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BDS5 oral disease > salivary gland disease > Flashcards

salivary gland disease Flashcards

1
Q

describe a ranula (what, presentation)

A
  • sublingual gland mucus extravasation cyst in FOM
  • 2-3cm fluctuant swelling, translucent
  • may limit mouth opening and mastication
  • can be plunging if it falls through discontinuous mylohyoid into neck
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2
Q

how does a ranula form/grow?

A
  • damage to sublingual gland duct
  • continuous flow of saliva without neural stimulation
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3
Q

list the 3 types of sialadentitis (inflammatory)

A
  • acute sialadenitis (infections)
  • chronic sialadenitis (obstruction)
  • end stage sialadenitis
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4
Q

describe the two types of acute sialadenitis (cause, presentation)

A

1 mumps (highly contagious, paramyxovirus)
- painful uni/bilateral parotid swelling, headache, malaise, fever, orchitis
2 acute suppurative/bacterial parotitis - Staph aureus, often parotid
- painful gland swelling +/- suppuration from gland orifice
- more frequent in those with severe xerostomia

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5
Q

describe chronic sialadenitis (cause, site, symptoms)

A
  • often duct obstruction (esp calculi)
  • submandibular gland >
  • unilateral swelling, asymptomatic or intermittently symptomatic +/- mealtime syndrome
  • xerostomia predisposes to stones (stones do not cause xerostomia)
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6
Q

what is mealtime syndrome?

A

intermittent salivary gland region swelling and pain during mealtimes (increased pressure)

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7
Q

why is chronic sialadenitis more common in the submandibular gland? (2)

A

long pathway/duct
supersaturated saliva

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8
Q

how do salivary calculi form?

A

calcium, magnesium and phosphate ions deposit around a central nidus (cell debris, thick mucus), layer by layer

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9
Q

how may a sialolith be located? (3)

A

palpated
plain film radiographs with sialography
ultrasound imaging

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10
Q

how does chronic sialadenitis appear histologically? (3)

A
  • loss of acini, ductal dilation, fibrosis
  • chronic inflammatory cell infiltrate
  • stone = dark, calcified, laminated appearance, often start in acini area
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11
Q

describe end stage sialadenitis (3)

A
  • prolonged sialadenitis; “Kuttner tumour”
  • hard fibrotic gland, no secretion or mealtime syndrome
  • intermittent low-grade pain
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12
Q

describe HIV-associated salivary gland disease (demographic, aetiology, symptoms, histology)

A
  • 5-10% of HIV-infected pts, children
  • unknown aetiology, but linked to opportunistic infections
  • uni/bilateral gland swelling +/- pain, often parotid
  • T cell infiltration destroying acini, fibrosis –> multiple lymphoepithelial cysts
  • low risk of lymphoma 1%
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13
Q

HIV-associated salivary gland disease management (2)

A

anti-retroviral therapy
+/- surgery or radiotherapy to decrease swelling

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14
Q

describe sialadenosis (what, symptoms, site, histology)

A
  • non-inflammatory enlargement of salivary glands +/- pain, +/- decreased salivary flow
  • often with associated systemic condition (endocrine, nutritional, neurological)
  • usually parotid, bilateral
  • 2-3x hypertrophy of gland acini with minimal inflammation
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15
Q

sialadenosis management (2)

A
  • treatment of underlying systemic condition
  • +/- surgery if significant cosmetic concerns
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16
Q

list salivary gland diseases/types (8)

A
  • sialadenitis = infection or obstructions, allergy
  • mucoceles, ranulas
  • salivary tumours – benign or malignant
  • systemic conditions:
    – sialadenosis
    – sarcoidosis
    – lymphoma
    – HIV-associated
    – autoimmune (Sjogren’s, IgG4)
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17
Q

describe IgG4 sclerosing disease (what, presentation, histology)

A
  • chronic autoimmune inflammation with dense enlarging fibrosis, mimics neoplastic conditions
  • any site, esp pancreas, lungs, salivary and lacrimal glands
  • uni/bilateral, parotid enlargement
  • diagnostic histology = storiform pattern, many IgG4-secreting plasma cells, dense fibrosis
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18
Q

IgG4 sclerosing disease histology (2)

A
  • storiform pattern
  • many IgG4-secreting plasma cells, dense fibrosis
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19
Q

IgG4 sclerosing disease management (2)

A
  • immediate corticosteroid therapy
  • investigate other organs
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20
Q

describe allergic/eosinophilic sialadenitis (what, demographic, treatment)

A
  • recurrent parotid swelling, mucus plugs, ductal abnormalities associated with eosinophilic-rich chronic inflammation
  • Japan
  • many pts atopic, with eosinophil presences suggests allergy component
  • often fails to respond to treatment
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21
Q

allergic/eosinophilic sialadenitis demographic (2)

A
  • Japanese
  • atopic pts
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22
Q

list some imaging modalities for salivary gland diseases (7)

A
  • ultrasound
  • endoscopy
  • scintigraphy and PET (nuclear medicine)
  • plain radiograph (lower 90º, posterior oblique)
  • sialography
  • CT
  • MRI
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23
Q

pros and cons of ultrasound imaging

A

+:
- simple, quick, non-invasive, cheap
- good compliance, no contrast or radiation
- high resolution, different orientations
- colour doppler for vascularity
-:
- operator-dependent, training
- messy with jelly
- superficial soft tissues only

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24
Q

salivary indications for ultrasound imaging (3)

A
  • salivary gland lumps
  • salivary gland obstructions
  • diagnosis and follow up of Sjogren’s
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25
Q

how does a sialolith appear on ultrasound? (3)

A
  • bright white, gently rounded
  • acoustic shadow
  • dilated duct associated
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26
Q

describe sialography

A
  • radiopaque contrast solution (iodine-based) injected into duct, radiological techniques used to view and demonstrate ductal anatomy
  • viewed live as injected or use plain film
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27
Q

indications for sialography (3)

A
  • identify filling defects (stones, plugs), strictures, duct architecture, dilations
  • suggests function of gland (clearance within 1 min normal)
  • planning interventional treatments for sialolith extraction/stricture dilation
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28
Q

contraindications for sialography (3)

A
  • iodine allergy
  • acute infection of gland
  • calculus at ostium of duct
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29
Q

what is punctate sialectasis? (2)

A
  • lobules of radiopaque contrast where there is salivary gland breakdown/damage
  • typical of Sjogren’s or recent sialadenitis
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30
Q

advantages of sialography (3)

A
  • superior resolution and detail
  • best sensitivity to differentiate stones and stenoses
  • fluoroscopic sialography allows live visualisation
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31
Q

which investigation has 100% sensitivity for salivary calculi?

A

CT scan

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32
Q

MI methods of removing sialoliths (4)

A
  • extracorporeal shock wave lithotripsy (ECSWL)
  • stone retrieval with baskets
  • intracorporeal shock wave lithotripsy
  • conservative surgery
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33
Q

explain briefly how extracorporeal shock wave lithotripsy works

A
  • ultrasound to identify location
  • piezoelectric shockwave generator targets stone
  • multiple visits to hit 10,000 times
  • aims to break down stone
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34
Q

indications and contraindications of stone retrieval with baskets

A
  • indications = stone ≤25% of lumen, mobile, accessible
  • contraindications = larger stone, small duct, unsuitable position, stricture distal to stone
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35
Q

briefly explain how balloon duct dilation helps with strictures

A

expandable balloon catheter introduced and inflated within salivary ductal system with guide wire

36
Q

indications for balloon duct dilation (2)

A
  • partial stenosis/multiple strictures of major gland duct
  • open pathway for sialoliths to be removed
37
Q

contraindications of balloon duct dilation (2)

A
  • complete ductal stenosis
  • asymptomatic or non-functioning gland
38
Q

ranula treatment (2)

A
  • marsupialisation/decompression
  • excision of whole gland by intra/extraoral approach under GA
39
Q

risks with submandibular gland removal (5)

A
  • marginal mandibular nerve (angle of mouth), hypoglossal nerve, lingual nerve damage
  • “stump” syndrome
  • scarring
  • haematoma (FOM)
  • damage to duct/salivary flow
40
Q

causes of false xerostomia (3)

A
  • mouth breathing
  • psychological
  • night dryness
41
Q

causes of true xerostomia (9)

A
  • medications
  • psychogenic (eg anxiety)
  • dehydration
  • systemic conditions (diabetes, cardiac and renal failure, hypovolaemic shock)
  • gland/nerve damage
  • Sjogren’s, SOX syndrome
  • irradiation, cytotoxic drugs
  • neurological damage
  • hypoplasia/aplasia of glands, vitamin A deficiency
42
Q

give some (types of) drugs which may cause xerostomia (up to 8)

A
  • atropine-like muscarinic drugs = atropine, hyoscine, anti-Parkinsonian, tricyclic antidepressants, antihistamines, antipsychotics, old antihypertensives
  • sympathomimetics = amphetamines, decongestants, monoamine oxidase inhibitors
  • opiate-based analgesics
  • benzodiazepines
  • appetite suppressants
  • H2 antagonists, PPIs
  • anti-HIV drugs (protease inhibitors)
  • alcohol, coffee
43
Q

which drugs/substances do not cause xerostomia even though you would think they might? (2)

A
  • beta blockers
  • smoking (subjective feeling due to mucosal thickening)
44
Q

what are the salivary flow rates for xerostomia? (2)

A
  • whole unstimulated flow <0.2ml/min in 10 mins
  • parotid flow <0.4ml/min per gland with citric acid used twice in 10 mins
45
Q

what are the normal salivary flow rates? (2)

A

10min unstimulated flow 0.2-0.3ml/min
10min stimulated parotid flow 1-2ml/min

46
Q

give some s/s of xerostomia (9 + indirect effects)

A
  • low salivary flow rate
  • mirror sticking to mucosa
  • sticky, stringy, frothy saliva with no pooling in FOM
  • absence of saliva
  • difficulty swallowing and speaking
  • general oral discomfort
  • decreased denture tolerance/retention
  • debris sticking to teeth
  • erythematous gingivae and loss of papillae
  • indirect effects = bad taste, caries, candidiasis, sialadentitis, lobulation or fissuring or depapillation of tongue dorsum, mucosal atrophy
47
Q

what questions may you ask in the history for a dry mouth? (8)

A
  • when? constant or intermittent
  • any associated features - anxiety, drugs, taste
  • smoking
  • drug history
  • any cancer treatment
  • mouth breathing, snoring
  • other mucosae
  • autoimmune disease
48
Q

what special investigations may you do for xerostomia? (7)

A
  • salivary flow rate (dribble into universal container
  • saliva sample for candida/pathogens
  • parotid saliva sample to culture if cloudy
  • urine glucose and osmolarity (diabetes)
  • refer for specialist neurological investigations and ultrasound
  • serology for inflammatory markers or auto-Abs
  • biopsy (focal lymphocytic sialadenitits)
49
Q

investigations for suspected Sjogren’s syndrome (4)

A
  • parotid flow rate
  • minor gland biopsy
  • blood test = FBC, film; ESR, Ig levels; autoantibody screen (ANA, SSA, SSB)
  • lacrimal flow (conjunctival staining and tear breakup time)
50
Q

what investigations may be done for dry eyes? (3)

A
  • Schirmer test (filter paper, 5mins)
  • ocular staining with Lissamine green
  • tear breakup time
51
Q

describe Sjogren’s syndrome (what, demographic, types)

A
  • chronic, autoimmune, rheumatic, progressive gland atrophy
  • middle aged females with 2 peaks (mid-30s, mid-50s)
  • may affect all exocrine glands
  • primary = dry eyes and mouth, non-glandular features
  • secondary = pre-existing connective tissue disease, usually less severe features
52
Q

ocular features of Sjogren’s syndrome (6)

A
  • failure of lacrimal secretion
  • drying of anterior conjunctiva
  • dry, gritty eyes
  • eyelids adherent in morning
  • burning soreness
  • keratoconjunctivitis sicca
53
Q

glandular features of Sjogren’s syndrome (7)

A
  • parotid swelling (more in primary SS)
  • lacrimal gland swelling
  • increased risk of lymphoma
  • dry vagina
  • dry skin
  • dry oesophagus
  • dry lungs +/- infections
54
Q

extraglandular s/s of Sjogren’s syndrome (9)

A
  • Raynaud’s phenomenon
  • excessive fatigue in waves
  • myalgia, arthralgia
  • peripheral neuropathy
  • lymphopaenia, thrombocytopaenia
  • hypergammaglobulinaemia and cryoglobulinaemia (sign of active SS)
  • CNS symptoms - brain fog to cognitive difficulties
  • renal = esp if pre-existing lupus
  • hepatobiliary chronic inflammation (primary biliary cirrhosis)
55
Q

what two features are uncommon in secondary Sjogren’s syndrome compared to primary?

A
  • gland swelling
  • lymphoma
56
Q

secondary Sjogren’s associated connective tissue disorders (3)

A
  • rheumatoid arthritis (50%)
  • systemic lupus erythematosus
  • systemic sclerosis
57
Q

what is the D/C for Sjogren’s syndrome?

A
  • autoantibodies (Ro, La, ANA, RF +/or positive minor gland biopsy)
    plus 2 of:
  • ocular symptoms >3 months
  • oral symptoms >3 months
  • ocular signs (Schirmer test, Rose Bengal stain)
  • salivary gland involvement with decreased flow
58
Q

what would the Schirmer test show with Sjogren’s?

A

<5mm wetting in 5 mins

59
Q

describe the pathogenesis of Sjogren’s syndrome (3)

A
  • failure of immune control and loss of tolerance (autoimmune)
  • systemic polyclonal B cell hyperreactivity
  • activated B cells infiltrate glands and collect around ducts, destroy acinar cells
60
Q

what may you expect the blood markers to look like for Sjogren’s syndrome? (2)

A
  • increased ESR and gammaglobulin
  • autoantibodies = ANF/ANA, Ro/SSA, La/SSB, RF, antithyroid, gastric parietal cells
61
Q

histology of Sjogren’s syndrome (3)

A
  • periductal CD4+ lymphocytic infiltrates
  • lymphoepithelial lesions (epimyoepithelial islands in background of lymphocytes)
  • atrophy of salivary acini
62
Q

where is a biopsy usually taken for Sjogren’s syndrome and why?

A

lower lip (easily accessible, similar features in major and minor glands)

63
Q

which type of Sjogren’s syndrome increases the risk of MALT lymphoma?

A

primary SS

64
Q

describe MALT-type lymphoma (AKA, presentation, prognosis)

A
  • extranodal marginal zone B cell lymphoma
  • persistent swelling of parotid (all swollen glands should be suspected)
  • low grade with good prognosis
65
Q

MALT-type lymphoma investigations (2)

A
  • biopsy
  • PCR and immunohistochemistry to detect clonality
66
Q

MALT-type lymphoma risk factors (5)

A
  • parotid enlargement, splenomegaly, lymphadenopathy
  • purpura, cryoglobulinaemic vasculitis
  • hypergammaglobulinaemia
  • neutropenia
  • low CD4+ count
67
Q

MALT-type lymphoma treatment options (2)

A

controversial:
- wait and watch
- low dose radiotherapy

68
Q

how does Sjogren’s syndrome appear on ultrasound and why?

A
  • honeycomb
  • lymphoepithelial infiltrates
69
Q

describe SOX syndrome (what, features)

A
  • mutation in SOX genes
  • Sialadenitis, Osteoarthritis, Xerostomia
  • symptomatic dry eyes and mouth, decreased whole flow but NORMAL stimulated flow
  • non-specific diffuse sialadenitis
  • primary generalised nodal osteoarthritis
  • NO RF or Ro/La auto-Abs
70
Q

oral management of Sjogren’s syndrome (6)

A
  • explain and reassure
  • preserve remaining flow, avoid drying drugs (liaise with GP)
  • salivary stimulation
  • salivary replacement
  • symptomatic treatment for soreness/dryness
  • monitor for caries, TW, candida, lymphoma
71
Q

what is involved in salivary stimulation for Sjogren’s disease? (3)

A
  • hydration - 1-1.5L water/day (consider renal)
  • sugar-free gum/sweets, saliva stimulating tablets (buffered, lemon)
  • pilocarpine 5mg 1-3x/day, parasympathomimetic
72
Q

contraindications to pilocarpine (3)

A

asthma
arrhythmias
glaucoma

73
Q

what is involved in salivary replacement for Sjogren’s syndrome?

A

sprays, gels, MW (eg Biotene)

74
Q

medical management for Sjogren’s syndrome (not oral) (5)

A
  • NSAID and paracetamol pain relief (arthralgia)
  • education to increase low intensity exercise (fatigue)
  • amlodipine or isoprolol (severe Raynaud’s)
  • hydroxychloroquine, methotrexate, prednisolone +/- steroid sparing (musculoskeletal pain)
  • rituximab considered for primary SS where conventional therapy has failed
75
Q

general advice for dry mouth or Sjogren’s syndrome pts (4)

A
  • regular dental review (6 monthly)
  • avoid strong soaps, use aqueous creams and emollients
  • avoid dry environments, smoking, XS alcohol
  • self help groups
76
Q

dry mouth differential diagnoses/causes (6)

A
  • dehydration (recent diarrhoea, vomiting; diabetes, fluid restrictions)
  • iatrogenic (drugs, radiotherapy, parotidectomy)
  • salivary gland diseases - agenesis (rare), infection, inflammatory
  • anxiety
  • local, mouth breathing
  • subjective feeling
77
Q

give the features measured by the clinical dryness scale (12)

A
  • mirror sticks to buccal mucosa
  • mirror sticks to both buccal mucosa
  • mirror sticks to tongue
  • frothy saliva
  • no pooling of saliva in FOM
  • tongue depapillation
  • highly fissured tongue
  • lobulated tongue
  • altered gingival architecture
  • glassy appearance of oral mucosa
  • cervical caries >2 teeth
  • debris on palate
78
Q

what is mild dryness and its management as guided by the clinical dryness scale? (4)

A
  • score 1-3 - may not need tx
  • sugar-free chewing gum 15mins BD
  • attention to hydration
  • routine check ups and monitoring
79
Q

what is moderate dryness and its management as guided by the clinical dryness scale? (5)

A
  • score 4-6, investigate if unclear cause
  • sugar-free gum or simple sialogogues
  • saliva substitutes
  • topical fluoride
  • regular monitoring
80
Q

what is severe dryness and its management as guided by the clinical dryness scale? (4)

A
  • score 7-10 - must ascertain cause and exclude Sjogren’s (REFER)
  • saliva substitutes
  • topical fluoride
  • monitored for changing s/s +/- specialist input
81
Q

functions of saliva (6)

A
  • lubrication (eating, speech)
  • cleansing
  • buffering (bicarb)
  • limits pathogen growth (lysozyme, IgA)
  • remineralisation
  • digestion (amylase)
82
Q

how does each part of the autonomic system affect salivary glands (normal function and if blocked)?

A
  • parasympathetic = secretory; blocked –> gland atrophy
  • sympathetic = protein secretion, little effect if blocked
83
Q

what factors influence salivary centres? (5)

A
  • taste
  • smell
  • chewing
  • anxiety
  • sleep/diurnal variation
84
Q

what is ptyalism?

A

excess salivation

85
Q

what may cause true ptyalism? (5)

A
  • local irritation/reflex (ulcers, ANUG, dentures)
  • lithium, anti-cholinergics (can also cause dry mouth)
  • waterbrash, idiopathic paroxysmal sialorrhoea (rare)
  • heavy metal poisoning, iodine
  • rabies
86
Q

what may cause false ptyalism? (4)

A
  • psychiatric
  • poor neuromuscular control (eg not swallowing) = Parkinson’s, stroke, Bell’s palsy
  • muscle wasting diseases
  • head-down posture in disability
87
Q

treatment for ptyalism (4)

A

(if not self-limiting)
- anticholinergic drugs - local (hyoscine patches) or systemic
- speech therapy (esp if previous stroke)
- botox into submandibular glands (can also be diagnostic) or surgical excision
- sectioning of chorda tympani

BDS5 oral disease (26 decks)

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