4 General Oto Flashcards

1
Q

1 Define sensitivity. (▶Fig. 4.1)

A

The ability of the test to identify correctly those patients with the disease TP/(TP+FN)

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2
Q

2 Define specificity.

A

The ability of the test to identify correctly those patients without the disease TN/(TN+FP)

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3
Q

3 Is high sensitivity or high specificity most important for a screening test?

A

Sensitivity

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4
Q

4 Define a type 1 error.

A

The chance of testing positive among those without the condition; false-positive rate = 1 specificity.

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5
Q

5 Define a type 2 error.

A

The chance of testing negative among those with the condition; false negative rate = 1-sensitivity.

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6
Q

6 Define positive predictive value.

A

The chance of having the condition among those that test positive TP/(TP+FP)

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7
Q

7 Define negative predictive value.

A

The chance of not having the condition among those that test negative TN/(TN+FN)

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8
Q

8 A cervical spine X-ray revealing a greater than 5- mm widening of the predentate space (between the anterior surface of the dens and the posterior surface of the C1 tubercle) is worrisome for what traumatic injury?

A

Atlantoaxial dissociation

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9
Q

9 Conventional radiography of the facial bones and neck has been largely replaced by computed tomography (CT). What traditional views were used to view the following:

  • Frontal, maxillary, and sphenoid sinus
  • Frontal sinuses, posterior ethmoid air cells, orbital floors
  • Maxillary sinuses, anterior ethmoid air cells, orbital floors
  • Sphenoid sinuses, anterior and posterior walls of the frontal sinuses
  • Soft tissue of the neck
A
  • Lateral view (5 degrees off true lateral)
  • Caldwell view (15 degrees off caudal angulation)
  • Waters view (neck in 33 degrees of extension)
  • Submentovertex view (anteroposterior [AP] projection, head in 90 degrees of extension)
  • AP and lateral views
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10
Q

10 In a stable pediatric patient with stridor, what radiography is appropriate?

A

AP and lateral neck films to evaluate for retropharyngeal abscess, croup, epiglottitis, and radiopaque foreign body

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11
Q

11 What are the most common findings on chest radiography in a patient with a witnessed foreign body aspiration and clinical signs suggestive of aspiration?

A

Mediastinal shift, unilateral hyperinflation, atelectasis, and a foreign object if radiopaque

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12
Q

12 Although they have been largely replaced by CT scan, radiographs of the temporal bone are occasionally necessary. Name the following views:

  • Lateral view of the mastoid with 30 degrees of cephalocaudad angulation
  • View of the petrous apex with patient facing the film, head slightly flexed and turned 45 degrees opposite the film
  • Comparison of both mastoid bones and petrous pyramids via AP view with a 30-degree tilt
A
  • Schüller view
  • Stenvers view
  • Towne view
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13
Q

13 Why is a CT scan typically a more appropriate imaging study in evaluating patients with a potential deep neck space infection instead of magnetic resonance imaging (MRI)?

A

Although MRI provides better soft tissue definition, it is expensive and requires a lengthy scan time compared with CT and therefore may necessitate sedation of a child or a distressed patient and increase the likelihood of airway compromise.

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14
Q

14 On T1-weighted MRI, contrast-enhancing tumors may be hidden by surrounding fat. What technique can be used to achieve better visualization of the tumor?

A

Fat suppression

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15
Q

15 Describe the T1-weighted appearance of water and fat on MRI.

A

Low intensity and high intensity, respectively

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16
Q

16 What are some of the contraindications to MRI use?

A

Electromagnetic force can cause serious malfunction to cardiac pacemakers and cochlear implants (although new techniques have been developed that allow cochlear implant recipients the ability to have MRI studies). Some older vascular clips and ossicular prostheses contain paramagnetic components, and unless these are known to be MRI compatible, another modality should be used.

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17
Q

17 What does SUV stand for in regard to positron emission tomography (PET) imaging?

A

Standardized uptake value, which provides a semiquantitative index of radio tracer uptake

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18
Q

18 What does the presence of an echogenic (fatty) hilum typically indicate during ultrasound examination of the neck?

A

Benign disease. Normal lymph nodes have an echogenic hilum, whereas it is reported that there is an absent hilum in 96 of metastatic lymph nodes.

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19
Q

19 Can the location of normal parathyroid glands be identified on ultrasound examination of the thyroid and neck?

A

Normal parathyroid glands are not usually visible because of their small size and similar echo texture to adjacent thyroid tissue.

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20
Q

20 What is acoustic shadowing in ultrasound imaging?

A

Diminished sound or loss of sound posterior to a strongly reflecting or attenuating structure

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21
Q

21 Review the differences between first-generation and second-generation antihistamines.

A

Compared with first-generation antihistamines, second-generation medications generally have a longer duration of action, have less central nervous system (CNS) penetration, and are less sedating.

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22
Q

22 Review contraindications to glucocorticoid steroid use.

A

Psychosis, severe diabetes, peptic ulcer disease, congestive heart failure, severe hypertension, systemic tuberculosis, osteoporosis

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23
Q

23 Describe the features of ototoxicity associated with salicylate use.

A

Reversible sensorineural hearing loss and tinnitus, hypothesized to result from disruption of oxidative phosphorylation. Its use does not produce histologic changes.

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24
Q

24 What severe neurologic side effect is associated with intramuscular administration of prochlorperazine?

A

Extrapyramidal side effects including focal dystonia

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25
Q

25 List the different amide and ester local anesthetics.

A

Amides have two “i’s,” whereas esters only have one “i” in their generic name. Examples of esters include benzocaine, cocaine, and tetracaine. Examples of amides include bupivacaine, lidocaine, and mepivacaine. Esters are more likely to cause an allergic reaction

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26
Q

26 What topical anesthetic reversibly binds to and inactivates sodium channels, thus inhibiting excitation of nerve endings and causing vasoconstriction?

A

Cocaine

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27
Q

27 What is the maximum dose of lidocaine hydrochloride?

A

4 to 5 mg/kg, maximum total dose of 300mg

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28
Q

28 What medication can be given to reverse the effects of local injectable epinephrine?

A

Local infusion of 1.5 to 5mg of phentolamine

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29
Q

29 What is the mechanism of action for β-lactam antibiotics?

A

Binds to DD-transpeptidase (also called penicillin-binding protein) and inhibits the formation of peptidoglycan crosslinks in the bacterial cell wall

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30
Q

30 What is the mechanism for acquiring penicillin resistance?

A

Enzymatic deactivation of penicillin G through β-lactamases and altered penicillin binding proteins

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31
Q

31 What is the mechanism of action of aminoglycosides?

A

They irreversibly bind to the 30S ribosome and freeze the 30S initiation complex. Additionally, they cause misreading of the mRNA code (bactericidal).

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32
Q

A mutation in which a gene may lead to increased aminoglycoside toxicity even at low doses?

A

Mitochondrial 12S ribosomal RNA gene

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33
Q

33 What are the earliest signs of aminoglycoside ototoxicity?

A

Tinnitus, high-frequency hearing loss, and dizziness

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34
Q

34 What is the mechanism of action of macrolides?

A

They inhibit translocation of the peptidyl tRNA from the A to the P site on the ribosome by binding to the 50S ribosomal RNA (bacteriostatic).

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35
Q

35 What is the treatment of Clostridium difficile colitis?

A

IV or oral (PO) metronidazole or PO vancomycin

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36
Q

36 What are the most common antibiotics that have been implicated in the development of C. difficile colitis?

A

Second- and third-generation cephalosporins, ampicillin/ amoxicillin, and clindamycin

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37
Q

37 A child develops gray staining of the teeth with a prominent horizontal line across the upper and lower teeth after being prescribed an antibiotic. Which antibiotic was most likely prescribed?

A

Tetracycline

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38
Q

38 What is the mechanism of action of aspirin?

A

Irreversible acetylation of serine 529 of cyclooxygenase (COX) 1. Rapid onset of action if dose is 160mg or greater. The effects of use last for the lifetime of the platelet, which is 7 to 10 days.

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39
Q

39 What is the mechanism of action of thienopyradines (e.g., clopidogrel bisulfate)?

A

Irreversible inhibition of the cysteine residue of the P2Y12 platelet receptor. Onset of action is rapid if patient is given a loading dose, and the effects last for the lifetime of the platelet (7 to 10 days).

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40
Q

40 What drug can be given to reverse the antiplatelet effects of nonsteroidal anti-inflammatory drugs (NSAIDs)?

A

Desmopressin acetate (DDAVP)

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41
Q

41 In the event of significant bleeding following administration of heparin, what medication should be considered?

A

Protamine. Give 1mg for every 100 units of heparin, and closely monitor activated partial thromboplastin time (aPTT).

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42
Q

42 What is the mechanism of action of warfarin?

A

It is a vitamin K antagonist that inhibits the production of vitamin K-dependent clotting factors.

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43
Q

43 Describe the mechanism of malignant hyperthermia.

A

It is caused by a combination of a volatile inhalational anesthetic (commonly halothane) and the short-acting paralytic succinylcholine. An abnormal ryanodine receptor causes overwhelming amounts of calcium to be released from the sarcoplasmic reticulum of skeletal muscle, thereby initiating prolonged and intense muscle contraction.

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44
Q

44 What is the initial treatment for malignant hyperthermia?

A

Stop the anesthetic, give dantrolene (which prevents the release of calcium from endoplasmic reticulum), increase oxygen, and initiate cooling measures including ice packs.

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45
Q

45 What are the physical examination findings of cardiac tamponade?

A

Tachycardia, paradoxical pulse with respirations, hypotension, jugular vein distension, muffled cardiac sounds, decreased QRS amplitude on electrocardiogram (ECG)

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46
Q

46 What are the four basic classifications of shock?

A
  • Hypovolemic shock: Loss of blood volume
  • Obstructive shock: Decreased circulation resulting from external or intrinsic compression
  • Septic shock: Related to vascular dilation
  • Cardiogenic shock: Impaired perfusion from lack of sufficient cardiac output
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47
Q

47 What is the formula describing the rate of fluid maintenance for the pediatric patient?

A

The 4:2:1 rule = 4 mL/kg hourly for the first 10 kg, adding 2 mL/kg per hour for the second 10 kg, and adding 1 mL/kg per hour for each kilogram over 20 kg

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48
Q

48 What is the formula used to calculate the rate of fluid resuscitation of a burn victim?

A

The Parkland formula: Fluid for the first 24 hours (milliliter) = 4 x patient weight (kg) x % body surface area involved; the first half is given over 8 hours, the second half over the remaining 16 hours. Rule of 9’s for determining percentage of burned: 9% = head, each arm; 18% = chest, back, each leg

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49
Q

49 What preoperative condition is associated with immunosuppression, poor wound healing, decreased basal metabolic rate, longer hospitalization, and an increased mortality rate?

A

Preoperative malnutrition

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50
Q

50 Why should gastric residuals be checked every 4 hours in a patient receiving enteral nutrition via tube feeds?

A

Regurgitation and aspiration are risks of tube feeding

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51
Q

51 What is involved in the refeeding syndrome that is observed in severely malnourished patients following initiation of feeds?

A

Malnourishment leads to hypoinsulinemia and electrolyte abnormalities including intracellular hypophosphatemia. Within 4 to 5 days of reinitiation of carbohydrate metabolism and subsequently increased insulin production, patients can develop severe hypophosphatemia.

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52
Q

52 You are rounding on a patient who underwent major surgery for polytrauma and required 20 units of packed red blood cells. The patient is complaining of perioral numbness and tingling. What is the likely diagnosis and treatment?

A

Citrate toxicity with subsequent hypocalcemia. Treat with calcium gluconate. This should be given for symptomatic patients only.

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53
Q

53 What medications can be given as pretreatment to prevent mild hypersensitivity and nonhemolytic febrile reactions in a patient receiving blood transfusion with a history of mild reactions?

A

Acetaminophen and antihistamines such as diphenhydramine

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54
Q

54 What complications may be encountered in a patient who has received massive intraoperative transfusions?

A

Volume overload, hyperplasia or hypokalemia, hyperammonemia, acidosis, thrombocytopenia, coagulation factor depletion, coagulopathy, hypothermia, transfusion related acute lung injury, and citrate toxicity

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55
Q

55 What is transfusion-related acute lung injury?

A

Acute respiratory distress and noncardiogenic pulmonary edema that develops during or within 6 hours of blood transfusion. Treatment includes supportive measures, often including mechanical ventilation, high-inspired oxygen, and positive end expiratory pressures.

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56
Q

56 Mechanical ventilation is most commonly delivered via positive-pressure ventilation (PPV). What are the two most common subtypes of PPV that focus on the transition from inspiration to expiration?

A

● Volume control: A set volume is delivered per breath ● Pressure control: A set pressure is delivered per breath

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57
Q

57 What common rule can be used to select the tidal volume and rate for a patient on assist control mechanical ventilation?

A

12–12 rule: 12 mL/kg of lean body mass delivered 12 times a minute. It is useful for patients without preexisting lung disease. It must be adjusted for patients with known chronic obstructive pulmonary disease (COPD), etc.

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58
Q

58 What technique can be used in mechanical ventilation to maintain a patient’s airway pressure above atmospheric pressure at the end of expiration?

A

Positive end expiratory pressure (PEEP)

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59
Q

59 What is the difference in the 1-second forced expiratory volume FEV1 to vital capacity (FVC) ratio in COPD compared with that in restricted lung disease?

A

In COPD, the FEV1/FVC ratio decreases, whereas the ratio is preserved or increased in restrictive lung disease.

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60
Q

60 Describe the difference between the two types of postobstructive pulmonary edema.

A

● Type 1. Follows an acute severe cause of upper airway obstruction (epiglottitis, laryngospasm, strangulation) and usually manifests within 1 hour of the event ● Type 2. Follows relief from a chronic obstruction (obstructive sleep apnea (OSA), choanal stenosis, subglottic stenosis) and usually manifests within 6 hours of reversing the obstruction

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61
Q

61 What is the treatment of postobstructive pulmonary edema?

A

Oxygen and supportive care in mild cases and PEEP in more severe cases. Diuretic therapy can be instituted, although the benefit is not clear.

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62
Q

62 What is the most common cause of fever in the immediate postoperative period?

A

Within the first 48 hours of surgery, fever is likely due to an inflammatory reaction to surgical insult or reaction to medication or blood product given intraoperatively. It is unlikely to be infectious. Evaluate for possible source of infection, but prophylactic antibiotics are not indicated. Patient may be treated with antipyretic and monitor for change in clinical status.

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63
Q

63 In the acute postoperative setting, how can the mnemonic “Wind, Water, Walk, Wound, Wonder Drugs, What did you do?” help in the evaluation of a febrile patient?

A

● Wind: Pneumonia? Aspiration? Atelectasis? ● Water: Urinary tract infection? ● Walk: Thrombophlebitis? Deep venous thrombosis? Pulmonary embolus? ● Wound: Surgical-site infection? ● Wonder drugs: Drug reaction (β-lactam antibiotic? Sulfa antibiotic?) ● What did we do? Catheter-related infection? IV site infection?

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64
Q

64 What is eosinophilic granuloma?

A

Eosinophilic granuloma is the most common form of Langerhans cell histiocytosis and is characterized by the formation of solitary or multiple discrete nodules within bones.

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65
Q

65 What is Hand-Schüller-Christian disease?

A

It is multifocal Langerhans cell histiocytosis with bone “granulomas,” associated with the triad of exophthalmos, lytic skull lesions, and diabetes inspidus.

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66
Q

66 True or false. Most patients with Langerhans cell histiocytosis have multisystem disease.

A

False. Approximately two-thirds of patients have disease involving one site.

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67
Q

67 What is Letterer-Siwe disease?

A

Systemic Langerhans cell histiocytosis is the rarest (~ 10% of cases) and the most severe form of disease. Initial symptoms often include generalized skin eruption, anemia, and hepatosplenomegaly.

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68
Q

68 Extranodal natural killer cell (NK)/T-cell lymphoma, nasal type, is commonly associated with which virus?

A

Epstein-Barr virus

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69
Q

69 How is extranodal NK/T-cell lymphoma, nasaltype, commonly treated?

A

Chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) in conjunction with radiotherapy

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70
Q

70 Compared with other types of lymphoma involving the head and neck, what is the prognosis for extranodal NK/T-cell lymphoma, nasal type?

A

Much poorer

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71
Q

71 What is the most common laryngeal manifestation of Wegener granulomatosis?

A

Subglottic stenosis

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72
Q

72 What is the most common otologic manifestation of Wegener granulomatosis?

A

Serous otitis media

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73
Q

73 What histopathologic findings are seen in Wegener disease?

A

Necrotizing granulomas and arteritis involving small vessels

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74
Q

74 What laboratory test is used to diagnose and follow Wegener disease?

A

Antineutrophil cytoplasmic antibody (C-ANCA). Test will be positive in more than 90% of cases.

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75
Q

75 What histopathological findings are seen in sarcoidosis?

A

Noncaseating granulomas

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76
Q

76 What condition is characterized by uveitis, parotid swelling, fever, and facial nerve palsy?

A

Heerfordt syndrome (uveoparotid fever), a manifestation of sarcoidosis

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77
Q

77 What is the most common site of laryngeal involvement of sarcoidosis?

A

Supraglottis

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78
Q

78 What is the most common head and neck manifestation of sarcoidosis?

A

Cervical lymphadenopathy

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79
Q

79 Describe a common presentation for pyogenic granuloma.

A

Less than 1-cm lobular red or purple lesion that develops on the gingiva or nasal mucosa that is friable and prone to bleeding. It occurs more commonly in women and is associated with trauma and pregnancy.

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80
Q

80 Describe the treatment of pyogenic granuloma.

A

Lesions frequently resolve spontaneously when associated with pregnancy. If frequent bleeding or cosmesis is a concern, conservative cauterization or excision can be pursued.

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81
Q

81 Describe the natural history of untreated necrotizing sialometaplasia.

A

Spontaneous resolution over weeks to months

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82
Q

82 How does blastomycosis typically manifest?

A

A common triad includes cutaneous disease, pulmonary involvement, and constitutional symptoms. Skin lesions may involve the face with verrucous growth and scarring. Oropharyngeal and laryngeal involvement are rare.

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83
Q

83 Describe the clinical manifestations of coccidiomycosis.

A

It is the cause of “valley fever.” Most patients have an influenza-like illness that includes malaise, fever, myalgia, arthralgia, and cough. Initial symptoms are pulmonary, mucocutaneous involvement with maculopapular rash, cervical lymphadenopathy, and/or meningeal involvement.

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84
Q

84 Where is Coccidioides immitis endemic?

A

Desert Southwest including New Mexico, Nevada, California, Texas, Utah, and northern Mexico

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85
Q

85 Histoplasmosis most commonly occurs in which geographic location?

A

The Ohio, Missouri, and Mississippi River valleys

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86
Q

86 Describe the head and neck manifestations of disseminated histoplasmosis.

A

Granulomatous lesions involving the lips, gingiva, tongue, larynx, and pharynx manifesting with painful ulcers containing heaped edges

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87
Q

87 What is the most common site of laryngeal involvement of histoplasmosis?

A

Supraglottis

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88
Q

88 How is histoplasmosis diagnosed?

A

Histoplasma antibody latex agglutination test, fungal stains, blood or urine antigens using enzyme-linked immunosorbent assay or polymerase chain reaction (PCR), or histoplasma skin test

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89
Q

89 What pathogen is responsible for the development of rhinosporidiosis?

A

The parasite Rhinosporidium seeberi

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90
Q

90 What are the common head and neck clinical manifestations of rhinosporidiosis?

A

Fleshy, friable strawberry-like lesions most commonly involving the inferior turbinate, oropharynx, conjunctiva, and perineum

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91
Q

91 What is the treatment for rhinosporidiosis?

A

Wide local excision or prolonged dapsone therapy

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92
Q

92 What is the causative organism in syphilis?

A

The spirochete Treponema pallidum

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93
Q

93 What is the treatment of syphilis?

A

Penicillin G benzathine

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94
Q

94 Describe the presentation of primary syphilis.

A

A painless ulcer (chancre) at the site of transmission demonstrating a rolled edge and punched-out base is present after 3 to 6 weeks at the site of exposure.

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95
Q

95 Describe the presentation of secondary syphilis.

A

Secondary syphilis is characterized by systemic spread of disease with manifestations including fever, myalgias, arthralgias, and lymphadenopathy. A mucocutaneous rash often develops including the oral mucosa and the palms and soles. Finally, condyloma lata and patchy alopecia may develop.

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96
Q

96 What are the three categories of tertiary syphilis?

A

The three categories are gummatous syphilis, cardiovascular syphilis, and neurosyphilis.

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97
Q

97 Describe the findings of congenital syphilis.

A

“Snuffles” with sinonasal drainage, saddle nose, saber shins, Hutchinson teeth, and mulberry molars

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98
Q

98 Describe the Argyll-Robertson pupil.

A

A pupil that does not react to light but does constrict during accommodation. Associated with syphilis

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99
Q

99 Describe the manifestation of otosyphillis.

A

Otosyphilis is associated with either congenital or tertiary acquired syphilis and manifests with sensorineural hearing loss beginning in the high frequencies, fluctuating tinnitus, and vertigo.

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100
Q

100 What is the Hennebert sign?

A

Rotary nystagmus when positive or negative pressure is applied to the tympanic membrane

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101
Q

101 Describe the Jarisch-Herxheimer reaction.

A

After treatment of syphilis, dying spirochetes may trigger a cytokine cascade that manifests with myalgias, fever, headache, and tachycardia.

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102
Q

102 What tests are commonly used for syphilis screening?

A

Venereal Disease Research Laboratory (VDRL), rapid plasma reagin (RPR) test

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103
Q

103 What confirmatory test should be ordered after a positive or equivocal screening test for syphilis?

A

FTA-ABS

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104
Q

104 What is the most common cause of subacute pediatric cervical lymphadenopathy?

A

Atypical Mycobacterium, most commonly M. avium-intracellulare, M. haemophilum, and M. scrofulaceum

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105
Q

105 How is brucellosis transmitted?

A

It is transmitted from contaminated meat or dairy products or via direct contact through broken skin.

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106
Q

106 What are the clinical manifestations of cat-scratch disease?

A

The primary lesion develops as an erythematous, nonpruritic pustule 1 week affter inoculation. Lymphadenitis of the axilla, neck, and inguinal region commonly develops 2 to 4 weeks after exposure. Suppuration with acute tenderness and fever frequently occurs. Lymphadenopathy usually resolves over 2 weeks but may persist for up to 2 years.

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107
Q

107 What are the pathogens associated with leprosy (Hansen disease)?

A

Mycobacterium leprae and Mycobacterium lepromatosis

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108
Q

108 What is the treatment for Hansen disease?

A

Dapsone

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109
Q

109 What pathogen is responsible for the development of rhinoscleroma?

A

Klebsiella rhinoscleromatis

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110
Q

110 What histologic findings are strongly suggestive of the diagnosis of rhinoscleroma?

A

Russell bodies (immunoglobulin containing inclusions in plasma cells), pseudoepitheliomatous hyperplasia, Mikulicz cells (foamy histiocytes containing Klebsiella)

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111
Q

111 What is the treatment for rhinoscleroma?

A

Tetracycline or ciprofloxacin

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112
Q

112 What tests are helpful in diagnosing systemic lupus erythematosus?

A

Antinuclear antibody (ANA), anti-Sm, anti-DNA, anti-ribonuclear protein (anti-RNP), and anticardiolipin antibody

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113
Q

113 What are the typical clinical manifestations of a patient with mixed connective tissue disease?

A
  1. Raynaud phenomenon
  2. Arthralgias
  3. Inflammatory myopathy
  4. Lymphadenitis
  5. Skin or mucosal lesions
  6. Serositis
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114
Q

114 What is the definition of mixed connective tissue disease?

A

Mixed connective tissue disease is characterized by a combination of overlapping features of systemic lupus erythematous, scleroderma, and polymyositis. Patients may manifest Raynaud phenomenon, arthralgias, inflammatory myopathy, lymphadenitis, skin or mucosal lesions, and serositis.

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115
Q

115 Which joints in the head and neck are most commonly affected by rheumatoid arthritis (RA)?

A

RA can affect any diarthrodial joint, including the temporomandibular, cricoarytenoid, and ossicular joints.

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116
Q

116 What does the acronym CREST stand for?

A

Calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasias. CREST syndrome is a limited cutaneous form of systemic scleroderma.

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117
Q

117 What are the histologic findings in a minor salivary gland lip biopsy performed in a patient with Sjogren disease?

A

Focal lymphocytic infiltrate with atrophic acini

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118
Q

118 What head and neck sites are commonly affected by relapsing polychondritis?

A

Ear, nasal septum, and larynx

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119
Q

119 What is the most common head and neck manifestation of relapsing polychondritis?

A

Episodic auricular chondritis, presenting with erythema and pain of the pinna with sparing of the fatty lobule. Eventually presents in ~ 90% of patients

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120
Q

120 What are common symptoms of giant cell arteritis?

A

Headache (predominantly temporal region), jaw claudication (~ 50% patients), vision loss or visual disturbance, fatigue, general malaise, fever, anorexia, weight loss, night sweats, and tongue pain

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121
Q

121 What histologic finding on temporal artery biopsy is suspicious for giant cell arteritis?

A

Inflammatory infiltrates in at least the adventitia and media, with elastic lamina fragmentation

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122
Q

122 What imaging study may be useful in the diagnosis of giant cell arteritis?

A

Duplex ultrasound. High-resolution MRI has been reported to have very similar diagnostic power, but more data are needed before it can be recommended as a diagnostic tool.

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123
Q

123 What is the classic triad of Wegener granulomatosis?

A

Granulomas of the respiratory tract, progressive glomerulonephritis, and necrotizing vasculitis of small to mediumsized arteries and veins

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124
Q

124 What condition is characterized by uveitis, oral aphthous ulcers, and genital ulcers?

A

Behçet disease

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125
Q

125 What are the two primary fascia networks of the neck? (▶Fig. 4.2)

A

Superficial cervical fascia and the deep cervical fascia

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126
Q

126 Describe the anatomy of the superficial cervical fascia.

A

It lies just deep to the dermis and superficial to the deep cervical fascia. It extends from the zygoma to the clavicle and envelops the platysma and muscles of facial expression.

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127
Q

127 Describe the anatomy of the deep cervical fascia.

A

It is composed of the superficial (investing), middle (visceral and muscular), and deep (prevertebral and alar) layer. The carotid sheath fascia is created by all three layers of the deep cervical fascia.

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128
Q

128 Describe the anatomy of the superficial (investing) layer of the deep cervical fascia.

A

It surrounds the neck and inserts superiorly at the nuchal ridge, mastoid, zygoma, and mandible and inferiorly at the clavicles, sternum, scapula, and acromion. It envelops the sternocleidomastoid muscle, trapezius, muscles of mastication, submandibular glands, and parotid gland. Inferiorly, its manubrial insertion splits to form the suprasternal space of Burns.

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129
Q

129 Describe the anatomy of the middle (visceral and muscular) layer of the deep cervical fascia.

A

It extends superior to the cranial base and inferiorly to the upper mediastinum. It is subdivided into the muscular and visceral layers. The muscular division surrounds the infrahyoid strap muscles; the visceral portion surrounds the pharyngeal constrictors, esophagus, trachea, and thyroid and creates the buccopharyngeal fascia. Both divisions contribute to the carotid sheath.

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130
Q

130 Describe the anatomy of the deep (prevertebral and alar) layer of the deep cervical fascia.

A

It is subdivided into the alar and prevertebral fascia. Both extend superiorly from the cranial base, but the alar fascia fuses with the middle cervical fascia and extends into the upper mediastinum, and the prevertebral fascia extends to the level of the coccyx. The alar fascia and prevertebral fascia fuse at the vertebral transverse processes and after joining, envelop the paraspinous muscles.

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131
Q

131 Describe the anatomy of the suprasternal space (space of Burns).

A

The inferior insertion of the superficial (investing) fascia splits just above the manubrium attaching anterior to the manubrium and posteriorly to the interclavicular ligament. This small potential space contains a portion of the anterior jugular veins, and the sternal heads of the sternocleidomastoid muscle.

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132
Q

132 Define the boundaries of the buccal space.

A

The buccal space is created by the buccinator muscle medially; the superficial layer of the deep cervical fascia and the muscles of facial expression laterally and anteriorly; and the muscles of mastication, mandible, and parotid gland posteriorly. It primarily contains adipose tissue (buccal fat pad), minor salivary glands, accessory parotid tissue, and facial/buccal arteries, veins, and lymphatics. The buccal fat pad is pierced by the parotid duct as it courses to the buccinator and eventually enters the mouth opposite the second upper molar.

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133
Q

133 Define the mechanism of spread of infection (or tumor) to and from the buccal space.

A

It permits spread between the mouth, parotid space, and masticator space from deficient fascial compartmentalization along the superior, inferior, and posterior limits.

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134
Q

134 Define the boundaries of the carotid space.

A

The carotid sheath contains the carotid artery, internal jugular vein, vagus nerve, and jugular lymphatic chain. All three divisions of the deep cervical fascia form the carotid sheath. It extends from the skull base to the mediastinum; anteriorly lies the sternocleidomastoid muscle, posteriorly the prevertebral space, and medially the visceral compartment.

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135
Q

135 Review the risk factors for carotid blowout.

A

Radiation, salivary fistula, malnutrition, hypothyroidism, Tincision over the great vessels, radical neck dissection

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136
Q

136 Define the boundaries of the danger space.

A

The danger space is a potential space that rests between the alar fascia and the prevertebral fascia. Infections in this area can communicate with the thorax (mediastinum) to the level of the diaphragm.

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137
Q

137 Define the boundaries of the masticator space.

A

The masticator space is created from the superficial layer of the deep cervical fascia surrounding the masseter laterally and the pterygoid muscles medially. It contains masseter muscle, pterygoid muscles, inferior tendon of the temporalis muscle, ramus, and posterior body of the mandible, internal maxillary artery, and the inferior alveolar neurovascular bundle.

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138
Q

138 Define the boundaries of the parapharyngeal space. (▶Fig. 4.3)

A

It is shaped as an inverted pyramid with the base at the cranial base and the apex at the hyoid bone. Anteriorly, it is bound by the pterygomandibular raphe, posteriorly be the prevertebral fascia, medially by the superior pharyngeal constrictor, and laterally by the parotid, mandible, and lateral pterygoid.

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139
Q

139 How is the parapharyngeal space commonly divided?

A

Prestyloid and poststyloid compartments are divided by the tensor-vascular-styloid fascia connecting the tensor veli palatini and the styloid process.

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140
Q

140 What structures are contained within the prestyloid space?

A

Fat, lymph nodes, minor salivary gland tissue, internal maxillary artery, and the inferior alveolar, auriculotemporal and lingual nerves

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141
Q

141 What structures are contained within the poststyloid space?

A

Carotid artery, internal jugular vein, cranial nerves 9 through 12, and the superior sympathetic chain

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142
Q

142 What is the syndrome that follows the parapharyngeal space or parotid surgery that causes pain with the onset of eating?

A

First-bite syndrome

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143
Q

143 Define the boundaries of the parotid space.

A

It is created by the superficial layer of deep cervical fascia as it surrounds the mandible and parotid gland and contains the parotid gland and parotid lymph nodes, the facial nerve, posterior facial vein, and facial artery.

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144
Q

144 Describe the mechanism of infection or tumor spread from the parotid space to the parapharyngeal space.

A

The superomedial parotid space fascia is deficient, allowing for direct spread into the parapharyngeal space via the stylomandibular tunnel.

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145
Q

145 Define the boundaries of the peritonsillar space.

A

It is bound by the palatine tonsil medially and the superior pharyngeal constrictor, palatoglossus, and palatopharyngeus medially, superiorly, inferiorly, anteriorly, and posteriorly. It contains loose areolar tissue and minor salivary glands.

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146
Q

146 Define the boundaries of the prevertebral space.

A

It extends from the skull base to the coccyx and is bordered anteriorly by the prevertebral fascia, posteriorly by vertebral bodies, and laterally by the transverse processes of vertebrae.

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147
Q

147 Describe the sequential layers and spaces (superficial to deep) of the posterior pharyngeal wall.

A

Mucosa, pharyngeal constrictor, buccopharyngeal fascia, retropharyngeal space, alar fascia, danger space, prevertebral fascia, prevertebral space

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148
Q

148 Define the boundaries of the sublingual space.

A
  • Contains the sublingual gland, Wharton duct, and lingual and hypoglossal nerves
  • Boundaries
    • Superiorly: mucosa of FOM
    • Laterally: mandible
    • Inferiorly: mylohyoid
    • Medially: genioglossus
    • Anteriorly: mandible.
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149
Q

149 What are the two divisions of the submandibular space?

A

It is subdivided into the sublingual and submaxillary spaces, which are separated by the mylohyoid. These two spaces communicate at approximately the second molar.

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150
Q

150 Define the boundaries of the submaxillary (submylohyoid) space.

A

It contains the submandibular gland and is bound superiorly and medially by the mylohyoid muscle, inferiorly and posteriorly by the digastric muscle, and laterally and anteriorly by the superficial layer of the deep cervical fascia and mandible.

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151
Q

151 Define the boundaries of the infratemporal fossa. (▶Fig. 4.4)

A

● Located inferior and medial to the zygomatic arch ● Anterior: Posterolateral portion of maxillary sinus ● Lateral: Ramus of the mandible ● Medial: Lateral pterygoid plate ● Superior: Greater wing of the sphenoid bone ● Inferior: Medial pterygoid muscle ● Posterior: Articular tubercle of the temporal bone, glenoid fossa

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152
Q

152 Describe the branches of the three segments of the internal maxillary artery. (▶Fig. 4.5)

A

● First (lateral) portion: Deep auricular artery, anterior tympanic artery, middle meningeal artery, inferior alveolar artery, accessory meningeal artery ● Second (middle) portion: Masseteric artery, pterygoid branches, anterior and posterior deep temporal arteries, buccal artery ● Third (medial) portion: Sphenopalatine artery (terminal branch), descending palatine artery, infraorbital artery, artery of the vidian canal, anterior, middle, and posterior superior alveolar artery

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153
Q

153 Define the boundaries of the pterygopalatine fossa.

A

● Located medial to the infratemporal fossa ● Anterior: Posteromedial portion of maxillary sinus ● Lateral: Pterygomaxillary fissure and infratemporal fossa ● Medial: Perpendicular plate of the palatine bone ● Superior: Body of the sphenoid bone ● Inferior: Pterygopalatine canal ● Posterior: Root of the pterygoid plates

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154
Q

154 Name the foramina communicating with the pterygopalatine fossa.

A

● Anterior: Inferior orbital fissure ● Lateral: Pterygomaxillary fissure ● Medial: Sphenopalatine foramen ● Interior: Greater palatine canal ● Posterior: Vidian canal, foramen rotundum

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155
Q

155 What important structure may be encountered if the vidian canal is followed posteriorly?

A

The second genu of the internal carotid artery

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156
Q

156 Define the boundaries of the temporal fossa.

A

It is located between the superficial layer of the temporalis fascia and the periosteum of the squamosal portion of the temporal bone and is subdivided into the superficial and deep layer by the temporalis muscle. It contains the internal maxillary artery and inferior alveolar nerve.

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157
Q

157 During submandibular gland excision, the marginal mandibular nerve cannot be readily identified. What strategy can be used to decrease the risk of marginal mandibular nerve injury?

A

The common facial vein can be identified low, ligated, and divided and then reflected superiorly because the marginal mandibular nerve rests superficial to the common facial vein and facial artery in the region of the mandibular notch.

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158
Q

158 Describe the location and course of the hypoglossal and lingual nerves in the region of the submandibular gland.

A

It is located deep to the digastric muscle and mylohyoid and superficial to the hypoglossus muscle. The lingual nerve is located cephalad to the hypoglossal nerve.

159
Q

159 What landmarks can be used for identification of the accessory nerve during level 2 neck dissection?

A

Transverse process of C1, anterolateral to the internal jugular vein, two fingerbreadths below the mastoid tip, or just as it runs posterior to the sternocleidomastoid 1 to 2cm above the Erb point

160
Q

160 Describe the location of the phrenic nerve and superior sympathetic chain.

A

It is located anterior to the anterior scalene muscle. The phrenic nerve runs lateral to the sympathetic chain.

161
Q

161 The hypoglossal nerve is “pinned” by what artery as it descends behind the digastric muscle?

A

The occipital artery

162
Q

162 Describe five methods or landmarks for identifying the facial nerve during parotidectomy.

A

The tragal pointer, tympanomastoid suture line, level of the digastric groove (posterior digastric muscle), retrograde from marginal mandibular nerve at mandibular notch, anterograde from the vertical segment of the mastoid

163
Q

163 During deep-lobe parotidectomy, what arteries must be divided for en bloc removal?

A

External carotid artery, superficial temporal artery, internal maxillary artery

164
Q

164 Which cervical rootlets contribute to the ansa cervicalis?

A

C1, C2, and C3

165
Q

165 Which deep neck spaces involve the entire length of the neck?

A

Four: the retropharyngeal, danger, prevertebral, and carotid spaces

166
Q

166 Describe the parasympathetic innervation to the parotid gland.

A

Inferior salivatory nucleus → cranial nerve IX (Jacobson nerve) → lesser superficial petrosal nerve → otic ganglion → auriculotemporal nerve (V3) → parotid gland

167
Q

167 Describe the parasympathetic innervation to the submandibular gland and sublingual glands.

A

Superior salivatory nucleus → nervus intermedius → cranial nerve VII → chorda tympani → lingual nerve → submandibular ganglion → submandibular gland

168
Q

168 Describe the parasympathetic innervation to the lacrimal gland.

A

Superior salivatory nucleus → greater superficial petrosal nerve → vidian nerve → sphenopalatine ganglion → lacrimal branch V1 → lacrimal gland

169
Q

169 Describe the condition of benign symmetric lipomatosis (location, sex, comorbidities).

A
  • Diffuse lipomatosis of the head, neck, shoulders, and proximal upper extremities.
  • M>F
  • Hx alcoholism and diabetes.
170
Q

170 True or False. Most liposarcomas develop from a preexisting benign lipoma.

A

False. Most liposarcomas develop de novo.

171
Q

171 What is the most common type of monomorphic adenoma?

A

Basal cell adenoma

172
Q

172 What is the most common paraganglioma of the head and neck? (▶Fig. 4.6)

A

Carotid body tumor, which develops within the adventitia of the carotid bifurcation and are of neural crest origin

173
Q

173 Describe the Lyre sign. (▶Fig. 4.7)

A

● Splaying of the internal carotid artery and the external carotid artery at the carotid bifurcation ● Seen with carotid body tumors ● Glomus vagale and sympathetic chain paragangliomas on the other hand displace the carotid system anteriorly.

174
Q

174 What percentage of head and neck paragangliomas are functional?

A

Less than 3%

175
Q

175 What cellular pattern is characteristically seen in paragangliomas?

A

Cells of Zellballen: alveolar-like clumps of tumor cells are surrounded by a network of thin-walled capillaries.

Thick bands of collagenous tissue divide the tumor.

Five to 20 epithelial cells compose a nest or group of cells.

176
Q

176 What percentage of head and neck paragangliomas are malignant?

A

Less than 10%.

Malignancy determined by the presence of lymph node metastasis, not by cellular atypia or local invasion.

177
Q

177 Familial paraganglioma syndromes are caused by a mutation in genes that encode for what enzyme?

A

Succinate dehydrogenase

178
Q

178 True or false. Neural fascicles can be more easily spared during resection of a schwannoma compared with a neurofibroma.

A

True

179
Q

179 What is the most common poststyloid parapharyngeal space tumor?

A

Schwannoma of the vagus or sympathetic chain

180
Q

180 Which benign salivary gland tumors have pronounced fluorodeoxyglucose (FDG) uptake on PET imaging?

A

Oncocytoma, and Warthin tumor. Both tumors are composed of large eosinophilic granular cells containing high mitochondrial concentrations.

181
Q

181 What is the most common type of tumor to arise within the prestyloid parapharyngeal space?

A

Benign salivary gland tumors

182
Q

182 Describe the MRI findings of pleomorphic adenoma.

A

Well-circumscribed mass with low intensity on T1- and hyperintensity on T2-weighted sequences. Frequently demonstrates homogeneous gadolinium uptake

183
Q

183 What is the most common prestyloid parapharyngeal space tumor?

A

Pleomorphic adenoma is the most common overall. Mucoepidermoid carcinoma is the most common malignancy.

184
Q

184 What are the main access routes to the parapharyngeal space?

A

Cervical, submandibular/cervical, cervical parotid, cervical parotid with mandibular osteotomy, transoral (not recommended)

185
Q

185 When should a mandibulotomy be considered for parapharyngeal space tumors?

A

● Tumors > 5 cm ● Tumors with extensive skull base disease ● Extensive invasion

186
Q

186 What are laryngoceles?

A

Air-filled dilations of the laryngeal ventricle that may be congenital or acquired

187
Q

187 Describe the three types of laryngoceles.

A

● Internal: Connects the ventricle with the paraglottic space, false cord, and aryepiglottic fold ● External: Ventricular dilation extends through the thyrohyoid membrane to the lateral neck. ● Combined: Both internal and external extension

188
Q

188 What are plunging ranulas, and how do they differ from nonplunging ranulas?

A

Plunging ranulas form from obstructed sublingual gland ducts leading to the formation of an epithelial-lined retention cyst. A plunging ranula requires that the cyst extend through the mylohyoid, most commonly to the submandibular space.

189
Q

189 Review the characteristic signs and symptoms of Kawasaki (lymphomucocutaneous) disease.

A

Fever for more than 5 days with at least four of the following five findings: ● Bilateral nonsuppurative conjunctivitis ● One or more changes of the mucous membranes of the upper respiratory tract, including pharyngeal injection, fissured or erythematous lips, and “strawberry” tongue ● One or more changes of the extremities, including peripheral erythema or edema and periungual and generalized desquamation ● Polymorphous rash ● Cervical lymphadenopathy > 1.5cm in diameter (usually unilateral)

190
Q

190 Describe the cardiac complications associated with Kawasaki disease.

A

Coronary artery aneurysms occur in up to 25% of untreated patients. Death may occur secondary to coronary artery thrombosis or aneurysm rupture. An ECG and echocardiogram should be obtained in all patients suspected of having Kawasaki disease.

191
Q

191 Describe the clinical manifestation of Kikuchi- Fujimoto disease.

A

A benign, self-limiting necrotizing lymphadenitis that most commonly affects young Japanese women. Initial symptoms may include malaise, fever, fatigue, arthralgias, weight loss, and hepatosplenomegaly.

192
Q

192 Describe Castleman disease.

A

Castleman disease is a rare lymphoproliferative disorder that can manifest with localized or multicentric disease. It is commonly associated with human immunodeficiency virus (HIV) and human herpes virus (HSV) 8.

193
Q

193 What is the most common cause of deep neck space infections in the adult population?

A

Odontogenic infection

194
Q

194 What is the most common cause of deep neck space infections within the pediatric population?

A

Tonsillitis

195
Q

195 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

196
Q

196 Describe the histologic appearance of Actinomyces israelii?

A

Gram-positive, non–acid-fast, anaerobic bacilli demonstrating a filamentous fungal-like growth pattern and “sulfur granule” formation

197
Q

197 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

198
Q

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

A

Persistent firm painless cervical adenopathy with overlying violaceous skin discoloration

199
Q

199 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, depending on the species.

200
Q

200 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

201
Q

201 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.

202
Q

202 Why are mycobacteria called acid-fast bacteria?

A

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

203
Q

203 What is the most common head and neck manifestation of tuberculosis?

A

Cervical lymphadenopathy

204
Q

204 What is the treatment of cervical lymphadenopathy associated with tuberculosis?

A

Isoniazid, rifampin, ethambutol, and pyrazinamide

205
Q

205 What pathogen is associated with cat-scratch disease?

A

Bartonella henselae

206
Q

206 Name the three types of Langerhans cell histiocytosis.

A

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

207
Q

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

A

Hand-Schüller-Christian disease (disseminated chronic)

208
Q

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

A

Letterer-Siwe (disseminated acute)

209
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.

210
Q

What is the most common cause of pediatric cervical lymphadenopathy?

A

Reactive lymphadenopathy from viral infection

211
Q

What is the most common cause(s) of pediatric suppurative lymphadenopathy?

A

Group A Streptococcus and Staphylococcus aureus

212
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.

NOT A SCREENING TEST.

213
Q

213 What are the symptoms of meningeal neurosyphilis?

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.

214
Q

214 What constitutes the Hutchinson triad of congenital syphilis?

A

Small notched teeth, deafness, and interstitial keratitis

215
Q

215 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

216
Q

216 What is the definition of otosyphilis?

A

The presence of a positive FTA-ABS in the setting of unexplained sensorineural hearing loss

217
Q

217 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.

218
Q

218 Describe the common initial symptoms of toxoplasmosis.

A
  1. Fever
  2. Malaise
  3. Pharyngitis
  4. Myalgias
  5. Cervical lymphadenopathy occurring in the most patients
219
Q

219 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

220
Q

220 What are the early symptoms of tularemia infection?

A

Fever, headache, chills, myalgia, photophobia, diminished visual acuity, and lymphadenopathy

221
Q

221 What are the possible side effects of amphotericin B?

A

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

222
Q

222 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.

223
Q

223 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

224
Q

224 What is the most common causative organism in chronic invasive fungal sinusitis?

A

Aspergillus fumigatus

225
Q

225 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.

226
Q

226 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.

227
Q

227 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.

228
Q

228 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.

229
Q

229 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.

230
Q

230 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

231
Q

231 What is the most common causative organism in necrotizing soft tissue infections?

A

Group A streptococcus

232
Q

232 What are the clinical characteristics of necrotizing fasciitis?

A

Tense edema, pain disproportionate to examination, skin discoloration, bullae, necrosis, and crepitus

233
Q

233 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. Broadspectrum antibiotics should be administered, and the patient should be monitored in an intensive care unit setting. Hyperbaric oxygen may provide additional benefit.

234
Q

234 Describe the clinical presentation of infectious mononucleosis.

A

Fever, fatigue, generalized lymphadenopathy, splenomegaly, and exudative pharyngitis with adenotonsillar hypertrophy

235
Q

235 Define the following terms: ● Ageusia ● Hypogeusia ● Dysgeusia

A

● Ageusia: Inability to taste ● Hypogeusia: Diminished ability to taste ● Dysgeusia: Distorted sense of taste

236
Q

236 Describe the taste innervation of each of the following upper aerodigestive locations:

  • Anterior two-thirds of the tongue
  • The posterior two-thirds of the tongue
  • The circumvallate papillae
  • Pharynx
  • Epiglottis
A
  • Chordae tympani of facial nerve
  • Glossopharyngeal nerve
  • Glossopharyngeal nerve
  • Glossopharyngeal and vagus
  • Superior laryngeal branch of vagus
237
Q

237 What is the most common cause of perceived taste dysfunction?

A

Olfactory dysfunction

238
Q

238 What tastes and odors are detected by the trigeminal nerve?

A

Spice and ammonia

239
Q

239 What is a Burton line?

A

A dark blue stippled line across the upper gingiva indicative of lead poisoning

240
Q

240 Oral cavity nevi most commonly occur where?

A

On the palate and gingiva

241
Q

241 Describe Peutz-Jeghers syndrome.

A

Autosomal dominant disorder characterized by intestinal hamartomatous polyps and mucocutaneous melanocytic macules involving the lips and buccal mucosa. It is associated with an increased risk of developing GI, pulmonary, and reproductive track malignancies.

242
Q

242 What is the most common intraoral pigmented lesion?

A

Amalgam tattoo resulting from amalgam implantation from prior dental work

243
Q

243 Review the risk factors for mucosal melanoma.

A

There are no known environmental risk factors. Smoking, chemical exposure, and sun exposure do not appear to be linked with an increased risk. A small subset may arise from junctional nevi.

244
Q

244 Which common medications are associated with gingival hyperplasia?

A

Phenytoin, calcium channel blockers, and cyclosporine

245
Q

245 Name several conditions associated with pseudoepitheliomatous hyperplasia.

A
  1. Rhinoscleroma
  2. Granular cell tumor
  3. Blastomycosis
  4. Syphilis
  5. Necrotizing sialometaplasia
246
Q

246 What benign process is often clinically and histologically mistaken for squamous cell carcinoma of the hard palate?

A

Necrotizing sialometaplasia

247
Q

247 Describe the important features of granular cell tumors of the head and neck.

A

Most commonly involve the tongue, palate and less commonly the larynx. They are sessile gray colored lesions that are of probable neurogenic origin; they stain strongly with s100 and histologically may be mistaken for squamous cell carcinoma since they exhibit pseudoepitheliomatous hyperplasia.

248
Q

248 Describe the common oral manifestations of Crohn disease.

A

Generalized mucosal swelling, cobblestoning of the buccal mucosa and gingiva, aphthous stomatitis, and angular cheilitis

249
Q

249 Describe the common oral manifestations of Sjogren disease.

A

Changes largely result from xerostomia, including difficulty in swallowing and eating, disturbances in taste and speech, dental caries, cobblestoning of the tongue, and increased risk of oral candidiasis.

250
Q

250 What is the most common oral manifestation of amyloidosis?

A

Macroglossia, occurring in 20% of patients

251
Q

251 What are the histologic findings with amyloidosis?

A

Apple-green birefringence, Congo red stain

252
Q

252 What is the most common intraoral malignancy associated with HIV?

A

Kaposi sarcoma

253
Q

253 Review the conditions associated with the development of hairy leukoplakia.

A

Immunocompromised states such as HIV/AIDS and prior organ transplantation. Hairy leukoplakia is associated with Epstein-Barr virus.

254
Q

254 What is the natural history of primary herpetic gingivostomatitis?

A

Mean duration of: ● Fever: 4.4 ± 2.4 days ● Oral lesions: 12 ± 3.4 days ● Extraoral lesions: 12 ± 3.9 days ● Dysphagia to food: 9.1 ± 3 days ● Dysphagia to liquid: 7.1 ± 2.5 days ● Viral shedding: 7.1 ± 2.5 days

255
Q

255 What is the most common presentation of a primary HSV infection in the pediatric population?

A

Herpetic gingivostomatitis

256
Q

256 General prodromal symptoms associated with primary herpetic gingivostomatitis include what?

A

General malaise, fever, anorexia, irritability, and headache

257
Q

257 What are primary and secondary clinical findings associated with primary herpetic gingivostomatitis?

A

● Primary: Painful pinhead vesicles that rupture to form ulcerative lesions, which are irregular and covered by a yellow gray membrane ● Secondary: Submandibular lymphadenitis, halitosis, and dehydration from refusal to take in adequate oral hydration

258
Q

258 What tests can be used to definitively diagnose an HSV-1 viral infection?

A

PCR, viral culture, serology, immunofluorescence. Note: Tzanck smear is not helpful for delineating HSV-1 from HSV-2.

259
Q

259 What are potential complications of herpetic gingivostomatitis?

A

Dehydration, herpetic whitlow, herpetic keratitis, secondary bacterial infection, esophagitis, epiglottitis, pneumonitis, encephalitis, eczema herpeticum

260
Q

260 What are the three most common antiviral agents used to treat herpetic gingivostomatitis, and what is their mechanism of action?

A

Acyclovir, valacyclovir, famciclovir. Metabolized by viral enzymes to form metabolites that interfere with DNA synthesis and cause cell death. It works best if initiated within 72 hours.

261
Q

261 What benefit does valacylcovir offer compared with acyclovir for the treatment of herpetic gingivostomatitis?

A

The dosing is twice a day compared with three to five times per day; however, it is more expensive.

262
Q

262 What is the generally accepted window of opportunity for prescribing oral acyclovir for effective treatment of primary herpetic gingivostomatitis?

A

Three days. This therapy has been shown to decrease the duration of the lesions (intraoral and extraoral), fever, dysphagia/odynophagia, and viral shedding.

263
Q

263 Recurrent oral HSV-1 infections can be associated with what important complications?

A

● Disfiguring lesions ● Erythema multiforme ● Aseptic meningitis ● Eczema herpeticum

264
Q

264 What noncontagious acute gingivitis is caused by an overgrowth of common bacterial species, including Prevotella intermedia, α-hemolytic streptococci, Actinomyces, or spirochetes, among others?

A

Acute necrotizing ulcerative gingivitis (trench mouth)

265
Q

265 In a patient with acute necrotizing gingivostomatitis, if the disease progresses beyond the gingiva to include other mucosal surfaces, what is this condition called?

A

Noma (cancrum oris)

266
Q

266 What are common risk factors for development of acute necrotizing ulcerative gingivitis?

A

Stress, immune incompetence (i.e., HIV infection), poor nutrition, poor oral hygiene, alcohol or tobacco use. This is not a contagious disease.

267
Q

267 What are common examination findings seen in acute necrotizing ulcerative gingivitis (“trench mouth”)?

A
  • Lymphadenopathy
  • Halitosis
  • Mucosal edema/ulceration/inflammation, with or without a pseudomembrane
268
Q

268 What is the treatment for acute necrotizing ulcerative gingivitis?

A
  • Analgesia (NSAID, narcotics, viscous lidocaine, etc.)
  • Antibacterial (clindamycin, penicillin, or erythromycin)
  • Oral hygiene (chlorhexidine 0.12% mouth rinse, brushing, flossing, etc.)
  • Dental consultation for debridement and definitive periodontal therapy
  • Management of underlying immunocompromised status is important if present
269
Q

269 What is the most common oral manifestation of HIV infection?

A

Oral candidiasis

270
Q

270 What are the common forms of oral candidiasis?

A
  • Pseudomembranous candidiasis (thrush)
  • Erythematous (atrophic) candidiasis
  • Angular cheilitis (perlèche)
  • Hyperplastic candidiasis
271
Q

271 What in-office diagnostic test can you perform to confirm the diagnosis of oral candidiasis?

A

Scraping of erosive lesion followed by potassium hydroxide (KOH) preparation and looking for budding yeast with or without pseudohyphae

272
Q

272 Review the initial treatment options for oral candidiasis.

A

Topical antifungal lozenges or solutions for 7–14 days: Clotrimazole troches, nystatin suspension, or nystatin pastilles

273
Q

273 What can you offer as treatment for moderate to severe oral candidiasis or for patients who do not respond to topical therapy for oral candidiasis?

A

Oral fluconazole for 7 to 14 days

274
Q

274 When is daily suppressive management with antifungals indicated for oral candidiasis?

A

Suppressive management Is usually unnecessary (even for HIV-positive patients).

Treating active infections and managing the underlying immunocompromised status are recommended. When indicated (usually assisted by ID Consult), management usually includes fluconazole, three times a week.

275
Q

275 The esophagus, an embryologic foregut derivative, undergoes what important process during week 8 to 10 of life?

A

Recanalization of the esophageal lumen

276
Q

276 Describe the muscular arrangement of the esophagus.

A
  • Outer longitudinal fibers, inner circular fibers
  • Superior thier skeletal, middle third mixed, inferior third smooth
277
Q

277 What are three physiologic areas of narrowing within the esophagus?

A
  • Upper esophageal sphincter (cricopharyngeus muscle, C6, narrowest segment)
  • Crossed by aorta and left main bronchus in mid chest
  • Lower esophageal sphincter (passes through diaphragm)
278
Q

278 What is the blood supply to the esophagus?

A

Arterial

  • Segmental blood supply, extensive submucosal anastomosis
  • Upper esophageal sphincter and cervical esophagus: Inferior thyroid artery
  • Thoracic esophagus: Paired esophageal arteries (terminal branches of bronchial arteries
  • Lower esophageal sphincter: Left gastric artery and left phrenic artery

Venous

  • Neck: Inferior thyroid veins
  • Mediastinum: Azygous and hemiazygous veins
  • Abdomen: Left gastric vein
279
Q

279 What is the innervation of the esophagus?

A
  • Sympathetic innervation from T6-T10 bilaterally
  • Greater and often lesser splanchnic nerves
  • Branches from the celiac plexus

Note: The vagal nerves form a plexus along the distal esophagus and then reform two distinct nerves on passage through the diaphragm.

280
Q

280 The upper, mid, and lower third of the esophagus drain into which nodal basin(s)?

A
  • Upper third = Paratracheal and internal jugular lymph nodes
  • Middle third = Mediastinal nodes
  • Lower third = Gastrohepatic and celiac axis lymph nodes
281
Q

281 What is the normal epithelial lining of the esophagus?

A

Nonkeratinizing stratified squamous epithelium

282
Q

282 What are the four layers of the esophageal wall?

A
  • Mucosa
  • Submucosa
  • Muscularis propria
  • Adventitia
283
Q

283 What key surgical landmarks must be kept in mind when operating on the esophagus in the neck?

A
  • It lies slightly left of midline.
  • Anterior: Trachea, thyroid lobe, and anterolaterally the recurrent laryngeal nerves bilaterally in the tracheoesophageal groove
  • Posterior: Vertebral column and longus colli muscles
  • Lateral: Thoracic duct on the left
284
Q

284 What key surgical landmarks are relevant when dilating an esophageal stricture in the mediastinum?

A
  • Superior mediastinum: Slightly left of midline
  • Posterior: Vertebral column, thoracic duct (not in direct contact, to left)
  • Anterior: Trachea, left mainstem bronchus, aortic arch
  • Left lateral: Descending aorta, left parietal pleura (direct contact)
  • Right lateral: Vena azygos
  • Inferior mediastinum: Returns to midline
  • Posterior: Vertebral column; inferiorly, the aorta moves posterior to the esophagus and esophagus.
  • Anterior: Pericardium
  • Left lateral: Parietal pleura (direct contact)
  • Right lateral: Parietal pleura (direct contact)
285
Q

285 At what thoracic level is the esophageal hiatus?

A

T10

286
Q

286 How many centimeters are the incisor teeth from the cricopharyngeus, aortic arch, left mainstem bronchus, and lower esophageal sphincter and diaphragm in an average adult?

A
  • 15cm
  • 25cm
  • 40cm
287
Q

287 What two types of peristalsis propel food through the esophagus?

A
  • Primary peristalsis: Triggered by swallowing
  • Secondary peristalsis: Triggered by esophageal dilation
288
Q

288 What are the functional muscular components of the upper esophageal sphincter?

A

The cricopharyngeus muscle, thyropharyngeus, and the proximal cervical esophagus

Note: Many muscles contribute to the function of the upper esophageal sphincter (e.g., movement of the larynx, infrahyoid musculature, etc.).

289
Q

289 What is the innervation of the upper esophageal sphincter?

A

At rest, the upper esophageal sphincter is contracted, and during oropharyngoesophageal events (swallowing, belching, emesis), the sphincter relaxes. The major tone effect stems from contraction of the cricopharyngeus, which is modulated by cranial nerve X.

Afferent information is primarily transmitted via cranial nerve IX.

290
Q

290 What is the innervation of the lower esophageal sphincter?

A

At rest, the lower esophageal sphincter is contracting as a result of neurotransmitter and hormonal influences. Swallow-induced relaxation occurs about 1 to 2 seconds after the bolus is swallowed. The vagal efferent motor neurons inhibit neurons within the myenteric plexus, which results in a decrease in the of the baseline tone.

291
Q

291 What anatomical relationship augments the function of the lower esophageal sphincter?

A

Diaphragmatic crura

292
Q

292 What are the four main protective mechanisms against esophageal reflux?

A
  1. Upper esophageal sphincter: Tonically closed
  2. Lower esophageal sphincter: Tonically closed
  3. Esophageal acid clearance: Peristalsis, gravity
  4. Epithelial resistance: Mucous layer, aqueous layer, cell membrane, and intracellular junctions
293
Q

293 When should esophagoscopy be considered after caustic ingestion?

A

Within the first 24 hours because the risk for perforation and complications may be greater at 2 to 3 days after injury

294
Q

294 What endoscopic findings suggest an increased risk of stricture formation after caustic ingestion?

A

Circumferential erythema with exudate and perforation

295
Q

295 Most esophageal foreign-body impactions occur at what level in the esophagus?

A

Cervical esophagus, just below the cricopharyngeus muscle

296
Q

296 Describe Boerhaave syndrome.

A

Elevated intraabdominal pressure results in a transmural tear within the distal esophageal wall after vomiting. This commonly occurs in the posterolateral wall of the distal esophagus.

297
Q

297 Describe Mallory-Weiss syndrome.

A

Incomplete tear of the esophageal wall involving the esophageal mucosa and submucosal arteries, often associated with retching

298
Q

298 What does the Hamman sign indicate?

A
  • Pneumomediastinum or pneumopericardium, often from tracheobronchial injury or Boerhaave syndrome
  • Demonstrated by a crunching sound that is synchronous with heartbeat
299
Q

299 What type of imaging study should be used In a patient with a suspected esophageal perforation?

A

Gastrografin swallow study

300
Q

300 Why should patients with findings concerning for esophageal diverticulum, complex stricture, or achalasia undergo esophageal barium swallow instead of initial endoscopy?

A

Barium swallow is sensitive for these findings, and these conditions are associated with a higher risk for esophageal perforation with endoscopy use.

301
Q

301 Is the barium swallow examination always performed using liquid barium?

A

No. It can be performed with barium tablets or barium-coated food objects, such as a marshmallow or bread, to identify more subtle lesions.

302
Q

302 What is esophageal impedance testing?

A

This test is performed by a catheter measuring multichannel intraluminal impedance, which measures the difference in resistance when a bolus (mucosa, gas, liquid, solid) passes the detecting channels on the device. It can be used in combination with manometry or pH monitoring and can identify directionality of bolus movement.

303
Q

303 What are the indications for esophageal impedance testing?

A
  1. Esophageal dysphasia
  2. Noncardiac chest pain
  3. Heartburn or regurgitation
  4. Preoperative evaluation for antireflux surgery
  5. Identification of the lower esophageal sphincter before pH catheter placement
304
Q

304 In a patient for whom twice-daily proton pump inhibitor (PPI) therapy has failed and who has a normal EGD, what test can be performed to confirm GERD?

A

Ambulatory esophageal pH monitoring, which may also be performed to assess adequacy of treatment

305
Q

305 What are the two available methods of ambulatory pH monitoring?

A

Ambulatory pH monitoring entails 24- to 48-hour monitoring of reflux events and clinical symptoms while eating an unrestricted diet with the patient off antacid medication for at least 7 days. It can be performed via a transnasal catheter positioned 5 cm above the lower esophageal sphincter or a capsule attached to mucosa 6 cm proximal to the Z-line

306
Q

306 What main outcome measure is used when evaluating the results of ambulatory pH monitoring?

A

Percentage of time the intraesophageal pH is <4, to distinguish physiologic from pathologic reflux

307
Q

307 What endoscopic test allows for evaluation of the oropharynx, esophagus, stomach, and upper duodenum?

A

EGD

308
Q

308 What test is often recommended as the initial test for GERD because it provides diagnostic (both visual and histologic via biopsy) and possibly therapeutic options to allow stratification of disease?

A

EGD

309
Q

309 Describe three methods for esophageal endoscopy.

A
  • Rigid transoral esophagoscopy performed with the patient under general anesthesia
  • Flexible transoral esophagoscopy performed with the patient under conscious sedation
  • Flexible transnasal esophagoscopy (TNE) performed with the patient under local and/or conscious sedation
310
Q

310 What benefit does endoscopy offer as the first step in evaluating a patient with esophageal dysphagia?

A

Endoscopy can provide visual evaluation and pathologic tissue samples and can also intervene and provide therapeutic benefit.

311
Q

311 What diagnostic test evaluates both the intraluminal pressures and coordination of the upper esophageal sphincter, esophageal body, and lower esophageal sphincter?

A

Esophageal manometry

312
Q

312 In a patient with dysphagia, noncardiac chest pain, or a possible esophageal motility disorder, what diagnostic test should be considered?

A

Esophageal manometry

313
Q

313 In a patient with dysphagia, how can you differentiate oropharyngeal from esophageal dysphagia based on symptoms?

A
  • Esophageal dysphagia: Food gets stuck after the swallow is completed because of structural or neuromuscular pathology; the problem is in the esophageal body or lower esophageal sphincter.
  • Oropharyngeal dysphagia: Difficult to complete swallow; disorders involve the oropharynx, hypopharynx, and upper esophageal sphincter.
314
Q

314 How does the differential diagnosis change if a patient with esophageal dysphagia complains of symptoms with solids only versus both solids and liquids?

A

Mechanical obstruction usually causes difficulty with solids (but it may progress to involve liquids later on). Motility disorders commonly result in concurrent solid and liquid dysphagia.

315
Q

315 What are the most common diagnoses in a patient with solid-food esophageal dysphagia?

A
  • Esophageal ring (intermittent)
  • Peptic stricture (progressive)
  • Malignancy (progressive)
316
Q

316 What is the most common cause of acute esophageal dysphagia?

A

Food impaction (meat); results in saliva expectoration

317
Q

317 What disease process is characterized by decreased or absent lower esophageal sphincter relaxation and decreased or absent esophageal peristalsis?

A

Achalasia (Greek: “does not relax”)

318
Q

318 Eagle syndrome is associated with what anatomical abnormality?

A

Elongated styloid process (about > 3 cm) and/or ossification or calcification of part or all the stylohyoid ligament. This syndrome was described in 1937 by Dr. Wyatt Eagle.

319
Q

319 Dysphagia lusoria is associated with what anatomical anomaly?

A

Aberrant right subclavian artery

320
Q

320 What histopathologic findings support the diagnosis of achalasia?

A

Decrease in total ganglion cells within the myenteric plexus, the presence of T cell, eosinophil, and mast cell infiltration, and increased neural fibrosis

321
Q

321 What is the general age group most commonly affected by achalasia?

A

20 to 60 years

322
Q

322 What are the primary complaints associated with loss of lower esophageal sphincter relaxation and esophageal aperistalsis (achalasia)?

A

Solid and liquid dysphagia, weight loss, chronic cough, chest pain, hiccups, regurgitation, heartburn, and globus

323
Q

323 What three associations are often included in triple A syndrome (Allgrove syndrome), which is most commonly found in children?

A
  • Achalasia
  • Adrenal insufficiency
  • Alacrima
324
Q

324 What infectious disease can lead to clinical manifestations of achalasia?

A

Chagas disease

325
Q

325 What management strategy can be used to reverse or stop the progression of achalasia?

A

None. The goal of management is to decrease lower esophageal sphincter tone and manage reflux.

326
Q

326 What is first-line therapy for patients with severe achalasia?

A

Surgical dilation or myotomy unless the patient is a poor operative candidate

327
Q

327 What medical options are available for patients with achalasia?

A

Nitrates and calcium channel blockers with the goal of decreasing lower esophageal sphincter tone

328
Q

328 What surgical interventions are available for achalasia?

A

Good operative candidates may undergo pneumatic dilation or myotomy. Poor operative candidates may undergo dilation with a bougie or botulinum toxin injection.

329
Q

329 What pathogen is associated with Chagas disease?

A

Parasite Trypanosoma cruzi

330
Q

330 What is the vector for Trypanosoma cruzi?

A

Reduviid bugs

331
Q

331 Describe the esophageal manifestations of Chagas disease?

A
  • Megaesophagus with dilation and muscular hypertrophy
  • Reduction in the number of neurons in the myenteric plexus
332
Q

332 What is the most common condition associated with chronic Chagas disease?

A
  • Cardiomyopathy
  • Arrhythmias
  • Conduction blocks
333
Q

333 What are the clinical manifestations of scleroderma?

A

Skin tightening, hyperpigmentation, and hypopigmentation of skin, sclerodactyly, Raynaud phenomenon, GERD, arthralgias, myalgias, Sicca syndrome, and dysphagia

334
Q

334 How common is esophageal involvement in patients with scleroderma?

A

90%; 50% experience significant symptoms

335
Q

335 The progressive fibrosis and atrophy within the smooth muscle of the esophagus associated with scleroderma manifest with what classic finding on esophageal manometry and barium esophagram?

A
  • Manometry: Progressive loss of esophageal body peristalsis in distal two-thirds and decreased lower esophageal sphincter pressure
  • Barium esophagram: Dilated esophagus, patulous gastroesophageal (GE) junction, and uninhibited reflux events into the distal esophagus
336
Q

336 What are common complications noted in patients with scleroderma and GERD?

A

Barrett esophagus, esophagitis, and strictures

337
Q

337 What laboratory test is most sensitive and specific for dermatomyositis?

A

Creatine kinase

338
Q

338 How is dermatomyositis commonly treated?

A

Systemic steroid therapy and potentially immunosuppressive and cytotoxic therapy, including methotrexate, azathioprine, and cyclophosphamide

339
Q

339 Describe the potential head and neck manifestations of dermatomyositis.

A

Heliotrope discoloration of upper eyelids, malar rash, dysphonia, dysphagia, scaly scalp, and hair loss

340
Q

340 What part of the aerodigestive tract is affected by polymyositis?

A

Hypopharynx and upper third of the esophagus

341
Q

341 What is the cause of diffuse esophageal spasm?

A

Neural and muscular defects triggered by reflux events, stress, extreme temperature variability in food or drink, carbonation, or particular smells

342
Q

342 What symptoms are associated with diffuse esophageal spasm?

A

Intermittent esophageal dysphagia, noncardiac chest pain, reflux/heartburn

343
Q

343 What are the classic esophageal manometric findings in patients with diffuse esophageal spasms?

A

>2 uncoordinated contractions during 10 consecutive swallows, aperistalsis in more than 30% of wet swallows, and a fifth of contractions being simultaneous

344
Q

344 What is the test(s) of choice to evaluate for cricopharyngeal dysfunction?

A

Videofluoroscopic swallow with esophagram

345
Q

345 What are the theories behind the relationship between cricopharyngeal dysfunction and dysphagia?

A

The cricopharyngeus is normally under tonic contraction but fails to relax with swallow. There is a lack of coordination between cricopharyngeus relaxation and the propulsion of food.

346
Q

346 Describe the relative contraindications to cricopharyngeal myotomy.

A
  • Advanced GERD
  • Progressive neurologic conditions such as bulbar palsy
  • Known proximal esophageal cancer
  • Hx radiation to the neck
347
Q

347 What is the proposed cause of epiphrenic esophageal diverticula?

A

Pulsion effect created superior to the cardioesophageal junction

348
Q

348 What is the proposed cause of traction esophageal diverticula?

A

Traction effect caused by inflammation associated with cervical adenopathy or adjacent fibrotic tissue

349
Q

349 Between what muscles does a Zenker diverticulum herniate? (▶Fig. 4.8)

A

Between the inferior pharyngeal constrictors and the cricopharyngeus (Killian triangle)

350
Q

350 Which side does a Zenker diverticulum most commonly involve and why?

A

It involves the left neck ~90% of the time and results from the convexity of the cervical esophagus to the left side and a more laterally positioned carotid artery on the left side, creating a space for the sac to protrude.

351
Q

351 Define the Killian-Jamieson area.

A

Dehiscence between the oblique and transverse fibers of the cricopharyngeus muscle

352
Q

352 Define the Laimer triangle.

A

Dehiscence between the cricopharyngeus muscles and the proximal esophageal muscles

353
Q

353 What nonmalignant complication of GERD can manifest with progressive esophageal dysphagia starting with solid-food dysphagia and progressing to both solid and liquid dysphagia?

A

Peptic stricture

354
Q

354 Describe the risk factors for developing a peptic stricture.

A
  • Older age
  • Male
  • Long history of reflux symptoms
  • GERD
  • Scleroderma
  • Zollinger-Ellison syndrome
  • Nasogastric tube placement
  • Hx of surgical management for achalasia (Heller myotomy)
355
Q

355 What is a Schatzki ring?

A

Smooth, thin (< 4mm) web of mucosa and submucosa at the squamocolumnar junction, marking the proximal margin of a hiatal hernia

356
Q

356 Describe the characteristics of a muscular esophageal ring.

A

Hypertrophic musculature within the esophageal body typically located within 2 cm of the GE junction

357
Q

357 What disease processes increase the likelihood of developing an esophageal ring?

A

GERD and eosinophilic esophagitis

358
Q

358 What is an esophageal web?

A

Thin mucosal fold covered in squamous epithelium that extends into the esophageal lumen, most commonly in the anterior cervical esophagus

359
Q

359 What is the most common cause of an esophageal web?

A

Most often, it is idiopathic and asymptomatic.

360
Q

360 What are common risk factors for the formation of an esophageal web?

A

Chronic GERD or iron deficiency associated with Plummer-Vinson syndrome.

361
Q

361 Describe the clinical features of Plummer-Vinson syndrome.

A

Triad of dysphagia, iron-deficiency anemia, and esophageal webs. Additionally associated with atrophic glossitis and squamous cell carcinoma of the oral cavity, esophagus, and hypopharynx

362
Q

362 What are common initial symptoms of GERD?

A

Heartburn 30 minutes to 2 hours after eating and regurgitation. Symptoms worsen with lying down or bending over. Less common symptoms include chest pain, chronic cough, laryngitis, asthma, and dental caries. Patients may complain of odynophagia and dysphagia in addition to belching.

363
Q

363 What symptoms are worrisome for a more sinister diagnosis than isolated GERD?

A

Dysphagia, odynophagia, choking, weight loss, chest pain, upper GI bleed, and no or poor response to an empiric trial of antacids. If these symptoms are present, or if a patient does not improve on empiric therapy, endoscopy should be considered.

364
Q

364 Why is an initial empiric trial of antacid therapy a reasonable first step in a patient with symptoms suggestive of GERD?

A

It is noninvasive, cost-effective, and in most cases diagnostic and therapeutic.

365
Q

365 What technique offers the best evaluation of a patient’s esophageal mucosa?

A

Endoscopic esophagoscopy

366
Q

366 What is commonly seen on esophagoscopy in a patient with reflux esophagitis?

A

Erosions or ulcerations at the squamocolumnar junction (Z line)

367
Q

367 To determine the severity of acid reflux, demonstrate reflux in a patient with normal endoscopic findings, or to evaluate response to therapy, a 24- hour pH probe test may be performed. What is the primary limitation of this test?

A

A fourth of patients with erosive esophagitis and a third of patients with nonerosive esophagitis will have normal results.

368
Q

368 When discussing lifestyle modifications for the management of GERD, what foods should be avoided?

A

Fatty foods, chocolate, coffee, excess alcohol, colas, red wine, orange juice, large meals, peppermint, basically anything that increases pH or decreases sphincter tone

369
Q

369 Beyond dietary considerations, what lifestyle modifications should be considered to improve mild GERD?

A

Elevate the head of bed while sleeping, avoid eating right before sleep, exercise regularly, and lose weight.

370
Q

370 Which histamine 2 (H2) blocker is the most effective for treating GERD, and what is the dose dependent relationship between symptoms and therapy?

A

When adjusted for potency, no H2 blocker has been shown to be stronger or more effective than another. There is not a dose-dependent relationship. If a patient is treated with 6 weeks of standard therapy and does not respond, it is time to look to additional intervention.

371
Q

371 In a patient diagnosed with erosive reflux disease, what medical management is indicated?

A

PPI therapy

372
Q

372 Is there any difference in treatment outcome for GERD when comparing once-daily proton pump inhibitor therapy with more frequent dosing regimens?

A

Yes. More frequent dosing schedules (twice a day) have been shown to result in a significant improvement in gastric pH and provide a longer duration of effect.

373
Q

373 After discontinuing a PPI for GERD, in what time frame do most patients who have recurrence begin to experience relapsing symptoms?

A

Three months

374
Q

374 What risks are associated with chronic suppressive PPI therapy for reflux disease?

A

Potentially decreased bone density, infections, and electrolyte abnormalities

375
Q

375 In a patient with long-standing esophageal reflux disease, the endoscopist identified specialized intestinal metaplasia or metaplastic cuboidal epithelium extending proximally to the natural squamocolumnar junction. What disease process is most likely associated with this finding?

A

Barrett esophagus

376
Q

376 To classify peptic esophagitis on endoscopy and decrease interobserver variability, several classification systems have been devised. The Los Angeles classification system is most commonly used. Describe the different grades involved in this system.

A

Los Angeles Classification

  • Grade A: One or more mucosal break, each ≤ 5mm long
  • Grade B: One or more mucosal break > 5mm long, without continuity between the tops of adjacent mucosal folds
  • Grade C: One or more mucosa breaks continuous between the tops of adjacent mucosal folds; not circumferential
  • Grade D: Circumferential mucosal break

Note: Historically the Savory-Miller grading system was the most prevalent; however, because of variable definitions, it is not as commonly used today.

377
Q

377 During endoscopy for erosive esophagitis, what is the strongest predictor of Barrett esophagitis on examination?

A

The length of the columnar appearing epithelium segment extending from the GE junction (long segment > 3 cm, short segment < 3 cm). Specialized intestinal metaplasia is required on pathology to confirm the diagnosis.

378
Q

378 What is the most feared complication of Barrett esophagus?

A

Esophageal adenocarcinoma. Annual incidence ranges between 0.12 and 0.5% in patients with Barrett esophagus.

379
Q

379 With Barrett esophagus, how often should a patient with (1) no evidence of dysplasia, (2) lowgrade dysplasia, and (3) high-grade dysplasia without eradication therapy be examined endoscopically?

A
  1. Every 3 to 5 years 2. Every 6 to 12 months 3. Every 3 months
380
Q

380 What three management strategies are available for patients with Barrett esophagus?

A

Controversy regarding optimal management is ongoing. Options include the following:

  • Management of GERD
  • Surveillance via serial endoscopy
  • Attempt to eradicate dysplasia
381
Q

381 What endoscopic options are available for dysplasia eradication in patients with Barrett esophagus?

A
  • Radiofrequency ablation
  • Photodynamic therapy
  • Endoscopic mucosal resection (recommended for patients with dysplasia and a visible mucosal irregularity to evaluate for T stage)
382
Q

382 Provide several reasons why the prognosis for esophageal cancer is poor.

A

It often manifests late in the disease, and the esophagus is without an outer serosal layer, which may lead to early spread.

383
Q

383 Describe the Müller maneuver.

A

Endoscopic evaluation during maximal inspiration, against a closed nose and mouth, at various levels in an attempt to identify anatomical regions of obstruction

384
Q

384 What is the Epworth sleepiness scale?

A

A commonly used, statistically validated questionnaire for daytime sleepiness. A score of 0 to 5 is supernormal, 5 to 10 is normal, 10 to 15 is sleepy, 15 to 20 is very sleepy, > 20 is dangerously sleepy.

385
Q

385 What is upper airway resistance syndrome (UARS)?

A

UARS is characterized by excessive daytime somnolence but normal sleep studies. Esophageal pressure monitoring shows abnormally increased negative intrathoracic pressures leading to increased work of breathing and sleep arousals. UARS is associated with crescendo snoring. In contrast to OSA, UARS is seen as frequently in women as in men, occurs in nonobese patients, and is more common in young adults than in elderly adults.

386
Q

386 What cephalometric findings are associated with OSA?

A

The skull base appears to be shorter. The sagittal dimension of both jaws is smaller and in a more retrognathic position. The height of the lower face is increased, as the mandible tends to be rotated posteriorly. The chin and tongue are retruded, the soft palate is elongated, and the upper airway space is narrowed.

387
Q

387 What is the definition of OSA?

A

OSA is a sleep disorder characterized by periodic complete or partial upper airway obstruction during sleep, causing intermittent apneas, hypopnea, or both despite ongoing respiratory effort. There is no universally accepted definition, but it is usually defined as a respiratory disturbance index (RDI) of 5 or greater. Measurements of the severity of OSA are based on the RDI, the severity of oxygen desaturation, and the level of daytime sleepiness.

388
Q

388 What medical therapies exist for treatment of OSA?

A
  • Weight control, CPAP (continuous positive airway pressure), and oral appliances
  • Medical conditions such as acromegaly and hypothyroidism should be ruled out.
  • Medications or substances such as alcohol, sedative hypnotics, narcotics, anesthetics, and sedating antihistamines should be avoided.
389
Q

389 What are potential complications or sequelae of Uvulopalatopharyngoplasty (UPPP)?

A

Persistent snoring or OSA, bleeding, nasopharyngeal regurgitation of liquids, oropharyngeal dryness, oropharyngeal dysphagia, and pharyngeal stenosis

390
Q

390 What does the Friedman staging system assess?

A

This staging system is used as a clinical predictor of which patients may have successful improvement of their OSA after UPPP surgery.

391
Q

391 What is the most common surgical treatment of children with OSA?

A

Adenotonsillectomy. Less commonly, lingual tonsillectomy may be performed.

392
Q

392 What craniofacial syndromes are closely associated with snoring and sleep apnea?

A
  • Achondroplasia
  • Pierre Robin syndrome
  • Treacher-Collins syndrome
  • Crouzon disease
  • Down syndrome
  • Prader-Willi syndrome
  • Apert syndrome
393
Q

393 What is the mechanism of radiofrequency tissue volume reduction used for the treatment of snoring?

A

Inserting electrodes and applying thermal energy will create a definable “thermal lesion” that over time will be replaced by stiff fibrotic tissue with reduced vibratory capacity.

394
Q

394 Describe tongue base and hyoid bone suspension procedures for treatment of OSA.

A

A screw, with two sutures attached, is drilled into the lingual cortex of the mandibular symphysis. The two sutures are then submucosally secured to the tongue base or wrapped around the hyoid and tied under tension.