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Oral medicine > Salivary Glands > Flashcards

Salivary Glands Flashcards

1
Q

Functions of saliva

A 
Tissue coating
Buffering
Digestion
Dental protection
Lubrication and viscoelasticity
Anti bacterial/fungal/viral
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2
Q

Sialosis

A

Non pathogenic, non neoplastic increase in salivary gland size

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3
Q

Sialadenitis

A

Ductal infection

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4
Q

Sialolithiasis

A

Duct obstruction

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5
Q

Sialectasis

A

Cystic dilatation of duct

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6
Q

Sialorrhoea

A

Excessive salivation/ drooling

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7
Q

What virus is acute viral sialadenitis often caused by?

A

Mumps

RNA virus paramyxovirus

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8
Q

Acute viral sialadenitis presentation

A 
Usually parotid (rarely SM)
Pain
Usually bilateral enlargement
Skin over unaffected 
Malaise, fever, headache
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9
Q

Acute viral sialadenitis spread

A

Droplet/direct contact

2-3 wks IP

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10
Q

Acute viral sialadenitis extrasalivary manifestations

A

Ochitis
Oophoritis
Pancreatitis

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11
Q

Acute viral sialadenitis histology

A

Accumulation of neutrophils and fluid in lumen of ductal structures

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12
Q

Management of acute viral sialadenitis

A

Clinical diagnosis
Fluid and pain meds
Second attack possible
Vaccination

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13
Q

Pathogenesis of acute bacterial sialadenitis

A

Retrograde contamination of salivary ducts and parenchymal tissues
- reduced flow can predispose pt - bacteria enter against flow
Stasis of flow caused by hypersalivation, dehydration, med induced hyposalivation, obstruction, strictures, adhesions, sialolithiasis

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14
Q

acute bacterial sialadenitis underlying causes

A 
ALWAYS
Dehydration and flow reduction 
Flow obstruction
DM
Immunosuppression
Abnormal anatomy

Most commonly affects : hospital inpts, elderly, H and N radio pts, SS pts, pre-existing salivary conditions

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15
Q

acute bacterial sialadenitis bacteria

A

S pyogenes, s aureus, prevotella spp

Rarely mycobacteria

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16
Q

acute bacterial sialadenitis presentation

A 
Painful and tender enlargement of one gland 
Pus discharge duct
Reddening of overlying skin
Trismus 
Pyrexia
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17
Q

acute bacterial sialadenitis histology

A

Acinar destruction with neutrophil infiltrates and bacterial presence

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18
Q

acute bacterial sialadenitis diagnosis

A

Clinical

Needle aspirate pus sample

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19
Q

acute bacterial sialadenitis tx

A

Antibiotics and analgesia
Fluids
Good OH
may need IV drainage

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20
Q

acute bacterial sialadenitis pathophysiology

A

Duct ectasia
Mucous metaplasia of ductal epithelium
Periductal fibrosis
Fusion of lobules

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21
Q

Chronic sialadenitis

A

Low grade bacterial invasion
Relapsing/radiation/sclerosing
Can develop after acute sialadenitis or calculi formation

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22
Q

Chronic sialadenitis clinical

A

Recurrent attacks of pain and swelling

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23
Q

Chronic sialadenitis histology

A

Atrophy of serous acini during chronic obstructions

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24
Q

Chronic sialadenitis diagnosis

A

Clinical and history

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25
Q

Chronic sialadenitis tx

A

Surgical excision

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26
Q

Chronic recurrent parotitis

A

Most common form of chronic sialadenitis
?aetiology
- semisolid material - coagulated albumin - as a result of gland inflammation, obstructs duct network, swelling

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27
Q

Chronic recurrent parotitis ages

A

Children 4m-15yrs

Adults 40-60 years

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28
Q

Chronic recurrent parotitis clinically

A 
Sudden onset parotid swelling
Usually unilateral
Varying discomfort
Overlying skin normal/slightly reddish, low-grade fever
Swelling 24-48 hrs, 1-2wks, months
Followed by clear periods weeks-years
Periodic as duct cleared by muscles/sialogogues 
Viscous and milky secretion (rarely pus)
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29
Q

Chronic recurrent parotitis tx

A

Short term steroids

Ductal clearance from ppt serum proteins

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30
Q

What is the most common benign minor SG lesion?

A

Mucocele

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31
Q

Main cause of mucocele

A

Mechanical trauma on discharge duct

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32
Q

Extravasation mucocele

A

Pseudocysts (no epithelial lining)
Mechanical trauma to excretory duct - transaction/rupture
Extravasation of mucin into CT - triggers inflammatory and granular reaction to contain Extravasation
Common minor SGs L lip, buccal mucosa and RM area

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33
Q

Retention mucocele

A

Lined by ductal epithelium , cystic dilatation
Often elderly
Due to duct obstruction- sialolith/periductal strictures/invasive tumour
Narrowing of ductal opening - reduced flow, subsequent distal distension - mucosal swelling
Common U lip, HP, FOM, MS

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34
Q

ranula

A

variant of mucocele on FOM which usually arises in body of SL gland and occ inducts of Rivini/Wharton’s duct
if extends through mylohyoid plunging ranula

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35
Q

mucocele most common sites

A

lip

FOM

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36
Q

mucocele clinical presentation

A 
surface smooth (can be rough/ulcerated)
colour: red/whitish/bluish/translucent
usually asymptomatic
fluctuant - rupture and release mucous - salty taste
often hx of trauma
usually bulging mass (can be polypoid/blister)
usually 0-2cm
most <30yrs, M
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37
Q

U lip mucocele

A

beware - likely a pathological lesion

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38
Q

mucocele diagnosis

A

hx and exam

US: cystic masses, sometimes contain fibrillar processes produced by FBs

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39
Q

mucocele recurrence

A

esp if traumatic habit persists

RFs - younger pt, ventral tongue

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40
Q

mucocele histology

A 
vascular GT surrounding a mucus pool
foam cells
macrophage lined cavity
severed duct if trauma
cystic cavity
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41
Q

mucocele tx

A 
usually surgical
 - surgery - complete excision/marsupialisation/dissection
 - cryosurgery
 - CO2 laser
 - electrocautery
non-surgical
 - IL injection of sclerosing agent
 - IL steroid injection
can resolve spontaneously
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42
Q

sialolith formation

A

small deposits of Ca etc that form on bacteria, mucus or epithelial cells, can block saliva flow and cause gland to swell

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43
Q

where are most sialoliths and why?

A

80% SMG
2x as much Ca as parotid, quite alkaline and mucous
tortous and uphill path

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44
Q

predisposing factors for sialolithiasis

A 
cause unknown
age
radio H+N
mouth injuries/trauma
meds affecting saliva production
SS
kidney problems
not drinking enough water
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45
Q

sialolithiasis clinical presentation

A

unilateral SG swelling
painful
intermittent
worst pain periprandial (flow)
gout link?
usually asymptomatic whilst forming, can sometimes disappear
affected gland can get infected - suppurative sialadenitis

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46
Q

sialolithiasis histology

A

dilated ducts with calculi
chronic inflammatory cells
calcified structure
metaplasia from columnar to SSE of lining - chronic irritation from stone

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47
Q

sialolithiasis diagnosis

A

hx
attempt to palpate calculus
radiograph (not always obvious - referral?)
sialography
CT - check for other causes of obstruction

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48
Q

sialolithiasis tx

A 
conservative
 - moist heat and gentle massage
 - hydration
 - sialogogues e.g. lemon drops - try to remove it if in 
   proximity of exit
 - NSAIDs
 - ABs if infection
surgery
lithotripsy
sialendoscopy
duct dilatation
surgical removal of gland: recurrent stones/irreversible damage to gland
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49
Q

other gland obstruction

A 
recurrent parotitis
 - HIV
 - duct stenosis
 - bacterial infection
chronic obstructive sialadenitis
 - usually caused by sialalithiasis
 - can be post-op
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50
Q

sialosis

A

non-inflammatory, non-neoplastic, chronic, diffuse enlargement of major SGs (usually parotid, occ SM, rarely minor)
painless/((tender))
bilateral
can be reactive mechanism e.g. EDs/alcoholism
clinical diagnosis
no tx

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51
Q

sialosis histology

A

hypertrophy (increase in cell size) of serous acini

oedema of interstitial CT

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52
Q

xerostomia

A

subjective feeling of oral dryness, may/may not be accompanied by hyposalivation

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53
Q

hyposalivation

A

objective reduction in salivary flow and production

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54
Q

causes of xerostomia

A 
dehydration
psychological
neurological dysfct
disease e.g. SS
medications
radio
SG tumour
SG trauma
nutritional deficiencies and/or EDs
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55
Q

meds which cause dry mouth

A 
tricyclics
B-blockers
antipsychotics
antihistamines
atropine
diuretics
cytotoxics
antimuscarinic cholinergic drugs
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56
Q

radiation

A

critical dose limits for parotid and SM tissue 40Gy, most regimens exceed this
declines during tx
fct deterioration in secretion up to several months after, concomitant with progressive, irreversible changes of the SG tissue with no significant recovery in gland fct

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57
Q

oral manifestations of xerostomia

A 
difficulties: speaking, sleeping, tasting, chewing, swallowing
caries - incisal edge and cervical
PDD
oral infections
 - fungal - candida, angular cheilitis
 - bacterial - staph
 - SG infections
atrophic lesions - depapillated tongue
traumatic lesions
reduced denture retention
halitosis
bad taste
frothy saliva
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58
Q

clinical evaluation of SG fct - history

A

systemic/local diseases
trauma
meds list

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59
Q

clinical evaluation of SG fct - symptom Qs

A

sip liquids to aid swallowing dry foods?
does mouth feel dry when eating?
diff swallowing any foods?
amount of saliva seem too little/much/don’t notice

= common complaints but don’t reliably predict SG hypofct

additional symptoms

  • speaking and eating difficulties
  • taste disturbances
  • halitosis, oral discomfort, intolerance of acidic/spicy
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60
Q

clinical evaluation of SG fct - physical exam

A

EO: major SGs, LNs
IO: STs, periodontium, dentition

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61
Q

challacombe scale oral dryness - about

A

additive score 1-10
symptoms will not necessarily progress in the order shown, but summated scores indicate likely pt needs
monitor symptom progression/regression

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62
Q

challacombe scale oral dryness - mild

A

1 - mirror sticks to buccal mucosa
2 - mirror sticks to tongue
3 - saliva frothy
= mild, may not need tx, SF gum, hydration, routine monitoring

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63
Q

challacombe scale oral dryness - mod

A

4 - no saliva pooling in FOM
5 - tongue mild depapillation
6 - altered gingival architecture i.e. smooth
= mod, SF gum/simple sialogogues, substitutes, F
investigate if reasons not clear
monitor regularly - decay and S+S

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64
Q

challacombe scale oral dryness - severe

A 
7 - glassy appearance esp palate
8 - tongue lobulated/fissured
9 - cervical caries (>2 teeth)
10 - debris on palate or sticking to teeth
 = severe, saliva substitutes and topical F
identify cause, exclude SS
refer
monitor, specialist input if worsening
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65
Q

xerostomia measurements and lab tests

A 
measure salivary output
 - UWSF, SWSF
 - ductal flow of major SGs
sialochemical analyses
serum lab studies
 - CBC with differential
 - AI markers
 - serum immunoglobulins
 - ESR
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66
Q

xerostomia imaging

A 
US: superficial
sonoelastography: (postradiation)
CT: tumours
*MRI: tumours
scintigraphy: fct - assess SG dysfct
PET: high cellular activity areas sign of tumour
sialography
radiograph
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67
Q

salivary biopsy

A 
FNA
major SG
minor labial SG
 - ≥5 minor glands
SS: focus score ≥1 per 4mm2
(focus score - ≥50 mononucleate cells per 4mm2)
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68
Q

pilocarpine SEs

A 
vision changes
hiccups
bradycardia
hypotension
bronchoconstriction
hyperhidrosis
nausea, vomiting, diarrhoea
cutaneous vasodilation
increased urinary freq
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69
Q

xerostomia therapy

A

water
tx cause if possible: hydration, modify drugs, control diseases
relief/substitutes - oralbalance
gustatory and tactile sialogogues
- SF acidic sweets, lemon pastilles, SF gum
pharmacologic sialogogues
- cevimeline (US only), pilocarpine (cholinergic),
betanechol chloride

70
Q

pilocarpine dose

A

5mg daily, up to 30mg

71
Q

pilocarpine contraindications

A 
iritis and narrow-angle glaucoma
CV disease
chronic pulmonary disease inc uncontrolled asthma
pts taking B-adrenergic blockers
active gastric ulcers
72
Q

hypersalivation/sialorrhea

A

increased saliva flow
drooling (salivary incontinence) not usually associated with increased production of saliva
- upset in coordinated control mechanism of orofacial and palato-lingual musculature leading to excessive pooling of saliva in anterior mouth
- unintentional loss of saliva from mouth

73
Q

drooling common causes

A

reduced swallowing
- NM diseases: CP, Parkinsons, stroke
- anatomic abnormalities: macroglossia, ortho problems
(incompetent lips, AOB), surgical defects following
major HandN resection, TMJ ankylosis)

74
Q

causes of hypersalivation

A

irritating oral disease (ulceration, infection, trauma)
med SEs (clozapine, risperidone, nitrazepam, bethanecol)
GORD
ENT diseases - can have oesophageal aetiologies - obstructive, inflammatory

75
Q

hypersalivation causes - medications

A

parasympathomimetic drugs causing an increase of salivary flow rate, low viscosity
directly working
- arecoline, bethanechol, cevimeline, methacholine,
muscarine, pilocarpine
indirectly working
- cisapride, neostigmine, nizatidine, physostigmine

76
Q

clinical features of drooling

A

repeated perioral cutaneous alterations
aspiration-related resp and pulmonary complications
altered speech and swallowing
social and psychological consequences

77
Q

assessment of drooling - freq

A

dry - never drools
occ drooling - not every day
freq - drooling every day
constant - constant drooling

78
Q

assessment of drooling - severity

A 
dry - never drools
mild - only lips wet
mod - lips and chin wet
severe - clothing soiled
profuse - hands and tray moist and wet
79
Q

drooling therapy

A 
oral motor training
speech therapy
behaviour therapy
drugs
 - antihistamines
 - glycopyrrolate (tablets)
 - scopolamine (patch)
 - Botox A - good in Parkinsons
surgery
radio
others
 - photocoagulation of salivary ducts
 - tongue acupuncture
80
Q

drooling surgical tx

A 
reduce flow/redirect flow to location more advantageous to promote swallowing
SMG excision
SM duct re-routing
parotid duct re-routing
parotid duct ligation
transtympanic neurectomy
81
Q

acute necrotising sialometaplasia about and predisposing factors

A

trauma induced
smokers
benign ulcerative lesion (resembles a SCC)
small vessel infarct

82
Q

acute necrotising sialometaplasia pathophysiology

A

ischaemic necrosis of minor SGs
lack of blood supply leads to death of the tissue and infarction of the SGs
vascular damage of palatine vessels

83
Q

acute necrotising sialometaplasia clinically

A

typically HP/SP jct
surface slough necrotic tissue
initially red tender swelling then central ulcer when overlying mucosa breaks down
anaesthesia can be associated to affected area

84
Q

acute necrotising sialometaplasia histology

A

hyperplasia
metaplasia of ducts
necrosis of salivary acini

85
Q

acute necrotising sialometaplasia diagnosis

A

usually biopsy to ensure not SCC

86
Q

acute necrotising sialometaplasia management

A

self-resolving within 6-10wks

antiseptic MW to tx ulceration

87
Q

SG neoplasms - locations with high risk of malignancy

A

SL gland

tongue

88
Q

what % of SG neoplasms are benign?

A

80%

89
Q

what % of SG neoplasms are parotid gland?

A

80% and 80% in superficial lobe

90
Q

SG neoplasms - clinically

A

asymptomatic swelling and eversion of ear lobes
no xerostomia
malignant - can be pain/ulcerate/facial palsy

91
Q

SG neoplasms management

A

surgical excision +/- radio

92
Q

Frey’s syndrome

A

if parotid gland tumour excision risk of damage to facial nerve - Frey’s syndrome
‘gustatory sweating’ - damaged nerve fibres regrow to supply the sweat glands of the skin
- when hungry you sweat

93
Q

SG neoplasms - indication of malignant change

A

rapid growth
pain
fixation to deep tissues
facial palsy

94
Q

which area is most affected by minor SG neoplasms?

A

palate

95
Q

usual benign locations of minor SG neoplasms

A

lip
buccal
palatal

96
Q

usual malignant locations of minor SG neoplasms

A

tongue
FOM
RM pad

97
Q

benign epithelial tumours

A

pleomorphic adenoma
Wharthin tumour
oncocytoma

98
Q

malignant epithelial tumours

A

mucoepidermoid carcinoma
adenoid cystic carcinoma
acinic cell carcinoma

99
Q

order of incidence of SG neoplasms

A 
pleomorphic adenoma
Warthin's tumour
adenoid cystic carcinoma
mucoepidermoid carcinoma
acinic cell carcinoma
100
Q

what is the most common SG tumour?

A

pleomorphic adenoma

101
Q

pleomorphic adenoma - site

A

parotid 90% then SM and minor palate (fixed mass)

102
Q

pleomorphic adenoma - clinical

A 
solitary, painless, slow-growing
unilateral swelling
not fixed to underlying tissues
skin overlying normal but can give bluish appearance
most parotid affect superficial lobe
103
Q

pleomorphic adenoma - histology

A

epithelial component: ducts or cystic structures
myoepithelial cells: angled, fusiform or rounded cells
stroma: CT, myxoid, chondroid, chondromyxoid, hyaline, fibrous
usually encapsulated with fibrous tissue (non/poorly encapsulated related to recurrence)

104
Q

pleomorphic adenoma - tx

A

surgery

105
Q

pleomorphic adenoma - outcome

A

can recur

risk of malignant transformation (3-13%)

106
Q

Warthin’s tumour - location

A

almost exclusively parotid and superficial lobe, can be bilateral (5-14%)

  • 2.3% SM
  • ext rare in minor
107
Q

Warthin’s tumour - usual age

A

> 40yrs

108
Q

Warthin’s tumour - clinical

A

painless, slow-growing, round/oval mass

sometimes fluctuant swelling

109
Q

Warthin’s tumour - histology

A

epithelial tissue, cystic formations
dense lymphoid tissue stroma
- can get germinal centres in this
well defined CT capsule

110
Q

Warthin’s tumour - tx

A

surgery (/monitor)

111
Q

Warthin’s tumour - outcome

A

low recurrence rate

1% malignant transformation of epithelial component

112
Q

oncocytoma - incidence

A

rare <1%

113
Q

oncocytoma - location

A

mostly parotid
rare minor
rarer SMG

114
Q

oncocytoma - clinical

A

painless, slow-growing, non-tender, firm, lobulated and mobile mass
occ pain/facial nerve paralysis

115
Q

oncocytoma - histology

A

monotonous, polygonal, eosinophilic (oncocytic) epithelial cells
round uniform nucleus
low nucleus-cytoplasm ratio

116
Q

oncocytoma - outcome

A

v low malignant potential
SMG best prognosis
recurrence 20% - insufficient surgery and occult multinodularity

117
Q

oncocytoma - tx

A

surgery

118
Q

what is the most common major SG malignant tumour?

A

mucoepidermoid carcinoma

119
Q

what is the most common minor SG malignant tumour?

A

adenoid cystic carcinoma

120
Q

mucoepidermoid carcinoma - site

A

50% parotid, but can affect any

121
Q

mucoepidermoid carcinoma - minor

A

most common on palate, rubbery/soft mass, may stimulate a mucocele/vascular tumour
also RM area

122
Q

mucoepidermoid carcinoma - clinical

A

swelling, pain, ulcer, infiltration, discolouration, facial paralysis

123
Q

mucoepidermoid carcinoma - histology

A

mucin secreting cells
intermediate cells
epidermoid cells

slow growth and can infiltrate surrounding tissues

124
Q

mucoepidermoid carcinoma - freq spread

A

perineural spread

40% show high-grade metastasis

125
Q

mucoepidermoid carcinoma - tx

A

surgery and radio

126
Q

mucoepidermoid carcinoma - outcome

A

high grade poorer survival

127
Q

adenoid cystic carcinoma - site

A

most common minor SG malignancy - often palate

can present in major

128
Q

adenoid cystic carcinoma - clinical

A

asymptomatic mass, can get ulcer
pain/cranial neuropathies - early and freq perineural invasion - parotid - facial n palsy
slow growing
locally invasive
metastasises
- cervical LNs, lung, liver, bone
haematogenous spread - to lungs most common which is unusual for a carcinoma

129
Q

adenoid cystic carcinoma - histology

A 
swiss cheese
no capsule
cribiform pattern most common
tubular type best prognosis
solid type least common - most aggressive and higher distant metastases
130
Q

adenoid cystic carcinoma - tx

A

surgery and radio

poor prognosis - local recurrence - hard to determine clinically how far tumour has spread

131
Q

acinic cell carcinoma - location

A

parotid >80%, can be bilateral

132
Q

acinic cell carcinoma - clinical

A 
slowly enlarging mass, few symptoms
occ involves nerves/regional nodes
usually solitary, encapsulated, soft, grey-white
invasive
slow growth, good prognosis
133
Q

acinic cell carcinoma - histology

A 
serous acinar cell differentiation
 - microcystic, solid, papillary cystic, follicular
clear/vacuolated cells
intercalated duct-like cells
non-specific glandular cells
134
Q

acinic cell carcinoma - tx

A

surgery

135
Q

polymorphous low-grade adenoma

A

rare
most common palate
M>F
slow growing

136
Q

which malignant tumours ten to have a slow growth pattern?

A

adenoid cystic carcinoma
low-grade MEC
acinic cell carcinoma

137
Q

prognostic factors for malignant SG tumour prognosis

A 
age
stage
histology
grading
lympho-vascular invasion
FN paralysis
cervical node involvement
neural spread
\+ surgical margins
site
gene mutations
138
Q

diagnosis of SG tumours - clinical S+S

A 
rapid growth rate
pain
facial nerve involvement
neck nodes
complete/partial parapharyngeal or palatal fullness
trismus
skin ulceration
fistulas
 = but be suspicious of every painless swelling of a SG
139
Q

diagnosis of SG tumours

A 
clinical S+S
US
MRI
pathology
TNM staging
140
Q

diagnosis of SG tumours - US

A

cheap, safe, accuracy 90%

141
Q

diagnosis of SG tumours - MRI

A

interface of tumour and tissue for surgical planning

142
Q

diagnosis of SG tumours - pathology

A

open biopsy not usually recommended due to risk of seeding
if small masses in minor SGs (palate, tongue) - punch biopsy
US guided FNA cytology

143
Q

tx of SG tumours

A

surgery
post-op radio recommended in selected pts
chemo only suitable for individual clinical use as palliative for unresectable disease, pts not amenable to radio, pts with metastatic disease

144
Q

TNM staging for SG tumours

A

Tx - T4b
Nx - N3
M0 - M1

145
Q

parotid gland

A

serous

stensen duct

146
Q

SMG

A

mixed

wharton duct

147
Q

SL gland

A

mucous

148
Q

aplasia

A

congenital absence of ≥ SGs

ectodermal dysplasia

149
Q

duct atresia

A

failure of a duct to canalise

can result in salivary retention cysts

150
Q

HIV

A

parotid enlargement in up to 10% pts

151
Q

CF

A

causes plugging of acinar ducts with precipitated secretions

essentially microscopic sialoliths

152
Q

sarcoidosis

A

collections of granulomas

can occur in any organ but often affect SGs causing large masses and facial palsy

153
Q

gland infiltration

A 
amyloidosis
 - build up of amyloid protein fibrils
 - lymphoepithelial cysts
haemachromatosis
 - causes xerostomia
154
Q

cancer tx that affects SGs

A

radio
GvHD
anti-neoplastic drugs (chemo)
radioiodine

155
Q

why are salivary tissues sensitive to radio?

A

due to their highly differentiated and specialised state

- not because of high mitotic figures

156
Q

radio and saliva

A

reduced quantity and quality of saliva
saliva usually reproduced after 4-8wks of finishing tx
- but can be thick, viscous and bad tasting
fibrosis of salivary tissue - end arteritis

157
Q

GvHD and saliva

A

mainly haematopoietic SC pts

results in SS

158
Q

chemo and saliva

A

reduced secretion

early apoptosis of SG cells

159
Q

radioiodine and saliva

A

reduction of gland fct

increased lymphocytic infiltrate

160
Q

saliva substitutes

A

glandosane
saliva orthana
biotene

161
Q

sugar substitutes

A

xylitol
mannitol
sorbitol

162
Q

salivary proteins

A

IgA
PRPs
mucins
histatin

163
Q

salivary enzymes

A

lipase
lysozyme
amylase

164
Q

what is Warthin’s tumour thought to originate from?

A

remnants of salivary duct epithelium trapped in LNs during embryogenesis

165
Q

parotid neoplasms

A

80% of all tumours

15% malignant

166
Q

SM neoplasms

A

10% of all tumours

30% malignant

167
Q

SL neoplasms

A

0.5% of all tumours

80% malignant

168
Q

minor neoplasms

A

10% of all tumours

45% malignant

169
Q

SS investigations

A 
dry eyes - subjective
dry eyes - objective
dry mouth - subjective
dry mouth - objective
autoAB findings
histopathology
American european consensus group revised international criteria
4 or more positive criteria (must inc 5 and/or 6)
170
Q

SS minor gland histology

A

focal lymphocytic sialadenitis
- collections of 50+ lymphocytes, one or more collections /4mm2
acinar loss
fibrosis

171
Q

SS major gland histology

A

lymphocytic infiltration
atrophy of acini
ductal epithelium shows hyperplasia which eventually occludes ducts - myoepithelial islands

Oral medicine (14 decks)

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