Salivary Glands Flashcards
Functions of saliva
Tissue coating Buffering Digestion Dental protection Lubrication and viscoelasticity Anti bacterial/fungal/viral
Sialosis
Non pathogenic, non neoplastic increase in salivary gland size
Sialadenitis
Ductal infection
Sialolithiasis
Duct obstruction
Sialectasis
Cystic dilatation of duct
Sialorrhoea
Excessive salivation/ drooling
What virus is acute viral sialadenitis often caused by?
Mumps
RNA virus paramyxovirus
Acute viral sialadenitis presentation
Usually parotid (rarely SM) Pain Usually bilateral enlargement Skin over unaffected Malaise, fever, headache
Acute viral sialadenitis spread
Droplet/direct contact
2-3 wks IP
Acute viral sialadenitis extrasalivary manifestations
Ochitis
Oophoritis
Pancreatitis
Acute viral sialadenitis histology
Accumulation of neutrophils and fluid in lumen of ductal structures
Management of acute viral sialadenitis
Clinical diagnosis
Fluid and pain meds
Second attack possible
Vaccination
Pathogenesis of acute bacterial sialadenitis
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
acute bacterial sialadenitis underlying causes
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
acute bacterial sialadenitis bacteria
S pyogenes, s aureus, prevotella spp
Rarely mycobacteria
acute bacterial sialadenitis presentation
Painful and tender enlargement of one gland Pus discharge duct Reddening of overlying skin Trismus Pyrexia
acute bacterial sialadenitis histology
Acinar destruction with neutrophil infiltrates and bacterial presence
acute bacterial sialadenitis diagnosis
Clinical
Needle aspirate pus sample
acute bacterial sialadenitis tx
Antibiotics and analgesia
Fluids
Good OH
may need IV drainage
acute bacterial sialadenitis pathophysiology
Duct ectasia
Mucous metaplasia of ductal epithelium
Periductal fibrosis
Fusion of lobules
Chronic sialadenitis
Low grade bacterial invasion
Relapsing/radiation/sclerosing
Can develop after acute sialadenitis or calculi formation
Chronic sialadenitis clinical
Recurrent attacks of pain and swelling
Chronic sialadenitis histology
Atrophy of serous acini during chronic obstructions
Chronic sialadenitis diagnosis
Clinical and history
Chronic sialadenitis tx
Surgical excision
Chronic recurrent parotitis
Most common form of chronic sialadenitis
?aetiology
- semisolid material - coagulated albumin - as a result of gland inflammation, obstructs duct network, swelling
Chronic recurrent parotitis ages
Children 4m-15yrs
Adults 40-60 years
Chronic recurrent parotitis clinically
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)
Chronic recurrent parotitis tx
Short term steroids
Ductal clearance from ppt serum proteins
What is the most common benign minor SG lesion?
Mucocele
Main cause of mucocele
Mechanical trauma on discharge duct
Extravasation mucocele
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
Retention mucocele
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
ranula
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
mucocele most common sites
lip
FOM
mucocele clinical presentation
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
U lip mucocele
beware - likely a pathological lesion
mucocele diagnosis
hx and exam
US: cystic masses, sometimes contain fibrillar processes produced by FBs
mucocele recurrence
esp if traumatic habit persists
RFs - younger pt, ventral tongue
mucocele histology
vascular GT surrounding a mucus pool foam cells macrophage lined cavity severed duct if trauma cystic cavity
mucocele tx
usually surgical - surgery - complete excision/marsupialisation/dissection - cryosurgery - CO2 laser - electrocautery non-surgical - IL injection of sclerosing agent - IL steroid injection can resolve spontaneously
sialolith formation
small deposits of Ca etc that form on bacteria, mucus or epithelial cells, can block saliva flow and cause gland to swell
where are most sialoliths and why?
80% SMG
2x as much Ca as parotid, quite alkaline and mucous
tortous and uphill path
predisposing factors for sialolithiasis
cause unknown age radio H+N mouth injuries/trauma meds affecting saliva production SS kidney problems not drinking enough water
sialolithiasis clinical presentation
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
sialolithiasis histology
dilated ducts with calculi
chronic inflammatory cells
calcified structure
metaplasia from columnar to SSE of lining - chronic irritation from stone
sialolithiasis diagnosis
hx
attempt to palpate calculus
radiograph (not always obvious - referral?)
sialography
CT - check for other causes of obstruction
sialolithiasis tx
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
other gland obstruction
recurrent parotitis - HIV - duct stenosis - bacterial infection chronic obstructive sialadenitis - usually caused by sialalithiasis - can be post-op
sialosis
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
sialosis histology
hypertrophy (increase in cell size) of serous acini
oedema of interstitial CT
xerostomia
subjective feeling of oral dryness, may/may not be accompanied by hyposalivation
hyposalivation
objective reduction in salivary flow and production
causes of xerostomia
dehydration psychological neurological dysfct disease e.g. SS medications radio SG tumour SG trauma nutritional deficiencies and/or EDs
meds which cause dry mouth
tricyclics B-blockers antipsychotics antihistamines atropine diuretics cytotoxics antimuscarinic cholinergic drugs
radiation
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
oral manifestations of xerostomia
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
clinical evaluation of SG fct - history
systemic/local diseases
trauma
meds list
clinical evaluation of SG fct - symptom Qs
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
clinical evaluation of SG fct - physical exam
EO: major SGs, LNs
IO: STs, periodontium, dentition
challacombe scale oral dryness - about
additive score 1-10
symptoms will not necessarily progress in the order shown, but summated scores indicate likely pt needs
monitor symptom progression/regression
challacombe scale oral dryness - mild
1 - mirror sticks to buccal mucosa
2 - mirror sticks to tongue
3 - saliva frothy
= mild, may not need tx, SF gum, hydration, routine monitoring
challacombe scale oral dryness - mod
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
challacombe scale oral dryness - severe
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
xerostomia measurements and lab tests
measure salivary output - UWSF, SWSF - ductal flow of major SGs sialochemical analyses serum lab studies - CBC with differential - AI markers - serum immunoglobulins - ESR
xerostomia imaging
US: superficial sonoelastography: (postradiation) CT: tumours *MRI: tumours scintigraphy: fct - assess SG dysfct PET: high cellular activity areas sign of tumour sialography radiograph
salivary biopsy
FNA major SG minor labial SG - ≥5 minor glands SS: focus score ≥1 per 4mm2 (focus score - ≥50 mononucleate cells per 4mm2)
pilocarpine SEs
vision changes hiccups bradycardia hypotension bronchoconstriction hyperhidrosis nausea, vomiting, diarrhoea cutaneous vasodilation increased urinary freq
xerostomia therapy
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
pilocarpine dose
5mg daily, up to 30mg
pilocarpine contraindications
iritis and narrow-angle glaucoma CV disease chronic pulmonary disease inc uncontrolled asthma pts taking B-adrenergic blockers active gastric ulcers
hypersalivation/sialorrhea
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
drooling common causes
reduced swallowing
- NM diseases: CP, Parkinsons, stroke
- anatomic abnormalities: macroglossia, ortho problems
(incompetent lips, AOB), surgical defects following
major HandN resection, TMJ ankylosis)
causes of hypersalivation
irritating oral disease (ulceration, infection, trauma)
med SEs (clozapine, risperidone, nitrazepam, bethanecol)
GORD
ENT diseases - can have oesophageal aetiologies - obstructive, inflammatory
hypersalivation causes - medications
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
clinical features of drooling
repeated perioral cutaneous alterations
aspiration-related resp and pulmonary complications
altered speech and swallowing
social and psychological consequences
assessment of drooling - freq
dry - never drools
occ drooling - not every day
freq - drooling every day
constant - constant drooling
assessment of drooling - severity
dry - never drools mild - only lips wet mod - lips and chin wet severe - clothing soiled profuse - hands and tray moist and wet
drooling therapy
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
drooling surgical tx
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
acute necrotising sialometaplasia about and predisposing factors
trauma induced
smokers
benign ulcerative lesion (resembles a SCC)
small vessel infarct
acute necrotising sialometaplasia pathophysiology
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
acute necrotising sialometaplasia clinically
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
acute necrotising sialometaplasia histology
hyperplasia
metaplasia of ducts
necrosis of salivary acini
acute necrotising sialometaplasia diagnosis
usually biopsy to ensure not SCC
acute necrotising sialometaplasia management
self-resolving within 6-10wks
antiseptic MW to tx ulceration
SG neoplasms - locations with high risk of malignancy
SL gland
tongue
what % of SG neoplasms are benign?
80%
what % of SG neoplasms are parotid gland?
80% and 80% in superficial lobe
SG neoplasms - clinically
asymptomatic swelling and eversion of ear lobes
no xerostomia
malignant - can be pain/ulcerate/facial palsy
SG neoplasms management
surgical excision +/- radio
Frey’s syndrome
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
SG neoplasms - indication of malignant change
rapid growth
pain
fixation to deep tissues
facial palsy
which area is most affected by minor SG neoplasms?
palate
usual benign locations of minor SG neoplasms
lip
buccal
palatal
usual malignant locations of minor SG neoplasms
tongue
FOM
RM pad
benign epithelial tumours
pleomorphic adenoma
Wharthin tumour
oncocytoma
malignant epithelial tumours
mucoepidermoid carcinoma
adenoid cystic carcinoma
acinic cell carcinoma
order of incidence of SG neoplasms
pleomorphic adenoma Warthin's tumour adenoid cystic carcinoma mucoepidermoid carcinoma acinic cell carcinoma
what is the most common SG tumour?
pleomorphic adenoma
pleomorphic adenoma - site
parotid 90% then SM and minor palate (fixed mass)
pleomorphic adenoma - clinical
solitary, painless, slow-growing unilateral swelling not fixed to underlying tissues skin overlying normal but can give bluish appearance most parotid affect superficial lobe
pleomorphic adenoma - histology
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)
pleomorphic adenoma - tx
surgery
pleomorphic adenoma - outcome
can recur
risk of malignant transformation (3-13%)
Warthin’s tumour - location
almost exclusively parotid and superficial lobe, can be bilateral (5-14%)
- 2.3% SM
- ext rare in minor
Warthin’s tumour - usual age
> 40yrs
Warthin’s tumour - clinical
painless, slow-growing, round/oval mass
sometimes fluctuant swelling
Warthin’s tumour - histology
epithelial tissue, cystic formations
dense lymphoid tissue stroma
- can get germinal centres in this
well defined CT capsule
Warthin’s tumour - tx
surgery (/monitor)
Warthin’s tumour - outcome
low recurrence rate
1% malignant transformation of epithelial component
oncocytoma - incidence
rare <1%
oncocytoma - location
mostly parotid
rare minor
rarer SMG
oncocytoma - clinical
painless, slow-growing, non-tender, firm, lobulated and mobile mass
occ pain/facial nerve paralysis
oncocytoma - histology
monotonous, polygonal, eosinophilic (oncocytic) epithelial cells
round uniform nucleus
low nucleus-cytoplasm ratio
oncocytoma - outcome
v low malignant potential
SMG best prognosis
recurrence 20% - insufficient surgery and occult multinodularity
oncocytoma - tx
surgery
what is the most common major SG malignant tumour?
mucoepidermoid carcinoma
what is the most common minor SG malignant tumour?
adenoid cystic carcinoma
mucoepidermoid carcinoma - site
50% parotid, but can affect any
mucoepidermoid carcinoma - minor
most common on palate, rubbery/soft mass, may stimulate a mucocele/vascular tumour
also RM area
mucoepidermoid carcinoma - clinical
swelling, pain, ulcer, infiltration, discolouration, facial paralysis
mucoepidermoid carcinoma - histology
mucin secreting cells
intermediate cells
epidermoid cells
slow growth and can infiltrate surrounding tissues
mucoepidermoid carcinoma - freq spread
perineural spread
40% show high-grade metastasis
mucoepidermoid carcinoma - tx
surgery and radio
mucoepidermoid carcinoma - outcome
high grade poorer survival
adenoid cystic carcinoma - site
most common minor SG malignancy - often palate
can present in major
adenoid cystic carcinoma - clinical
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
adenoid cystic carcinoma - histology
swiss cheese no capsule cribiform pattern most common tubular type best prognosis solid type least common - most aggressive and higher distant metastases
adenoid cystic carcinoma - tx
surgery and radio
poor prognosis - local recurrence - hard to determine clinically how far tumour has spread
acinic cell carcinoma - location
parotid >80%, can be bilateral
acinic cell carcinoma - clinical
slowly enlarging mass, few symptoms occ involves nerves/regional nodes usually solitary, encapsulated, soft, grey-white invasive slow growth, good prognosis
acinic cell carcinoma - histology
serous acinar cell differentiation - microcystic, solid, papillary cystic, follicular clear/vacuolated cells intercalated duct-like cells non-specific glandular cells
acinic cell carcinoma - tx
surgery
polymorphous low-grade adenoma
rare
most common palate
M>F
slow growing
which malignant tumours ten to have a slow growth pattern?
adenoid cystic carcinoma
low-grade MEC
acinic cell carcinoma
prognostic factors for malignant SG tumour prognosis
age stage histology grading lympho-vascular invasion FN paralysis cervical node involvement neural spread \+ surgical margins site gene mutations
diagnosis of SG tumours - clinical S+S
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
diagnosis of SG tumours
clinical S+S US MRI pathology TNM staging
diagnosis of SG tumours - US
cheap, safe, accuracy 90%
diagnosis of SG tumours - MRI
interface of tumour and tissue for surgical planning
diagnosis of SG tumours - pathology
open biopsy not usually recommended due to risk of seeding
if small masses in minor SGs (palate, tongue) - punch biopsy
US guided FNA cytology
tx of SG tumours
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
TNM staging for SG tumours
Tx - T4b
Nx - N3
M0 - M1
parotid gland
serous
stensen duct
SMG
mixed
wharton duct
SL gland
mucous
aplasia
congenital absence of ≥ SGs
ectodermal dysplasia
duct atresia
failure of a duct to canalise
can result in salivary retention cysts
HIV
parotid enlargement in up to 10% pts
CF
causes plugging of acinar ducts with precipitated secretions
essentially microscopic sialoliths
sarcoidosis
collections of granulomas
can occur in any organ but often affect SGs causing large masses and facial palsy
gland infiltration
amyloidosis - build up of amyloid protein fibrils - lymphoepithelial cysts haemachromatosis - causes xerostomia
cancer tx that affects SGs
radio
GvHD
anti-neoplastic drugs (chemo)
radioiodine
why are salivary tissues sensitive to radio?
due to their highly differentiated and specialised state
- not because of high mitotic figures
radio and saliva
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
GvHD and saliva
mainly haematopoietic SC pts
results in SS
chemo and saliva
reduced secretion
early apoptosis of SG cells
radioiodine and saliva
reduction of gland fct
increased lymphocytic infiltrate
saliva substitutes
glandosane
saliva orthana
biotene
sugar substitutes
xylitol
mannitol
sorbitol
salivary proteins
IgA
PRPs
mucins
histatin
salivary enzymes
lipase
lysozyme
amylase
what is Warthin’s tumour thought to originate from?
remnants of salivary duct epithelium trapped in LNs during embryogenesis
parotid neoplasms
80% of all tumours
15% malignant
SM neoplasms
10% of all tumours
30% malignant
SL neoplasms
0.5% of all tumours
80% malignant
minor neoplasms
10% of all tumours
45% malignant
SS investigations
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)
SS minor gland histology
focal lymphocytic sialadenitis
- collections of 50+ lymphocytes, one or more collections /4mm2
acinar loss
fibrosis
SS major gland histology
lymphocytic infiltration
atrophy of acini
ductal epithelium shows hyperplasia which eventually occludes ducts - myoepithelial islands
