General oto infectious diseases of the neck Flashcards

1
Q

What is the most common cause of deep neck

space infections in the adult population?

A

Odontogenic infection

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2
Q

What is the most common cause of deep neck

space infections within the pediatric population?

A

Tonsillitis

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3
Q

Describe the head and neck manifestations of

Actinomyces israelii infection?

A

Development of a “lumpy jaw” and multiple painless, red or
bluish raised, firm lesions containing multiple draining sinus
tracts

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4
Q

Describe the histologic appearance of Actinomyces

israelii?

A

Gram-positive, non–acid-fast, anaerobic bacilli demon-

strating a filamentous fungal-like growth pattern and “sulfur granule” formation

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5
Q

What are the most common sites of the head and

neck to develop Mycobacterium infections?

A

Anterior superior cervical region near the submandibular
space, followed by the posterior cervical, middle cervical, and supraclavicular regions. Atypical mycobacterial infection is sometimes found in the preauricular region

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6
Q

What is the most common manifestation for atypical Mycobacterium infections involving the
neck?

A

Persistent firm painless cervical adenopathy with overlying

violaceous skin discoloration

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7
Q

What is the current recommended management
of atypical Mycobacterium infections involving the
neck?

A

Persistent lesions are best managed by surgical excision or incision and curettage. Common antibiotic choices include clarithromycin, ethambutol, isoniazid, and rifampin, de-
pending on the species.

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8
Q

What tests should be ordered for patients with suspected mycobacterial infections involving the
head and neck?

A

PPD, chest plain film, cultures (Ziehl-Neelson stain,

Lowenstein-Jensen medium), nucleic acid probes, and PCR

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9
Q

Are PPD tests usually positive in patients with atypical mycobacterial infections of the head and neck?

A

No. PPD tests are generally negative or weakly reactive.

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10
Q

Why are mycobacteria called acid-fast bacteria?

A

Once they are colorized with a red dye, they cannot be decolorized with acid solutions.

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11
Q

What is the most common head and neck mani-

festation of tuberculosis?

A

Cervical lymphadenopathy

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12
Q

What is the treatment of cervical lymphadenop-

athy associated with tuberculosis?

A

Isoniazid, rifampin, ethambutol, and pyrazinamide

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13
Q

What pathogen is associated with catscratch

disease?

A

Bartonella henselae

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14
Q

Name the three types of Langerhans cell histiocytosis.

A

● Eosinophilic granuloma
● Hand-Schüller-Christian (disseminated chronic)
● Letterer-Siwe (disseminated acute)

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15
Q

What condition manifests with the triad of osteolytic skull lesions, exophthalmos, and diabetes insipidus?

A

Hand-Schüller-Christian disease (disseminated chronic)

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16
Q

Which type of Langerhans cell histiocytosis is
associated with early in life onset and a rapidly
progressive course?

A

Letterer-Siwe (disseminated acute)

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17
Q

What is Lemierre syndrome?

A

Septic thrombophlebitis of the neck that most commonly
results from Fusobacterium necrophorum. It often begins
with pharyngitis progressing to lymphadenopathy, fevers,
chills, and rigors. Septic emboli may involve the lung, brain,
spleen, and liver, among other sites.

18
Q

What is the most common cause of pediatric

cervical lymphadenopathy?

A

Reactive lymphadenopathy from viral infection

19
Q

What is the most common cause(s) of pediatric

suppurative lymphadenopathy?

A

Group A Streptococcus and Staphylococcus aureus

20
Q

What is the test of choice for primary syphilis?

A

The FTA-ABS test evaluates for the presence of treponemal
antibodies. The test is positive in 90% of patients who seek
therapy for primary syphilis and remains positive for life.

21
Q

What are the symptoms of meningeal neuro-

syphilis?

A

Headache, nuchal rigidity, nausea, and vomiting. Cranial
nerve involvement is seen in 40% of patients resulting in
hearing loss, facial paralysis, and visual disturbances.

22
Q

What constitutes the Hutchinson triad of congenital syphilis?

A

Small notched teeth, deafness, and interstitial keratitis

23
Q

What test is most useful in establishing the diagnosis of neurosyphilis?

A

Reactive cerebrospinal fluid (CSF) VDRL and a CSF white

blood cell count of 20 cells/μL or greater

24
Q

What is the definition of otosyphilis?

A

The presence of a positive FTA-ABS in the setting of

unexplained sensorineural hearing loss

25
Q

What are the causes of syphilis-associated

hoarseness?

A

Laryngeal chancres, mucous membrane manifestations of
secondary syphilis involving the upper aerodigestive tract,
and gummata of the larynx may directly cause hoarseness.
Long-term syphilis may result in infraglottic stenosis,
adhesions between vocal folds or arytenoid fixation.
Neurosyphilis may result in recurrent laryngeal nerve
paresis.

26
Q

Describe the common initial symptoms of toxoplasmosis.

A

Fever, malaise, pharyngitis, and myalgias, with cervical

lymphadenopathy occurring in the most patients

27
Q

What are the pathogen, vector, and carrier

responsible for the development of tularemia?

A

Francisella tularensis, Amblyomma americanum (lone star tick), rabbits, and wild rodents, respectively

28
Q

What are the early symptoms of tularemia

infection?

A

Fever, headache, chills, myalgia, photophobia, diminished

visual acuity, and lymphadenopathy

29
Q

What are the possible side effects of amphotericin

B?

A

Nephrotoxicity, anemia, fever, chills, nausea, and vomiting

30
Q

What is the mechanism of action of the “azole”

antifungal medications?

A

Fungistatic. All azoles work by inhibiting a cytochrome P-

450–dependent enzyme that is required to convert lanosterol to ergosterol.

31
Q

What are the five recognized forms of fungal

sinusitis?

A

● Acute fulminant invasive fungal sinusitis
● Chronic invasive fungal sinusitis
● Granulomatous invasive fungal sinusitis
● Fungus ball
● Allergic fungal rhinosinusitis

32
Q

What is the most common causative organism in

chronic invasive fungal sinusitis?

A

Aspergillus fumigatus

33
Q

Describe the condition of HIV lymphadenopathy.

A
Diffuse lymphadenopathy (> 2 cm) involving two or more
extrainguinal sites for longer than 3 months. Two thirds of
patients infected with HIV will develop this syndrome
shortly after seroconversion.
34
Q

What are the anatomical boundaries of the deep

neck space involved in Ludwig angina?

A

The submandibular space is bound superiorly by the
mucosa of the floor of mouth, laterally and anteriorly by the
mandible, and inferiorly by the superficial layer of the deep
cervical fascia. It contains two divisions (sublingual and
submaxillary), separated by the mylohyoid muscle.

35
Q

How do submandibular infections spread to other deep neck space compartments?

A

Communication between potential spaces exists at the
buccopharyngeal gap, which connects the submandibular
and lateral pharyngeal spaces.

36
Q

Why is there a lack of trismus in patients suffering

from Ludwig angina?

A

Trismus develops from irritation of the masticatory muscles
(masseter and pterygoids), which insert into the mandibular
ramus. The submandibular space is not contiguous with
these muscles.

37
Q

What is the mechanism of airway compromise in

patients with Ludwig angina?

A

Increased swelling in the bilateral submandibular space
pushes the tongue superiorly and posteriorly, thereby
causing progressive airway obstruction.

38
Q

What is the best management of the airway in a

patient with a progressive infection of the submandibular space with increasing airway compromise?

A

Awake intubation or tracheostomy

39
Q

What is the most common causative organism in

necrotizing soft tissue infections?

A

Group A streptococcus

40
Q

What are the clinical characteristics of necrotizing

fasciitis?

A

Tense edema, pain disproportionate to examination, skin

discoloration, bullae, necrosis, and crepitus

41
Q

What is the treatment of necrotizing fasciitis?

A

Incision and drainage are inadequate. Necrotic tissue must be debrided and the wound left open with packing. Broad-
spectrum antibiotics should be administered, and the patient should be monitored in an intensive care unit
setting. Hyperbaric oxygen may provide additional benefit.

42
Q

Describe the clinical presentation of infectious

mononucleosis.

A

Fever, fatigue, generalized lymphadenopathy, splenomegaly,

and exudative pharyngitis with adenotonsillar hypertrophy