Salivary Gland Disorders Flashcards

1
Q

salivary gland disorders

A
  1. mucocele/ranula
  2. sialolithiasis
  3. acute/chronic sialadenitis
  4. sialadenosis
  5. xerostomia
  6. benign lymphoepithelial lesion (BLEL)
  7. Sjogren syndrome
  8. necrotizing sialometaplasia
  9. sialorrhea
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2
Q

T/F: salivary gland neoplasia is benign

A

false, it is benign and malignant

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3
Q

mucocele

A

oral mucosal swelling caused by rupture of salivary gland DUCT

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4
Q

what does the rupture of a salivary gland duct lead to?

A

spillage of mucin

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5
Q

T/F: mucocele is common

A

true

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6
Q

who is affected by mucocele?

A

all ages but especially children, young adults

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7
Q

what is the most common site for a mucocele?

A

lower lip (82%)

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8
Q

what sites are affected by mucocele?

A
  1. lower lip
  2. buccal mucosa
  3. ventral tongue
  4. floor of mouth
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9
Q

clinical features of mucocele

A
  1. non-tender, soft swelling
  2. may be fluctuant or firm
  3. color: translucent to bluish
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10
Q

T/F: reoccurance does not happen with mucocele

A

false, may have history of repeated swelling and resolution

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11
Q

ranula

A

type of mucocele seen on the floor of the mouth

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12
Q

what does ranula arise from?

A

sublingual gland

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13
Q

T/F: ranula develops on the floor of the mouth to the right of midline

A

false, can be right or left of midline

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14
Q

clinical features of ranula

A

similar as mucocele

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15
Q

histopathologic features of mucocele/ranula

A
  1. extravasated mucin

2. granulation tissue with variable numbers of inflammatory cells

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16
Q

treatment of mucocele/ranula

A
  1. microscopic exam to rule out neoplasm

2. excision of mucous deposit including involved gland

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17
Q

T/F: some mucocele/ranula resolve without treatment especially superficial ones

A

true

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18
Q

T/F: treatment for ranula may include marsupialization (“unroofing”)

A

true

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19
Q

marsupialization

A

making incision into the lesion and suturing the edges so inner and external surfaces are continuous

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20
Q

prognosis of mucocele/ranula

A

excellent

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21
Q

mucocele/ranula will occasionally recur if what?

A

if the involved gland is not excised

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22
Q

sialolithiasis

A

deposition of calcium salts around nidus of debris in lumen

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23
Q

what causes sialolithiasis?

A

unclear but can possibly due to

  1. chronic sialadenitis
  2. partial ductal obstruction
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24
Q

where does sialolithiasis occur?

A

submandibular gland, parotid or minor glands

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25
Q

what percent of sialolithiasis occur in the submandibular gland?

A

80%

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26
Q

clinical features of sialolithiasis

A
  1. hard submucosal mass in soft tissue
  2. ± symptoms
  3. may have swelling prior to or during meals
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27
Q

radiographic features of sialolithiasis

A

soft tissue film shows opaque, lamellated structure

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28
Q

histopathologic features of sialolithiasis

A
  1. concentric laminatiosn that may surround a nidus of amorphous debris
  2. periductal inflammation
  3. acute or chronic sialadenitis of the feeding gland
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29
Q

if the duct associated with sialolithiasis is removed, then it often demonstrates what histopathologically?

A

squamous metaplasia

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30
Q

treatment for sialolithiasis

A
  1. gentle massage to “milk” saliva toward orifice
  2. sialogogues (medications which stimulate saliva)
  3. sour sugarless candies
  4. increase fluid intake to “flush”
  5. moist heat
  6. surgical removal, may include gland if significant inflammatory damage
  7. lithotripsy, sialendoscopy with basket retrieval (major gland)
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31
Q

prognosis of sialolithiasis in minor glands

A

good

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32
Q

prognosis of sialolithiasis in major glands

A

good, but morbidity if gland requires removal

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33
Q

acute/chronic sialadenitis

A

inflammation of the salivary gland

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34
Q

causes of acute/chronic sialadenitis

A
  1. bacterial
  2. viral
  3. ductal obstruction, retrograde infection
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35
Q

bacteria that causes acute/chronic sialadenitis

A

often penicillinase-producing staph

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36
Q

virus that causes acute/chronic sialadenitis

A

most often mumps

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37
Q

acute/chronic sialadenitis caused by ductal obstruction, retrograde infection is associated with what?

A

xerostomia, may follow general anesthesia

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38
Q

T/F: chronic may follow acute sialadenitis due to ductal damage

A

true

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39
Q

clinical features of acute/chronic sialadenitis

A
  1. diffuse
  2. unilateral swelling
  3. painful/tender, especially around meal times
  4. may feel warm
  5. overlying skin may be erythematous
  6. may have low-grade fever
  7. may have trismus
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40
Q

acute sialadenitis usually affects which gland?

A

parotid

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41
Q

what may be expressed in acute sialadenitis?

A

purulent exudate expressed from the parotid papilla

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42
Q

chronic sialadenitis usually affects which gland?

A

submandibular gland

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43
Q

radiographic feature of chronic sialadenitis

A

sialography: “sausage-link” appearance of ductal system due to ductal dilatation

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44
Q

histopathologic features of acute/chronic sialadenitis

A
  1. chronic inflammatory cell infiltrate
  2. dilated ducts
  3. acinar atrophy
  4. fibrosis
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45
Q

treatment of acute/chronic sialadenitis

A
  1. screening radiograph to rule-out sialolith
  2. antibiotic therapy - broad spectrum (i.e. tetracycline)
  3. culture and sensitivity if purulence
  4. massage (with caution)
  5. warm compress
  6. sialogogues with hydration (or sugarless lemon drops)
  7. ductal stenting
  8. sialoendoscopy with saline irrigation
  9. surgical drainage
  10. surgical removal of affected gland may be needed
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46
Q

T/F: antibiotics prescribed for acute/chronic sialadenitis may adjusted depending on culture and sensitivity result

A

true

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47
Q

prognosis of acute/chronic sialadenitis

A

can range from excellent to poor if gland must be removed

48
Q

why does acute sialadenitis reported to have 20-50% mortality rate in debilitated patients?

A

because of the spread of the infection and sepsis

49
Q

treatment for chronic sialadenitis

A

conservative therapy to surgical intervention

50
Q

T/F: the etiology of sialadenosis is infectious

A

false, non-infectious etiology

51
Q

what is sialadenosis associated with?

A

associated with underlying systemic condition

  • diabetes
  • malnutrition
  • alcoholism
  • bulimia
52
Q

treatment for sialadenosis

A
  1. often unsatisfactory - control of underlying disease
  2. partial parotidectomy cosmetic reasons
  3. pilocarpine reported to be beneficial
53
Q

prognosis of sialadenosis

A

fair-poor, depending on disease

54
Q

xerostomia

A

subjective symptom of dryness

55
Q

xerostomia predisposes people to what?

A
  1. mucosa susceptible to injury due to lack of lubrication
  2. oral candidiasis
  3. increased caries, especially cervical
56
Q

causes of xerostomia

A
  1. medications especially polypharmacy
  2. glandular aplasia or hypofunction
  3. radiation therapy
  4. graft vs host disease
  5. Sjogren syndrome
57
Q

polypharmacy medications

A
  1. antihistamines
  2. antidepressants
  3. sedatives and anxiolytic agents
  4. antihypertensive agents
58
Q

clinical features of xerostomia

A
  1. meticulous oral hygiene and early disease
  2. absence of pool of saliva at FoM
  3. lipstick on teeth
  4. glove, gauze or mirror sticks to mucosa
  5. saliva frothy, stringy or sticky
  6. oral malodor
59
Q

treatment for xerostomia

A
  1. good hydration/frequent sips of water
  2. artificial saliva/lubricants
  3. sialogogues, SUGAR-FREE lemon drops
  4. 1% neutral sodium fluoride gel or toothpaste nightly
  5. antifungal therapy as needed
  6. more frequent dental recall
60
Q

prognosis of xerostomia

A

variable

61
Q

T/F: people with xerostomia are at a high risk for caries

A

true, think prevention

62
Q

benign lymphoepithelial lesion (BLEL)

A

an autoimmune condition that causes proliferation of epithelial cells and lymphocytes (mainly parotid and lacrimal glands)

63
Q

what might BLEL be associated with?

A

Sjogren syndrome

64
Q

recent data suggests that a portion of the infiltrate in BLEL is monoclonal, perhaps representing what?

A

a low-grade lymphoma in situ

65
Q

who is affected by BLEL?

A

female predilection, middle-aged or older

66
Q

clinical feature of BLEL

A

unilateral or bilateral, firm, non-tender swelling of the parotid area

67
Q

radiographic feature of BLEL

A

sialography: “blossoms on a tree” pattern of punctate sialectasis often observed

68
Q

histopathologic features of BLEL

A
  1. destruction of the normal parotid parencyma with replacement by a diffuse lymphocytic infiltrate
  2. occasionally see germinal centers
  3. remnants of ductal epithelium “epimyoepithelial islands”
69
Q

what does epimyoepithelial islands represent when seen histopathologically in BLEL?

A

residual ductal structures

70
Q

epimyoepithelial islands are also seen histopathologically in what other disease besides BLEL?

A

lymphoma

71
Q

why does treatment for BLEL vary?

A

varies depending on how much appearance bothers patient

72
Q

treatment for BLEL

A
  1. do nothing
  2. low-dose radiation
  3. corticosteroid therapy
73
Q

prognosis for BLEL

A

good

74
Q

can BLEL transform?

A

yes, malignant transformation of lymphoid or epithelial components have been reported

75
Q

what are the 2 forms of Sjorgen syndrome?

A
  1. primary

2. secondary

76
Q

T/F: Sjogren sydrome is an acquired condition

A

false, autoimmune condition

77
Q

Sjogren syndrome is thought to be a continuation of what condition?

A

BLEL

78
Q

primary Sjogren syndrome

A

aka sicca syndrome

- xerostomia and keratoconjunctivitis sicca (dry eyes)

79
Q

secondary Sjogren syndrome

A

sicca syndrome plus any other autoimmune disease (e.g. rheumatoid arthritis, systemic lupus erythematosus, Hashimoto’s thyroiditis, mixed CT disease, etc.)

80
Q

Sjogren syndrome

A

autoimmune process attacks lacrimal and salivary glands

81
Q

who is affected by Sjogren syndrome?

A

usually middle-age to older adults, but has been seen in children

82
Q

T/F: Sjogren syndrome has a 9:1 male predilection

A

false, 9:1 FEMALE predilection

83
Q

clinical features of Sjogren syndrome

A
  1. partoid swelling (BLEL) may or may not be dramatic
  2. patients often complain of dry, gritty feeling in eyes and a dry mouth
  3. cervical caries, often rampant
  4. increased prevalence of oral candidiasis
  5. burning feeling on tongue
  6. angular cheilitis
  7. atrophy of dorsal tongue papillae
84
Q

diagnosis of Sjogren syndrome

A
  1. serology
  2. laboratory
  3. international classification criteria for Sjogren syndrome
  4. labial salivary gland biopsy
85
Q

How do people with Sjogren syndrome measure their salivary flow on the Schirmer tear test?

A

normal salivary flow wets the entire strip; Sjogren less than 5 mm

86
Q

T/F: most of the time, serology tests are relatively specific

A

false, relatively NON-SPECIFIC

87
Q

how do patients with Sjogren syndrome score on serology test?

A

patients tend to have an elevated erythrocyte sedimentation rate (ESR) and polyhypergammaglobulinemia, especially IgG

88
Q

T/F: laboratory tests used to diagnose Sjogren syndrome tests a variety of autoantibiodies, which are characteristic but specific

A

false, characteristic but NOT specific

89
Q

how do patients with Sjogren syndrome score on laboratory tests?

A
  1. positive rheumatoid factor (RF) in ~60%

2. anti-nuclear autoantibodies (ANAs) in ~80%: anti-Rho and anti-La

90
Q

labial salivary gland biopsy technique

A
  1. lower labial mucosa, lateral to midline, uninflammed
  2. 1 cm incision, parallel to vermilion zone
  3. remove at least 5 minor glands through the incision and place them in routine 10% buffered formalin
91
Q

histopathologic features of Sjogren syndrome

A
  1. aggregates (foci) of >50 lymphocytes ± plasma cells scattered throughout glandular parenchyma
  2. 1 or more foci of 50 or more cells per 4-mm^2 of glandular tissue supports Dx of
    Sjögren syndrome
92
Q

why are lobules of gland exhibiting acinar atrophy and interstitial fibrosis excluded from diagnosing Sjogren syndrome?

A

these are non-specific features related to aging

93
Q

treatment for Sjogren syndrome

A
  1. hydration
  2. artificial tears and artificial saliva/lubricants
  3. sialogogues
  4. daily topical fluorides for natural teeth
  5. anti-fungal agents for candidiasis, as needed
  6. more frequent dental prophylaxis; plaque control
  7. for secondary Sjogren syndrome, appropriate therapy for other autoimmune processes
94
Q

prognosis of Sjogren syndrome

A

fair

95
Q

patients with Sjogren syndrome have a what increase in lymphoma compared to age- and sex-matched population?

A

44x increase

96
Q

what causes nectrotizing sialometaplasia?

A

thought to be due to ischemic necrosis

  • traumatic injury
  • dental injections
  • ill-fitting dentures
  • upper respiratory infection
  • eating disorders (binge-purge)
  • adjacenet tumor
  • previous surgery
97
Q

who is affected by nectrotizing sialometaplasia

A

adults, rare in children

98
Q

T/F: nectrotizing sialometaplasia has a female predilection

A

false, male

99
Q

where is the most common location for nectrotizing sialometaplasia?

A

possterior hard palate/anterior soft palate

100
Q

clinical features of nectrotizing sialometaplasia

A
  1. swelling ± pain, paresthesia
  2. sharply demarcated ulcer, non-elevated margins
  3. minimal peripheral erythema
101
Q

what do patients with nectrotizing sialometaplasia usually report ~2 weeks after diagnosis?

A

“a piece of my palate fell out”

102
Q

how long does it take for nectrotizing sialometaplasia heal?

A

4-6 weeks

103
Q

what is nectrotizing sialometaplasia easily mistaken for?

A

SCC or mucoepidermoid carcinoma (a cancer of salivary gland) by an inexperienced pathologist

104
Q

early stages of nectrotizing sialometaplasia show what?

A

only lobular ischemic necrosis

105
Q

histopathologic features of nectrotizing sialometaplasia

A
  1. pseudoepitheliomatous hyperplasia (PEH) of surface epithelium
  2. acinar necrosis, but overall architecture of involved gland is preserved
  3. squamous metaplasia of the ductal epithelium - confined to normal boundaries of the gland
106
Q

pseudoepitheliomatous hyperplasia (PEH)

A

nonspecific reactive hyperplasia (no separation) stratified mucocutaneous epithelia, which simulates squamous cell carcinoma (diagnostic pitfall)

107
Q

sialorrhea

A

constant hypersalivation (“pool and drool”)

108
Q

primary sialorrhea causes what?

A

increased salivary flow

109
Q

secondary sialorrhea causes what?

A

impaired swallowing

110
Q

what is the most common cause of sialorrhea?

A

neuromuscular dysfunction

111
Q

causes of sialorrhea

A
  1. neuromuscular dysfunction
  2. hypersecretion
  3. motor or sensory dysfunction
  4. drug-induced (antipsychotics esp. chozapine, meds for Alzheimer’s dementia and myasthenia gravis, exposure to heavy metal toxins, insecticides, nerve agents)
112
Q

why may sialorrhea be problematic?

A
  1. social implications
  2. skin irritation
  3. requirement for numerous clothing changes
113
Q

sialorrhea in more severe cases may cause what?

A

dehydration and aspiration pneumonia

114
Q

treatment for sialorrhea

A
  1. surgical
  2. botulinum toxin A (Botox)
  3. anticholinergics
115
Q

surgical treatment for sialorrhea

A
  1. submandibular duct relocation
  2. ductal ligation
  3. removal of gland
116
Q

T/F: management of sialorrhea is a challenge for it depends on underlying condition and individual’s response to therapies

A

true