Salivary gland disease Flashcards
function of saliva
clearance taste - zinc/mucin remineralisation - phosphate acid buffeing antimicrobial antifungal digestion - amylase lubrication
local causes of dry mouth
mouth breathing drugs - inhalers for asthma alcohol smoking candidosis cancer therapy - chemo
systemic causes of dry mouth
- drugs - diuretics/antihypertensive/antidepressants/antipsychotic/benzodiazepines/opiod analgesics/anticonvulsants/ litium/ antimuscarinics (amitriptyline)
- MH - diabetes/sarcoidosis/sjogren’s syndrome/CF/alzheimer’s/haemochromatosis/HIV/hep C
- dehydrated
xerostomia - clinical features
jacob's cracker sign - swallowing issues food stuck to palate shiny mucosa >caries denture control issues oral malodour clicking speech altered taste oral candidosis ascending inf of salivary glands
how to assess xerostomia
- dry mouth - produce unstimulated saliva <1.5ml in 15min
- associated tear production issue - schirmer paper in 5 min
- bloods - antibodies (ro/la/ana), random blood glucose - esr/crp and FBC
- other inv - MRI/ultrasound/chest Rg
what is the challacombe scale of clinical oral dryness
-name the 10 signs
additive score of 1-10 - symptoms not progress in order but score up (can be used to monitor)
- mirror sticks to buccal mucosa
- mirror sticks to tongue
- frothy saliva
- 4.no saliva pooling at FoM
- 5.generalised shortening of tongue papillae
- 6.altered gingival architecture
- 7.glassy appearance of mucosa (palate)
- 8.tongue fissured/lobulated
- 9.cervical caries
- debris on palate
what is a ranula
large FoM mucous extravasation cyst (sublingual)
what is a necrotising sialometaplasia
- cause
- most likely patient
- signs
- diff diagnosis
- histological apearance
small vessel ishaemia and resultant infarction
- smoker/trauma/LA
- Swelling and ulceration. Painless and self limiting
- -Sq cell carconoma/salivary gland carcinoma
- Surface slough and hyperplasia of surface ep
- squamous metaplasia of ducts and necrosis of salivary acini
- inflamation
systemic disease that can cause dehydration
- chronic
- acute
Chronic - diabetes mellitus / diabetes insipidus / addison’s disease / renal failure
acute - persistent vomiting/haemorrhage
somatisation symps
oral dysaesthesia / headache / neck and back pain
TMD pain/ fibromyalgia / dyspepsia
criteria for sjogren’s
subjective dry mouth - >3mth/frequent liquid sip
subjective dry eye - >3mth/tear replacement 3xd
objective dry mouth - unstimulated <1.5ml in 15min
objective dry eyes - schirmer test 5min
histopathology findings (labial minor gland biopsy)
autoimmune findings - anti la/ro
4/6 for diagnosis
positive histopathological findings of salivary gland disease
- minor
- major
-minor - focal lymphocytic sialadentits/acinar loss/fibrosis
focal collection of lymphocytes >50 lymphocytes,
>1 collection/4mm squared
-major - lymphocytic infiltrate/ epithelial hyperplasia/ atrophy of acina
ductal epithelium hyperplasia eventually occulding duct=myoepithelial islands
sjogren’s syndrome complications
caries oral candidosis infection function loss denture retention salivary lymphoma - non hodgkins lymphoma
xerostomia management
alternative drug - liase with GP regular sips of water chew sugar free gum salivary replacement stop smoking moderate caffiene intake monitorblood sugar levels change to SLS free toothpaste refer if mouth breathing during sleep drink more water
Prevention - high F conc toothpaste
name 2 types of hypersalivation
true - stroke/ degenerative CNS disease - MS/parkinson’s/alzheimers
perceived.
saliva substitutes
- sprays - xerotin/saliveze (pH neutral) glandosane (pH5.75)
- lozenges - saliva orthana/salivix/saliva stimulating tablets
- saliva stimulants - pilocarpine
- oral care systems - biotene oralbalance
drugs that cause HYPERsalivation
haloperidol/anticholinesterases/clonazepam/clozapine/nicardipine
causes of hypersalivation
swallowing failure (anxiety/stroke/MND/MS) postural drooling - cerbral palsy
subacute obstruction - associated with what symps
- cause
- inv
swelling associated with meals - submandibular.
slowly progressing
eventually fixed and painful
=duct obstruction
-INV - plain Rg low true occ, ultrasonography, sialography (inf free)
treating excess saliva
- deal with anxiety
- drugs to reduce salivation - antimuscarinics
- biofeedback training - swallowing control
- surgery = duct reposition/gland removal
reasons for a change in gland size
- secretion retention - mucocele/duct obstruction
- chronic sialadenitis
- gland hyperplasia - sialosis/sjogren’s
- salivary neoplasm
salivary gland infection
- viral
- bacterial
- why are these more likely to happen
viral - paramyxovirus(mumps) - uni/bilateral
common in childhood
bacterial - underlying cause dehydration/flow reduction diabetes mellitus immune suppression abnormal anatomy recurrent patotitis of childhood
management of a subacute obstruction -surgical -viral -bacterial outcomes
-surgical - sialolith removal
no stone - sialography (washing)
-gland removal - if fixed swelling
reformation of stone/duct deformity/gland damage
viral - supportive/fluids and analgesia
bacterial - supportive/fluids/analgesia and antibiotics
ascending oral microorganisms = amoxicillin with/out metronidazole
chronic sialadenitis -aetiology =submand =parotid what follows
obstruction
submand - stone
parotid - stricture
-infection follows = acinar atropy, fibrosis and inflammation
salivary tumours
-major gland
-neurological change due to?
symps
major - localised swelling
facial n branches withing parotid - n disturbance
-painless, slow growing, well defined
aetiology of salivary gland tumours
-of h&n neoplasms
what % are benign overall
3% of h&n neoplasms
75% benign overall
clinical features of
- major gland neoplasms
- minor gland neoplasms
- major = lump in affected gland, asymmetry, obstruction, pain/facial palsy (later)
- minor= junction of h&s, palate, upper lip/cheek, ulcerate (late) = malignant
gland percentages - % of all tumours and % malignant
- parotid
- submand
- subling
- minor
parotid - 80% all, 15% malignant
submand - 10% all, 30% malignant
subling - 0.5% all, 80% malignant
minor - 10% all, 45% malignant
diagnosis of salivary gland neoplasm
FNA, core biopsy, incisional biopsy
what issues can arise from diagnosis
many tumour types variation in tissue (pathology complex) common features between types not all tumours fit class immunohistochemistry needed to differentiate
Pleomorphoc adenoma
- how common
- where most common
- growth rate
- histological features
-75% all tumours
- PAROTID
vsried histology = duct epithelium, myoepithelial cells, myxoid and chondroid areas
treatment of pleomorphic adenoma
issue?
progression to carcinoma %
wide local incision
recurrence (multifocal)
5% carcinoma progression
Warthin’s tumour
- % of all tumours
- where found mostly
- histology
- treatment
15% all tumours
PAROTID
cystic, distinct ep, lymphoid tissue
treated by excision
adenoid cystic carcinoma
- % of tumours
- where found
- patterns
- local spread to?
- late spread
- treatment
-5% of tumours
-cribriform or tubular/solid
-local spread - nerves and bone
-difficult to treat, recurrence = poor prognosis at 20yr
metastisis by blood to lung
Highly invasive – muscle/nerve Sensory symps – facial weakness, Poor Prognosis, Slow growing Diag – FNA/Biopsy/excision Lymphnode metastasis - unusual
histology of warthin’s tumour
oncocytic epithelium (pink)
cystic spaces
lymphoid tissue
Most common salivary gland neoplasms in order of incidence
- pleomorphic adenoma
- adenoid cystic carcinoma
- warthin’s tumour
- acinic cell carcinoma
- mucal epidermoid carcinoma
Pleomorphic adenoma Warthin’s tumour Adenoid cystic cell carcinoma Mucal epidermoid carcinoma Acinic cell carcinoma
Mucoepidermoid carcinoma
- histology
- grading
- behaviour
- lymphatic spread
2 cell types - squamous (epidermoid) glandular (mucous) Unpredictable behaviour Lymphatic spread - rare
