear

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109
Q

What are the symptoms of sensorineural hearing loss?

A

Distortion of hearing, impaired speech discrimination, tinnitus

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110
Q

What are the signs of sensorineural hearing loss?

A

Air conduction is better than bone conduction (positive Rinne test), Weber materializes to the side without the defect.
Audiogram most commonly shows greatest loss in high-frequency tones.

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111
Q

What is the Weber test?

A

Tuning fork on middle of head (lateral louder = either ipsilateral conductive loss or contralateral sensorineural)

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112
Q

What is the Rinne test?

A

Tuning fork on mastoid and then next to ear (conductive loss louder on mastoid)

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113
Q

What are the causes of sensorineural hearing loss?

A

Aging (presbycusis); acoustic injury from sudden or prolonged exposure to loud noises; perilymph fistula; congenital (TORCHES); Meniere’s disease; drug or toxin; acoustic neuroma; pseudotumor cerebri; CNS disease; endocrine disorders; sarcoidosis

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114
Q

What is the most common cause of sensorineural hearing loss in children?

A

Meningitis (bacterial)

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115
Q

What is the treatment for sensorineural hearing loss?

A

Treatment of underlying cause, hearing aids, lip reading, cochlear implant

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116
Q

What is vertigo?

A

Sensation of head/body movement, or movement of surroundings (usually rotational)

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117
Q

What is the cause of vertigo?

A

Asymmetric neuronal activity between right and left vestibular systems

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118
Q

What is the history of peripheral vertigo?

A

Severe vertigo, N/V, always accompanied by horizontal or rotatory nystagmus (fast component almost always to side opposite disease), other evidence of inner ear disease (tinnitus, hearing loss)

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119
Q

What are the risk factors for peripheral vertigo?

A

Frequently associated with a previously operated ear, a chronic draining ear, barotrauma, or head trauma

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120
Q

What is the history of central vertigo?

A

Found in brainstem or cerebellum: insidious onset, less intense and more subtle sensation of vertigo.
Occasionally, vertical nystagmus.

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121
Q

What are the steps in diagnostic evaluation of vertigo?

A

Careful neurologic and otologic examinations are required.

May need FTA/VDRL, temporal bone scans, CT, MRI, ENG, position testing, audiometric testing.

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122
Q

What is the most common etiology of vertigo?

A

Benign Paroxysmal Positional Vertigo (BPPV):

History of brief spells of severe vertigo with specific head positions.

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123
Q

What is the differential diagnosis for vertigo?

A
  1. Central: vertebral basilar insufficiency, Wallenberg syndrome, MS, epilepsy, migraine.
  2. Peripheral: BPPV, motion sickness, syphilis, Meniere’s disease, vestibular neuronitis, labyrinthitis, acoustic neuroma, perilymph fistula.
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124
Q

What is Tullio’s phenomenon?

A

Induction of vertigo by loud noises.

Classically, result of otosyphilis.

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125
Q

What is Meniere’s disease?

A

Disorder of the membranous labyrinth, causing fluctuating sensorineural hearing loss, episodic vertigo, nystagmus, tinnitus, aural fullness, N/V

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126
Q

What is the classic triad of Meniere’s disease?

A
  1. Hearing loss
  2. Tinnitus
  3. Vertigo
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127
Q

What is the pathophysiology of Meniere’s disease?

A

Obscure, but most experts believe excessive production or defective resorption of endolymph

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128
Q

What is the medical treatment for Meniere’s disease?

A

Salt restriction, diuretics (thiazides), anti-nausea agents, occasionally diazepam

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129
Q

What are the indications for surgery with Meniere’s disease?

A

Surgery is offered to those who fail medical treatment or who have incapacitating vertigo

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130
Q

What are the surgical options for Meniere’s disease?

A
  1. Shunt from membranous labyrinth to subarachnoid space
  2. Vestibular neurectomy
  3. Labyrinthectomy
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131
Q

What are glomus tumors?

A

Benign, slow-growing tumors arising in glomus bodies found in the adventitial layer of blood vessels.
Often associated with CN IX and X in the middle ear.

132
Q

What is the usual location for glomus tumors?

A

Middle ear, jugular bulb, course of CN IX-XII

133
Q

How common are glomus tumors?

A

Most common benign tumor of the temporal bone

134
Q

What is the treatment for glomus tumors?

A

Surgical resection, radiation therapy for poor operative candidates or for recurrences

135
Q

What is epistaxis?

A

Bleeding from the nose

136
Q

What are the predisposing factors for epistaxis?

A

Trauma, “nose picking,” sinus infection, allergic or atrophic rhinitis, blood dyscrasias, tumor, environmental extremes (hot, dry climates, winters)

137
Q

What is the usual cause of epistaxis?

A

Rupture of superficial mucosal blood vessels (Kiesselbach’s plexus if anterior, sphenopalatine artery if posterior)

138
Q

What is the most common type of epistaxis?

A

Anterior (90%), usually from trauma

139
Q

Which type of epistaxis is more serious?

A

Posterior:

Usually occurs in the elderly or is associated with a systemic disorder (hypertension, tumor, arteriosclerosis)

140
Q

What is the treatment for epistaxis?

A

Direct pressure; proceed to anterior nasal packing with gauze strips, followed by posterior packing with Foley catheter or lamb’s wool.
Packs must be removed in

141
Q

What is the treatment of last resort for epistaxis?

A

Ligation or embolization of the sphenopalatine artery (posterior) or ethmoidal artery (anterior)

142
Q

What infectious disease syndrome is seen with nasal packing?

A

Toxic shock syndrome:

Fever, shock, rash caused by exotoxin from Staph aureus

143
Q

What is the treatment for toxic shock syndrome?

A

Supportive with removal of nasal packing, IVF, O2, anti-Staph antibiotics

144
Q

What is acute rhinitis?

A

Inflammation of nasal mucous membrane

145
Q

What is the most common cause of acute rhinitis?

A

URI.
Rhinovirus is the most common agent in adults (other non-allergic causes: nasal deformities and tumors, polyps, atrophy, immune diseases, vasomotor problems)

146
Q

What are the symptoms of allergic rhinitis?

A

Nasal stuffiness; watery rhinorrhea; paroxysms of morning sneezing; itching of nose, conjunctiva, or palate

147
Q

How is allergic rhinitis characterized?

A

Early onset (before 20 years), familial tendency, history of atopy, elevated serum IgE, eosinophilia on nasal smear

148
Q

What are the findings on physical exam in allergic rhinitis?

A

Pale, boggy, bluish nasal turbinates coated with thin, clear secretions.
In children, a transverse nasal crease sometimes results from repeated “allergic salute”.

149
Q

What is the treatment for allergic rhinitis?

A

Allergen avoidance, antihistamines, decongestants.

Steroids or sodium cromylate in severe cases.

150
Q

What is the typical history for acute sinusitis?

A

Previously healthy patient with unrelenting progression of a viral URI or acute rhinitis beyond the normal 5-7-day course

151
Q

What are the symptoms of acute sinusitis?

A

Periorbital pressure or pain, nasal obstruction, nasal or post-nasal mucopurulent discharge, fatigue, fever, headache

152
Q

What are the signs of acute sinusitis?

A

Tenderness over affected sinuses, pus in the nasal cavity.

May also see reason for obstruction (septal deviation, spur, tight osteomeatal complex).

153
Q

What is the pathophysiology of acute sinusitis?

A

Thought to be secondary to decreased ciliary action of the sinus mucosa and edema causing obstruction of the sinus ostia, lowering intrasinus O2 tension and predisposing patients to bacterial infection

154
Q

What are the causative organisms in acute sinusitis?

A

Strep pneumo, GABHS, H. flu

155
Q

What is the treatment for acute sinusitis?

A

14-day course of antibiotics (penicillin G, amoxicillin, Ceclor, Augmentin are common), topical and systemic decongestants, and saline nasal irrigation

156
Q

What is the treatment for fungal sinusitis?

A

Fungal sinusitis is commonly caused by Mucor and seen in immunosuppressed patients.
Treatment is IV antifungals (amphotericin or caspofungin) and surgical debridement of all necrotic tissue.

157
Q

What is chronic sinusitis?

A

Infection of nasal sinuses lasting longer than 4 weeks, or pattern of recurrent acute sinusitis punctuated by brief asymptomatic periods

158
Q

What is the pathology of chronic sinusitis?

A

Permanent mucosal changes secondary to inadequately treated acute sinusitis, consisting of mucosal fibrosis, polypoid growth, and inadequate ciliary action, hyperostosis (increased bone density on CT)

159
Q

What are the symptoms of chronic sinusitis?

A

Chronic nasal obstruction, postnasal drip, mucopurulent rhinorrhea, low-grade facial and periorbital pressure or pain

160
Q

What are the causative organisms in chronic sinusitis?

A 
Usually anaerobes (Bacteroides, Veillonella, Rhinobacterium).
Also H. flu, Strep viridans, Staph aureus, Staph epidermidis.
161
Q

What is the treatment for chronic sinusitis?

A

Medical management with decongestion, mucolytics, topical steroids, and antibiotics.
If this fails, proceed to endoscopic or external surgical intervention.

162
Q

What is FESS?

A

Functional Endoscopic Sinus Surgery

163
Q

What are the complications of sinusitis?

A

Orbital cellulitis (if ethmoid sinusitis), meningitis, epidural or brain abscess (frontal sinusitis), cavernous sinus thrombosis (ethmoid or sphenoid sinusitis), osteomyelitis

164
Q

What are the usual locations of cancer of the nasal cavity and paranasal sinuses?

A

Maxillary sinus, nasal cavity, ethmoid sinus

165
Q

What are the associated cell types in cancer of the nasal cavity and paranasal sinuses?

A

Squamous cell (80%), adenocellular (15%)

166
Q

What rare tumor arises from olfactory epithelium?

A

Esthesioneuroblastoma.

Usually arises high in the nose (cribriform plate) and is locally invasive.

167
Q

What are the signs and symptoms of cancer of the nasal cavity and paranasal sinuses?

A

Early: nasal obstruction, blood-tinged mucus, epistaxis
Late: localized pain, cranial nerve deficits, facial/palate asymmetry, loose teeth

168
Q

How is the diagnosis of cancer of the nasal cavity and paranasal sinuses made?

A

CT (extent of disease and local invasion); MRI (soft-tissue disease)

169
Q

What is the treatment for cancer of the nasal cavity and paranasal sinuses?

A

Surgery +/- XRT

170
Q

What is the prognosis for cancer of the nasal cavity and paranasal sinuses?

A

5-year survival for T1-2 lesions: 70%

171
Q

What us juvenile nasopharyngeal angiofibroma?

A

Most commonly encountered vascular mass in the nasal cavity.

Locally aggressive but non-metastasizing.

172
Q

What is the usual history for juvenile nasopharyngeal angiofibroma?

A

Adolescent boys who present with nasal obstruction, recurrent massive epistaxis, possibly anosmia

173
Q

What is the usual location for juvenile nasopharyngeal angiofibroma?

A

Site of origin is the roof of the nasal cavity at the superior margin of sphenopalatine foramen

174
Q

Into what can a juvenile nasopharyngeal angiofibroma transform?

A

Fibrosarcoma

175
Q

How is the diagnosis of juvenile nasopharyngeal angiofibroma made?

A

Carotid arteriography, CT.

Biopsy is contraindicated secondary to risk of uncontrollable hemorrhage.

176
Q

What are indications for biopsy in juvenile nasopharyngeal angiofibroma?

A

None

177
Q

What is the treatment for juvenile nasopharyngeal angiofibroma?

A

Surgery via lateral rhinotomy or sublabial maxillotomy with bleeding controlled by internal maxillary artery ligation or preoperative embolization, in the setting of hypotensive anesthesia.
Preoperative irradiation has also been used to shrink the tumor.

178
Q

What is the common site of referred throat pain?

A

Ear

179
Q

What is pharyngotonsillitis?

A

Acute or chronic infection of the nasopharynx or oropharynx and/or Waldeyer’s ring of lymphoid tissue (consisting of palatine, lingual, and pharyngeal tonsils and the adenoids)

180
Q

What is the etiology of pharyngotonsillitis?

A

Acute attacks can be viral (adenovirus, enterovirus, coxsackievirus, EBV) or bacterial (GABHS).
Chronic tonsillitis often with mixed population, including Strep, Staph, and Moraxella.

181
Q

What are the symptoms of pharyngotonsillitis?

A

Acute: sore throat, fever, local LAD, chills, headache, malaise.
Chronic: noisy mouth breathing, speech and swallowing difficulties, apnea, halitosis.

182
Q

What are the signs of pharyngotonsillitis?

A

Viral: injected tonsils and pharyngeal mucosa, exudate may occur, but less often than with bacterial tonsillitis.
Bacterial: swollen, inflamed tonsils with white-yellow exudate in crypts and on surface, cervical LAD.

183
Q

How is the diagnosis of pharyngotonsillitis made?

A

CBC, throat culture, Monospot test

184
Q

What are the possible complications of pharyngotonsillitis?

A

Peritonsillar abscess (quinsy), retropharyngeal abscess (causing airway compression), rheumatic fever, post-strep glomerulonephritis

185
Q

What is the treatment for pharyngotonsillitis?

A

Viral: acetaminophen, warm saline gargles, anesthetic throat spray.
Bacterial: 10 days penicillin (erythromycin if allergic).

186
Q

What are the indications for tonsillectomy in pharyngotonsillitis?

A

Sleep apnea or cor pulmonale secondary to airway obstruction; suspicion of malignancy; hypertrophy causing malocclusion; peritonsillar abscess; recurrent acute or chronic tonsillitis

187
Q

What are the possible complications of tonsillectomy?

A

Acute or delayed hemorrhage

188
Q

What is the clinical setting of peritonsillar abscess?

A

Inadequately treated recurrent acute or chronic tonsillitis

189
Q

What is the associated microbiology of peritonsillar abscess?

A

Mixed aerobes and anaerobes (which may be penicillin-resistant)

190
Q

What is the site of peritonsillar abscess formation?

A

Begins at the superior pole of the tonsil

191
Q

What are the symptoms of peritonsillar abscess?

A

Severe throat pain, drooling dysphagia, odynophagia, trismus, cervical LAD, fever, chills, malaise

192
Q

What is the classic description of voice with peritonsillar abscess?

A

Hot-potato voice

193
Q

What are the signs of peritonsillar abscess?

A

Bulging, erythematous, edematous tonsillar pillar.

Swelling of uvula and displacement to contralateral side.

194
Q

What is the treatment for peritonsillar abscess?

A

IV antibiotics and surgical evacuation by incision and drainage.
Most experts recommend tonsillectomy after resolution of inflammatory changes.

195
Q

What is Ludwig angina?

A

Infection and inflammation of the floor of the mouth (sublingual and submandibular)

196
Q

What is the source of Ludwig angina?

A

Dental infection

197
Q

What is the treatment for Ludwig angina?

A

Antibiotics, emergency airway, I&D

198
Q

What is the usual cell type in cancer of the oral cavity?

A

Squamous cell (>90%)

199
Q

What are the most common sites of cancer of the oral cavity?

A

Lip, tongue, floor of mouth, gingiva, cheek, palate

200
Q

What is the etiology of cancer of the oral cavity?

A

Linked to smoking, alcohol, and smokeless tobacco products

201
Q

What is the frequency of nodal metastasis of cancer of the oral cavity?

A

10-60%, usually to jugular and jugulodigastric nodes, submandibular nodes

202
Q

How is the diagnosis of cancer of the oral cavity made?

A

H&P, dental assessment, Panorex or bone scan if mandible is thought to be involved, CT/MRI for extent of tumor and nodal disease, FNA

203
Q

What is the treatment for cancer of the oral cavity?

A

Radiation, surgery, or both for small lesions.
Localized lesions can usually be treated surgically.
Larger lesions require combination therapy, possible mandibulectomy and neck dissection.

204
Q

What is the prognosis for cancer of the oral cavity?

A

Tongue: 20-70%

Floor of mouth: 30-80%

205
Q

What is the frequency of gland involvement amongst salivary gland tumors?

A

Parotid (80%)
Submandibular (15%)
Minor salivary glands (5%)

206
Q

What is the potential for malignancy with salivary gland tumors?

A

Greatest in minor salivary gland tumors (80% malignant), least in parotid (80% benign)

207
Q

How do benign and malignant salivary gland tumors differ in terms of H&P?

A

Benign: mobile, nontender, no node involvement or facial weakness
Malignant: painful, fixed mass with evidence of local metastasis and facial paresis/paralysis

208
Q

What is the diagnostic procedure for salivary gland tumors?

A

FNA.
Never perform an excisional biopsy of a parotid mass, superficial parotidectomy is the procedure of choice for benign lesions of the lateral lobe.

209
Q

What is the treatment for salivary gland tumors?

A

Involves adequate surgical resection, sparing facial nerve if possible, neck dissection for node-positive necks

210
Q

What are the indications for post-op XRT for salivary gland tumors?

A

Postoperative XRT if high-grade cancer, recurrent cancer, residual disease, invasion of adjacent structures, any T3-4 parotid tumors

211
Q

What is the most common benign salivary tumor?

A

Pleomorphic adenoma (benign mixed tumor)

212
Q

What is the usual location of pleomorphic adenoma?

A

Parotid gland

213
Q

What is the clinical course of pleomorphic adenoma?

A

They are well-delineated and slow-growing

214
Q

What is the second most common benign salivary tumor?

A

Warthin’s tumor

215
Q

What is the usual location of Warthin’s tumor?

A

Parotid gland

216
Q

What is Warthin’s tumor?

A

Slow-growing, cystic mass, usually located in the tail of the superficial portion of the parotid.
Rarely becomes malignant.

217
Q

What is the most common malignant salivary tumor?

A

Mucoepidermoid carcinoma

218
Q

What is the second most common malignant salivary tumor?

A

Adenoid cystic carcinoma

219
Q

What are the 3 parts of the larynx?

A
  1. Glottis: begins halfway between the true and false cords (in the ventricle) and extends inferiorly 1 cm below the edge of the vocal folds.
  2. Supraglottis: extends from superior glottis to superior border of hyoid and tip of epiglottis.
  3. Subglottis: extends from lower border of glottis to inferior edge of cricoid cartilage.
220
Q

What is the innervation of the larynx?

A

Vagus nerve: superior laryngeal and recurrent laryngeal nerves.
Superior laryngeal supplies sensory to supraglottis and motor to inferior constrictor and cricothyroid muscle.
Recurrent laryngeal supplies sensory to glottis and sub glottis and motor to all remaining intrinsic laryngeal muscles.

221
Q

What is croup?

A

Viral infection of the larynx and trachea generally affecting children

222
Q

What is the usual cause of croup?

A

Parainfluenza virus

223
Q

What age group is affected most by croup?

A

6 months - 3 years

224
Q

Is croup considered seasonal?

A

Yes (most often in autumn)

225
Q

What are the precipitating events in croup?

A

Usually preceded by URI

226
Q

What is the classic symptom of croup?

A

Barking (seal-like), non-productive cough

227
Q

Other than barking cough, what are the symptoms of croup?

A

Respiratory distress, low-grade fever

228
Q

What are the signs of croup?

A

Tachypnea, inspiratory retractions, prolonged inspiration, inspiratory stridor, expiratory rhonchi/wheezes

229
Q

What is the differential diagnosis of croup?

A

Epiglottitis, bacterial tracheitis, foreign body, diphtheria, retropharyngeal abscess, peritonsillar abscess, asthma

230
Q

How is the diagnosis of croup made?

A

AP neck XR shows classic “steeple sign”, indicating subglottic narrowing.
ABG may show hypoxemia plus hypercapnia.

231
Q

What is the treatment for croup?

A

Keep child calm, cool mist, steroids, aerosolized racemic epinephrine may be administered to reduce edema and airway obstruction

232
Q

What are the indications for intubation in croup?

A

If airway obstruction is severe or child becomes exhausted

233
Q

What is the usual course of croup?

A

Resolves in 3-4 days

234
Q

What type of secondary infection occurs with croup?

A

Secondary bacterial infection (Strep, Staph)

235
Q

What is epiglottitis?

A

Severe, rapidly progressive infection of the epiglottis

236
Q

What is the usual causative agent of epiglottitis?

A

H. flu type B

237
Q

What age group is affected by epiglottitis?

A

2-5 years

238
Q

What are the signs and symptoms of epiglottitis?

A

Sudden onset, high fever, “hot-potato” voice, dysphagia, drooling, no cough, patient prefers to sit upright, lean foreword, toxic, stridulous

239
Q

How is the diagnosis of epiglottitis made?

A

Can usually be made clinically

240
Q

What is the treatment for epiglottitis?

A

Involves immediate airway support in the OR: intubation or possibly tracheostomy, medical treatment is comprised of steroids and IV antibiotics agains H. flu

241
Q

What is the incidence of malignant laryngeal tumors?

A

2% of malignancies

242
Q

What is the most common site for laryngeal malignancies?

A

Glottis

243
Q

What is the second most common site for laryngeal malignancies?

A

Supraglottis

244
Q

Which type of laryngeal malignancy has the worst prognosis?

A

Subglottic tumors

245
Q

What are the risk factors for laryngeal malignancies?

A

Tobacco, alcohol

246
Q

What is the pathology of laryngeal malignancies?

A

Squamous cell carcinoma (90%)

247
Q

What are the symptoms of laryngeal malignancies?

A

Hoarseness, throat pain, dysphagia, odynophagia, neck mass, referred ear pain

248
Q

What is the usual location for supraglottic malignant lesions?

A

Laryngeal surface of epiglottis

249
Q

What area is often involved in supraglottic malignant lesions?

A

Pre-epiglottic space

250
Q

What is the typical extension of supraglottic malignant lesions?

A

Tend to remain confined to supraglottic region, though may extend to vallecula or base of tongue

251
Q

What is the associated type of metastasis with supraglottic malignant lesions?

A

High propensity for nodal metastasis

252
Q

What is the treatment for supraglottic malignant lesions?

A

Early: XRT
Late: laryngectomy

253
Q

What is the usual location for glottic malignant lesions?

A

Anterior part of true cords

254
Q

What is the typical extension of glottic malignant lesions?

A

May invade thyroid cartilage, cross midline to invade contralateral cord, or invade paraglottic space

255
Q

What is the associated type of metastasis with glottic malignant lesions?

A

Rare nodal metastasis

256
Q

What is the treatment for glottic malignant lesions?

A

Early: XRT
Late: laryngectomy

257
Q

What is the usual etiology of neck mass in infants?

A

Congenital (branchial cleft cyst, thyroglossal duct cyst)

258
Q

What is the usual etiology of neck mass in adolescents?

A

Inflammatory (cervical adenitis), with congenital also possible

259
Q

What is the usual etiology of neck mass in adults?

A

Malignancy, especially if painless and immobile

260
Q

What is the 80% rule of neck masses?

A

80% are benign in children

80% are malignant in adults > 40 years

261
Q

What are the 7 cardinal symptoms of neck masses?

A

Dysphagia, odynophagia, hoarseness, stridor, globus, speech disorder, referred ear pain

262
Q

What comprises the workup of a neck mass?

A 
Full head and neck exam, indirect laryngoscopy, CT, MRI, FNA for tissue diagnosis.
Biopsy contraindicated (may adversely affect survival if malignant).
263
Q

What is the differential diagnosis for neck mass?

A

Inflammatory: cervical lymphadenitis, cat-scratch disease, infectious mono, infection in neck spaces.
Congenital: thyroglossal duct cyst (midline, elevates with tongue protrusion), branchial cleft cyst (lateral), dermoid cyst (midline submental), hemangioma, cystic hygroma.
Neoplastic: primary or metastatic.

264
Q

What is the workup of node-positive squamous cell carcinoma in the neck and no primary site?

A

Triple endoscopy (laryngoscopy, esophagoscopy, bronchoscopy) and blind biopsies

265
Q

What is the treatment for neck mass?

A

Surgical excision for congenital or neoplastic.

2 most important procedures for cancer treatment are radical and modified neck dissection.

266
Q

What is the role of adjuvant therapy in head and neck cancer?

A

Postoperative chemotherapy/XRT

267
Q

What is involved in radical neck dissection?

A

Removal of nodes from clavicle to mandible, SCM muscle, submandibular gland, tail of parotid, internal jugular vein, digastric muscles, stylohyoid and omohyoid muscles, fascia within the anterior and posterior triangles, CN XI, and cervical plexus sensory nerves

268
Q

What are the indications for radical neck dissection?

A
  1. Clinically positive nodes that likely contain metastatic cancer.
  2. Clinically negative nodes in neck, but high probability of metastasis from a primary tumor elsewhere.
  3. Fixed cervical mass that is resectable.
269
Q

What are the contraindications against radical neck dissection?

A
  1. Distant metastasis.
  2. Fixation to structure that cannot be removed (e.g. carotid artery).
  3. Low neck masses.
270
Q

What is type I modified neck dissection?

A

Spinal accessory nerve preserved

271
Q

What is type II modified neck dissection?

A

Spinal accessory nerve and internal jugular vein preserved

272
Q

What is type III modified neck dissection?

A

Spinal accessory nerve, internal jugular vein, and SCM nerves are preserved

273
Q

What are the advantages of modified neck dissections?

A

Increased postoperative function and decreased morbidity (especially if bilateral).
These modifications are usually intra-operative decisions based on the location and extent of tumor growth.

274
Q

What are the disadvantages of modified neck dissections?

A

May result in increased mortality from local recurrence

275
Q

What are the symptoms of mandible fractures?

A

Gross disfigurement, pain, malocclusion, drooling

276
Q

What are the signs of mandible fractures?

A

Trismus, fragment mobility and lacerations of gingiva, hematoma in floor of mouth

277
Q

What are the possible complications of mandible fractures?

A

Malunion, nonunion, osteomyelitis, TMJ ankylosis

278
Q

What is the treatment for mandible fractures?

A

Open or closed reduction, MMF

279
Q

What is MMF

A

MaxilloMandibular Fixation

280
Q

How are midface fractures evaluated?

A

Careful physical and CT

281
Q

What is a Le Fort I fracture?

A

Transverse maxillary fracture above the dental apices, which also traverses the pterygoid plate.
Palate is mobile, but nasal complex is stable.

282
Q

What is a Le Fort II fracture?

A

Fracture through the frontal process of the maxilla, through the orbital floor and pterygoid plate.
Midface is mobile.

283
Q

What is a Le Fort III fracture?

A

Complete craniofacial separation.

Differs from a Le Fort II in that it extends through the nasofrontal suture and frontozygomatic sutures.

284
Q

What is a tripod fracture?

A

Fracture of the zygomatic complex, involving 4 fractures:

  1. Frontozygomatic suture
  2. Inferior orbital rim
  3. Zygomaticomaxillary suture
  4. Zygomaticotemporal suture
285
Q

What is a blowout orbital fracture?

A

Orbital fracture with blowout of supporting bony structural support of orbital floor.
Patient has enophlalmos (sunken-in eyeball).

286
Q

What is entrapment in an orbital fracture?

A

Entrapment of periorbital tissues within the fracture opening, including entrapment of extraocular muscles.
Loss of extraocular muscle mobility and diplopia.

287
Q

What is a step off orbital fracture?

A

Orbital fracture with palpable step off of bony orbital rum (inferior or lateral)

288
Q

Are mandibular fractures usually a single fracture?

A

No, because the mandible forms an anatomic ring, > 95% of mandible fractures have more than one fracture site

289
Q

What is the best XR study for mandibular fractures?

A

Panorex

290
Q

What must be ruled out and treated with a broken nose?

A

Septal hematoma.

Must drain to remove chance of pressure-induced septal necrosis.

291
Q

How can otitis externs be distinguished from otitis media on examination?

A

Otitis externa is characterized by severe pain upon manipulation of the auricle

292
Q

What causes otitis media?

A

Most cases are caused by Strep pneumo and H. flu

293
Q

What causes otitis externa?

A

Pseudomonas

294
Q

What must be considered in unilateral serous otitis?

A

Nasopharyngeal carcinoma

295
Q

What is the most common cause of facial paralysis?

A

Bell’s palsy, which has an unidentified etiology

296
Q

What is the single most important prognostic factor in Bell’s palsy?

A

Whether the affected muscles are completely paralyzed

297
Q

What is the most common cause of parotid swelling?

A

Mumps

298
Q

Wat is Heerfordt’s syndrome?

A

Sarcoidosis with parotid enlargement, facial nerve paralysis, and uveitis

299
Q

Which systemic disease causes salivary gland stones?

A

Gout

300
Q

What is the most common salivary gland site of stone formation?

A

Submandibular gland

301
Q

What is Mikulicz’s syndrome?

A

Any cause of bilateral enlargement of the parotid, lacrimal, and submandibular glands

302
Q

What are the 3 major functions of the larynx?

A
  1. Airway protection
  2. Airway/respiration
  3. Phonation
303
Q

What is a cricothyroidotomy?

A

Emergent surgical airway by incising the cricothyroid membrane

304
Q

What are the 4 major indications for a tracheostomy?

A
  1. Prolonged mechanical ventilation (> 2 weeks)
  2. Upper airway obstruction
  3. Poor life-threatening pulmonary toilet
  4. Severe obstructive sleep apnea
305
Q

What is a ranula?

A

Sublingual retention cyst arising from sublingual salivary glands

306
Q

What is Frey’s syndrome?

A

Flushing, pain, and diaphoresis in the auriculotemporal nerve distribution initiated by chewing

307
Q

What causes Frey’s syndrome?

A

Cutting the auriculotemporal nerve causes abnormal regeneration of the sympathetic and parasympathetic nerves, which, once destined for the parotid gland, find new targets in skin sweat glands.
Thus people sweat when eating.

308
Q

What is the classic triad of Meniere’s disease?

A
  1. Hearing loss
  2. Tinnitus
  3. Vertigo
309
Q

What is the most common posterior fossa tumor and where is it located?

A

Acoustic neuroma, usually occurring at the cerebellopontine angle

310
Q

What is the most common site of sinus cancer?

A

Maxillary sinus

311
Q

What tumor arises from olfactory epithelium?

A

Esthesioneuroblastoma

312
Q

What cell type is most common in head and neck cancer?

A

Squamous cell

313
Q

What are the most important predisposing factors to head and neck cancer?

A

Excessive alcohol use and tobacco abuse

314
Q

What is the most frequent site of salivary gland tumor?

A

Parotid gland

315
Q

What is the most common benign salivary gland tumor?

A

Pleomorphic adenoma

316
Q

What is the most common malignant salivary gland tumor?

A

Mucoepidermoid carcinoma

317
Q

What is the classic feature of croup?

A

Barking, seal-like cough

318
Q

What are the classic features of epiglottitis?

A

Hot-potato voice, sitting up, drooling, toxic appearance, high fever, leaning forward

319
Q

What comprises the workup of neck mass?

A

FNA and complete head and neck exam.

Do not biopsy.

320
Q

What is Ramsay-Hunt syndrome?

A

Painful facial nerve paralysis from herpes zoster of the ear

321
Q

What is the most common malignant neck mass in children, adolescents, and young adults?

A

Lymphoma

322
Q

What is the most common primary malignant solid tumor of the head and neck in children?

A

Rhabdomyosarcoma

323
Q

To where is throat pain most often referred?

A

Ear

324
Q

What ENT condition is described as crocodile tears?

A

Frey’s syndrome

325
Q

What is Brown’s sign?

A

Tympanic membrane pulsations that cease with positive pressure.
Seen with middle ear tumor mass.

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