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doctor stuff Flashcards

1
Q

What is lichen planus?

A

Chronic inflammatory condition affecting skin and mucous membranes - wrists, ankles, genitals mouth
Often see white lines called Wickham’s striae

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2
Q

What is the prevalence of lichen planus?

A

1% of population
Mainly age 30-50
If skin cases found, 50% chance for oral lesions

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3
Q

What are the causes of lichen planus?

A

Autoimmune reaction
Viral - Hep C, HSV
Medications - ACE inhibitors, beta blockers, diuretics, NSAIDs, DMARDs
Amalgam restorations

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4
Q

What are the signs and symptoms of oral lichen planus?

A

Reticular white pattern on buccal mucosa, gingivae, tongue palate
Ulceration
Erythema
Often no symptoms
Sensitivity to hot and spicy foods
Burning sensation in the mucosa - thinning of epithelium caused by atrophy changes from LP

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5
Q

What special investigations are carried out for lichen planus?

A

Biopsy for histopathological analysis
Patch testing for allergens or irritants
Blood test - haematinics and FBC for underlying conditions such as Hep C, LSE - (Anti La, Anti Ro)

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6
Q

What is the malignant potential of lichen planus?

A

1% over 10 years

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7
Q

How is mild, intermittent lichen planus treated?

A

Chlorhexidine mouthwash
Benzydamine mouthwash
Avoid SLS containing toothpaste

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8
Q

How is persisting symptomatic lichen planus managed in a primary care setting?

A

Topical steroids for ulcers:
- beclometasone MDI inhaler
- betamethasone rinse

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9
Q

How is persisting symptomatic lichen planus treated in a hospital setting?

A

Oral prednisolone
Topical tacrolimus - ointment or mouthwash
Hydroxychloroquine
Systemic immunomodulators - azathioprine and mycophenolate

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10
Q

What is seen histologically in lichen planus

A

Saw tooth rete-ridges
Acanthosis of epithelial layer
Parakeratosis of superficial epithelium
Band like infiltration of T lymphocytes

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11
Q

What are the different clinical presentations of lichen planus?

A

Reticular
Ulcerative
Papular
Bullous
Atrophic
Plaque like

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12
Q

Name 2 lichen like lesions

A

GVHD
Lupus erythematosus

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13
Q

What is erythema multiforme?

A

Immunologically generated skin and mucosal ulceration
Target like patches with red centre surrounded by pale ring, which is surrounded by a red ring
Heals within 2 weeks
Affects anterior mouth and lips

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14
Q

How is erythema multiforme treated?

A

Systemic steroids
Systemic aciclovir if secondary care
Fluid intake
Analgesia

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15
Q

What causes erythema multiforme?

A

Viral - HSV
Medications - antibiotics or anticonvulsants

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16
Q

What may erythema multiforme progress to?

A

Stevens-Johnson syndrome

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17
Q

What is angina bullosa haemorhagica?

A

Blood filled blisters in the oral cavity
Rapid onset then burst within hours
Heals with no scarring within days

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18
Q

How is angina bullosa haemorrhagica treated?

A

No tx
Chlorhexidine mouthwash and benzydamine spray
Reassure pt its benign

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19
Q

What causes angina bullosa haemorrhagica?

A

Eating - thermal trauma
Steroids inhalers

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20
Q

What is pemphigoid?

A

Autoimmune blistering disease
Clear or blood filled, thick walled blisters
Exposed connective tissue when blisters burst

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21
Q

What are the different types of pemphigoid?

A

Bullous pemphigoid - affects skin
Mucous membrane pemphigoid - all mucous membranes - eye, genital, oral
Cicatritial pemphigoid - mucosal with scarring

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22
Q

What is seen histologically in pemphigoid?

A

Sub epithelial split
Antibodies attack the hemidesmosomes at the basement membrane that attach the epithelium to the connective tissue

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23
Q

What special investigations are carried out for pemphigoid and pemphigus?

A

Direct immunofluorescence
Biopsy for histopathological analysis
Blood test for antibodies C3, IgG and IgA

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24
Q

What is seen in DIF in pemphigoid?

A

Linear staining seen along the basement membrane
C3 and IgG antibodies detected in this area
IgA occasionally found

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25
Q

How does DIF work?

A

Tissue sample is taken and are incubated with fluorescently labelled antibodies that specifically bind to immunoglobulins (IgG and IgA) and complement proteins (C3)
Slides are examined under a fluorescent microscope to visualise the distribution of autoantibodies and complement proteins

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26
Q

How is pemphigoid and pemphigus treated?

A

Benzydamine spray
Beclometasone MDI inhaler
Betamethasone rinse
Oral prednisolone
Immunomodulators - azothioprine, mycophenolate

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27
Q

What is pemphigus?

A

Autoimmune blistering disease
Causes intraepithelial bullae found in skin and mucosa

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28
Q

What is the most common type of pemphigus?

A

Pemphigus vulgaris

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29
Q

What is seen histologically in pemphigus?

A

Antibodies attack the desmosomes joining epithelial cells
Loss of epithelium
Basal cells attached to the basement membrane
Tzank cells seen

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30
Q

What is seen in DIF in pemphigus?

A

Antibodies binding all around cells as desmosomes role is to attach epithelial cells to each other
Basket-weave pattern
C3 and IgG antibodies

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31
Q

What is the main clinical difference between pemphigoid and pemphigus?

A

In pemphigus you rarely see intact bullae, you see erosions instead

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32
Q

What are the causes of nutritional/metabolic ulcers?

A

Children/teenagers associated with growth
Adults with GI pathology
Anaemia
Malnourishment

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33
Q

What conditions cause immunological ulcers?

A

Behçet’s disease
Vesiculobullous disease
Lichen planus
CT diseases eg - SLE

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34
Q

What infections can cause ulcers?

A

HSV
VZV
Coxsackie virus
EBV
HIV

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35
Q

Describe a high risk ulcer

A

Exophytic
Rolled borders
Raised
Hard to touch - indurated

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36
Q

What are the different causes of ulcers?

A

Trauma
Immunological
Carcinoma
Infection
Medical conditions

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37
Q

What are recurrent herpetic lesions and where are they most found?

A

Ulceration limited to one nerve group/branch
Lesions recur in the same place
Prodromal period
Often occurs on hard palate

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38
Q

What is recurrent aphthous stomatitis?

A

Immunologically generated recurring ulcers that follow a set pattern depending on type

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39
Q

Describe minor aphthous ulcers

A

Less than 10mm diameter
Last up to 2 weeks
Only affects non-keratinised mucosa
Heals without scarring
Responds well to topical steroids
Commonest type of recurrent oral ulceration

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40
Q

Describe major aphthous ulcers

A

Can last for months
Can affect any part of the oral mucosa
May scar when healing
Responds poorly to topical steroids - intralesional steroids more helpful
Usually larger than 10mm - diagnose from worst ulcer

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41
Q

Describe herpetiform apthae

A

Rarest form of aphthous ulcers
Multiple small ulcers on non-keratinised mucosa
Heal within 2 weeks
Similarly to primary herpetic gingivostomatitis in site and number but without systemic effects
Can coalesce into larger areas of ulceration
Not to do with HSV as keratinised epithelium is involved

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42
Q

How is oral and genital ulceration diagnosed?

A

3 episodes of mouth ulcers in a year
At least two of the folllowing:
- genital sores
- eye inflammation
- skin ulcers
- pathergy

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43
Q

What are the signs of Behçet’s disease?

A

Primarily vasculitis
Oral and genital ulceration
Eye disease
Bowel ulceration
May involve heart, lungs, brain and joints

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44
Q

How is Behçet’s disease managed?

A

Treat RAS
Systemic immunomodulation where multiple systems involved

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45
Q

What are the predisposing factors for RAS?

A

Genetic predisposition
Systemic disease
Stress
Mechanical injuries
Hormone level fluctuations
Micro element deficiencies
Viral and bacterial infection

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46
Q

What special investigations are used for RAS?

A

Blood tests:
- haematinic deficiencies - iron, B12 and folic acid
- coeliac disease (TTG)
Allergy tests

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47
Q

How is RAS treated?

A

Correct haematinic deficiency
Refer if coeliac positive
Avoid dietary triggers identified from testing
Chlorhexidine mouthwash
Benzydamine spray
Beclometasone MDI inhaler
Betamethasone rinse
Oral prednisolone
Immunomodulators

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48
Q

What are the causes of dry mouth?

A

Salivary gland disease
Drugs - reduce stimulation of glands to produce saliva
Medical conditions
Anxiety and somatisation disorders

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49
Q

What drugs cause dry mouth?

A

Antimuscarinic cholinergic drugs:
- tricyclic antidepressants
- antihistamines
- antipsychotics
- diuretics

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50
Q

What special investigations are carried out for a dry mouth?

A

Salivary flow tests - <1.5ml unstimulated flow in 15 minutes
Blood tests - FBC, U&E, ANA, anti La, anti Ro, C3 and C4 complement
Imaging - salivary ultrasound, sialography
Dry eyes screen - Schirmer’s tests - <5mm wetting of paper in 5 minutes
Labial gland biopsy of lower lip

51
Q

What are the functions of saliva?

A

Acid buffering
Mucosal lubrication
Taste facilitation
Antibacterial

52
Q

What conditions directly affect the salivary glands?

A

Aplasia
Sarcoidosis
HIV
Gland infiltration - amyloidosis and haemachromatosis
Cystic fibrosis

53
Q

What is sarcoidosis?

A

Granulomatous condition causing infiltrate within the SG preventing proper function

54
Q

What is amyloidosis?

A

Deposition of protein within SG, preventing proper function

55
Q

What is haemachromatosis?

A

Excess storage of iron in SG preventing proper function
High level of ferritin in blood

56
Q

How can radiation and cancer treatment lead to a dry mouth?

A

Radiation causes loss of vascular supply
Anti-neoplastic drugs and radioiodine can accumulate and kill acinar cells

57
Q

What are the causes of salivary gland enlargement?

A

Viral - mumps, HIV
Secretion retention - mucoceles and duct obstruction
Gland hyperplasia - sialosis when cause unknown
Sjögren’s syndrome

58
Q

How does HIV salivary disease present?

A

Unexplained salivary swelling
Doesn’t improve with treatment
Lympho-proliferative enlargement of the glands

59
Q

How does subacute salivary obstruction present?

A

Swelling associated with meals - increases as salivary flow starts and decreases as flow stops
Causes duct obstruction
Usually submandibular but can be parotid

60
Q

What are the causes of subacute salivary obstruction?

A

Sialolith (stones)
Mucous (plugging)
Ductal damage from chronic infection (scarring)

61
Q

What special investigations are carried out for subacute obstruction?

A

Plain radiography - lower occlusal or periapical in cheek
Sialography
Isotope scan
Ultrasound of duct system

62
Q

What is chronic non-specific sialadenitis?

A

Damage to salivary glands over many years
Acinai and ducts lost and replaced with fibrous tissue

63
Q

How is salivary subacute obstruction managed?

A

Surgical sialolith removed if present
Sialography if no stones present
Consider gland removal if fixed swelling and no obvious cause for obstruction

64
Q

What is sialosis?

A

Persisting and unexplained enlargement of one or more salivary gland with no identified glandular cause

65
Q

What special investigations can be carried out for sialosis?

A

Blood tests - glucose, FBC, U&E’s, Anti La, Anti Ro
MRI of major salivary glands
Ultrasound for Sjögren’s changes
Labial gland biopsy to exclude Sjögren’s
Tear films
Sialography
Clinical photographs

66
Q

What is Sjögren’s syndrome?

A

A chronic autoimmune disorder where the body’s immune system attacks its own salivary glands and lacrimal glands resulting in dry eyes and dry mouth

67
Q

What is the incidence of SS?

A

0.2-1.2% of people affected
Female: male ratio 10:1

68
Q

What are the signs and symptoms of SS?

A

Dry eyes and mouth
General fatigue
Joint pain and swelling
Muscle pain
Salivary gland enlargement

69
Q

What are the consequences of SS?

A

Gradual loss of salivary/lacrimal gland tissue through inflammatory destruction
Enlargement of major salivary glands
Increased risk of any lymphoma (5%) and MALT lymphoma
Oral and ocular effects of loss of saliva and tears

70
Q

How is SS diagnosed?

A

ACR-EULAR 2016 - if pt scores ≥4, they can be diagnosed
Histopathological findings (Labial biopsy) - 3
Autoantibodies (anti la, anti ro) - 3
Dry eyes/mouth through salivary flow and Schirmer’s test - 1
Ultrasound - 1
Ocular staining score - 1

71
Q

What are the oral signs and symptoms of SS?

A

Symptoms:
- daily feeling of dry mouth for >3 months
- recurrent swelling of salivary glands as an adult
- frequent sips of water to aid swallowing dry food
Signs:
- abnormal unstimulated whole salivary flow (UWS) - <1.5ml in 15 minutes

72
Q

What are the ocular signs and symptoms of SS?

A

Symptoms:
- persistent dry eyes for >3 months
- recurrent sensation of sand/gravel in eyes
- tear substitutes used >3 times daily
Signs:
- abnormal Schirmer test - <5mm wetting in 5 minutes
- green stain in fluorescein tear film assessment

73
Q

What is seen histologically in SS?

A

Generalised lymphocytic infiltration
Collection of >50 lymphocytes around a duct - lymphocytic focus (foci)
Acinar tissue destruction
Fibrosis of glandular tissue

74
Q

How is SS treated?

A

Prevention - diet, OHI, fluoride
Symptomatic treatment of oral dryness with salivary stimulants (Prilocarpine) or salivary substitutes (saliva orthana)
Immune modulating treatment - hydroxychloroquine and methotrexate (DMARDs)

75
Q

What are the causes of white patches?

A

Abnormal or increased keratin
Increased epithelial thickness
Candida infection

76
Q

What are the risk factors for oral candidiasis?

A

Immunocompromised
Dentures
Smoking
Inhaler use
Dry mouth
Antibiotics
HIV

77
Q

What are the different types of oral candidiasis?

A

Pseudomembranous
Erythematous
Hyperplastic
Angular cheilitis

78
Q

How is candidiasis managed?

A

Denture and oral hygiene
Check diabetes
Microbiological check
Haematinics
Topical antifungals - miconazole, chlorhexidine, nystatin
Systemic antifungals - fluconazole, itraconazole

79
Q

Describe pseudomembranous candidiasis

A

White, curd like patches
Can be wiped away, leaving red underneath
Seen immunocompromised, inhalers and infants

80
Q

Describe erythematous candidiasis

A

Red, atrophic areas
Burning sensation
Bleeding areas
Seen in immunocompromised, denture wearers and people with xerostomia

81
Q

Describe hyperplastic candidiasis

A

Chronic, persistent white patches
Cannot be wiped away
Found in immunocompromised and poor fitting dentures
Malignant potential

82
Q

Describe angular cheilitis

A

Found on corners of mouth
Erythema and fissuring
Due to poor fitting dentures, immunocompromised and nutritional deficiency

83
Q

What is traumatic keratosis and how is it treated?

A

Increased keratin deposition at site of trauma as protective mechanism
Smoking cessation and clinical photograph

84
Q

What is hairy leukoplakia?

A

Non-removable white patch found mostly on lateral border of tongue
Acanthotic and parakeratinised tissue
Triggered in EBV
Found in HIV pts - immunocompromised

85
Q

What is granulomatosis with polyangiitis and how is it managed?

A

Systemic vasculitis
May have fever and weight loss
Potentially fatal
Manage with immunosuppressants

86
Q

Which oral tissues are keratinised and non-keratinised?

A

Keratinised:
- gingiva, hard palate, dorsum of tongue
Non-keratinised:
- buccal and labial mucosa, soft palate, floor of mouth, inner lining of lips

87
Q

Give examples of connective tissue (vascular) diseases

A

Large vessel disease - giant cell arteritis
Medium vessel disease - Kawasaki disease
Small vessel disease - granulomatosis with polyangiitis

88
Q

What are the general causes of brown/black lesions

A

Racial
Smoking
Drugs
Addison’s disease

89
Q

What are the local causes of brown/black lesions

A

Amalgam
Melanotic macule
Melanotic naevus
Malignant melanoma

90
Q

What are the features of a melanoma?

A

Variable pigmentation
Irregular outline
Raised surface
Symptomatic - itch or bleed

91
Q

When should a white lesion be referred?

A

If becoming more raised and thickened
If it has an inflammatory margin
If the lesion is without cause

92
Q

What are fordyce spots, where are they found and what is the incidence?

A

Sebaceous glands - look like yellowish bumps
Found on buccal mucosa and lips
60-75% of adults

93
Q

What is linea alba?

A

Horizontal, asymptomatic white lesion found along the occlusal plane of the buccal mucosa

94
Q

How does linea alba appear histologically?

A

Hyperkeratosis
Prominent or reduced granular layer
Acanthosis

95
Q

What is geographic tongue and what is its incidence?

A

Loss of Filiform papillae - areas of tongue atrophy and hyperkeratinisation
Comes and goes and changes appearance
Affects 3% of population

96
Q

What are the symptoms of geographic tongue and how is it managed?

A

Mainly asymptomatic
Sometimes sensitive to hot and spicy foods and toothpaste
Avoid trigger foods and use SLS free toothpaste

97
Q

What is a fissured tongue and how is it treated?

A

Variation of normal anatomy
Deep grooves and fissures on tongue surface
OHI
Lightly brushing tongue

98
Q

What is black hairy tongue, what causes it and how is it treated?

A

Hyperplasia of the Filiform papillae
Build up of commensal bacteria and food debris, pigmented fungi and bacteria
Associated with smoking and antibiotics, chlorhexidine and poor OH
Reassure pt, smoking cessation, stay hydrated, lightly brush tongue and gently exfoliate with peach/nectarine stone

99
Q

What is desquamative gingivitis?

A

Full thickness erythema of the gingivae
Descriptive term not a diagnosis
Not caused by plaque but exacerbated by it

100
Q

What are bony exostoses, what is the incidence and give examples?

A

Usually benign overgrowth of calcified bone - can be associated with parafunction
Affects 30-40% of the population
Torus palatinus
Torus mandibularis

101
Q

Why should bony exostoses be monitored?

A

Can be a manifestation of rare polyposis syndromes such as Gardner’s syndrome

102
Q

What is oral dysaesthesia?

A

An abnormal sensory perception in the absence of abnormal stimuli

103
Q

What are the types of oral dysaesthesia?

A

Somatoform - perception and understanding of information is wrong
Neuropathic - abnormal sensory stimulus and nerves function incorrectly

104
Q

Give examples of common dysaesthesias

A

Burning mouth feeling
Dysgeusia - bad/salty/metallic taste
Paraesthesia feeling
Dry mouth feeling

105
Q

What are the predisposing factors for oral dysaesthesias?

A

Deficiencies - haematinics, zinc, vitamin B1 and B6
Fungal and viral infections
Anxiety and stress
Gender - woman more likely to present

106
Q

What is burning mouth syndrome most associated with?

A

Haematinic deficiency

107
Q

What is touch dysaesthesia and what should be done?

A

Pins and needles feeling
Normal sensation to testing despite pins and needles feeling
Must test CNs
MRI to check demyelination or tumour

108
Q

How is a dry mouth dysaesthesia treated?

A

Associated with anxiety disorder
Test as if patient has SS, should get no positive findings

109
Q

How are dysaesthesias managed?

A

Explain condition to patient - mouth may be normal but the way your feeling isn’t
Assess degree of anxiety
Anxiolytic meds - nortriptyline
Neuropathic meds - Gabapentin, pregabalin

110
Q

What is neuralgia?

A

An intense stabbing pain
Usually brief but severe
Pain extends along course of affected nerve
Usually caused by irritation or damage to a nerve

111
Q

What is the incidence of TN?

A

4.3 in 100,000
Female:male ratio is 5.9:3.4
Usually older people

112
Q

What are the causes of TN?

A

Idiopathic
Classical - vascular compression of CNV
Secondary to:
- MS
- space-occupying lesion
- CT disease

113
Q

What are the triggers of TN?

A

Cutaneous
Wind and cold
Touch
Chewing

114
Q

What are the red flags in TN?

A

Younger pts
Sensory deficit in facial region
Hearing loss
Other CN lesions - test CNs and get MRI

115
Q

What is the first and second line drug therapy for TN?

A

First line - carbamazepine, oxycarbamazepine, lamtrigine
Second line - Gabapentin, pregabalin, phenytoin, baclofen

116
Q

What are the side effects of carbamazepine?

A

Blood disorders - thrombocytopenia, neutropenia
Electrolyte imbalance
Neurological deficit
Liver toxicity
Potentially fatal skin reactions

117
Q

What are the surgical options for TN?

A

Microvascular decompression (MVD) - preferred
Stereotactic radiosurgery
Destructive central procedures
Destructive peripheral neurectomies

118
Q

What are trigeminal autonomic cephalalgias and give examples?

A

Unilateral head pain - predominately from V1
Very severe, excruciating pain
Include cluster headache, paroxysmal hemicrania and SUNCT

119
Q

What is the main difference between cluster headache, PH and SUNCT?

A

Cluster headache - cycles of frequent attacks followed by periods of remission
PH - frequent attacks multiple times per day
SUNCT - very frequent shorter attacks, dozens per day

120
Q

What is OFG?

A

Oedema in the oral and facial soft tissues by blockage of lymphatic drainage due to an immune reaction
Swelling comes up quickly and settles very slowly over weeks and months

121
Q

What is angio-oedema?

A

Oedema of the oral facial soft tissues due to an increase in fluid exudate from capillaries with no lymphatic drainage
Swelling comes up quickly and settles within 24-48 hours

122
Q

What are the signs and symptoms of OFG?

A

Lip and facial swelling
Cobblestoning appearance of mucosa
Mucosal tags
Oral ulceration
Angular cheilitis

123
Q

What investigations should be carried out for OFG?

A

Blood tests - deficiencies
Faecal calprotectin
Endoscopy
Biopsy for histopathological analysis

124
Q

How is OFG managed?

A

Avoidance of benzoates, cinnamon, chocolate, sorbetes
Topical steroids - Betamethasone rinse, beclomethasone MDI inhaler
Intralesional steroids - triamcinolone
Tacrolimus
Oral prednisolone
Azathioprine, mycophenolate

4 - misc (10 decks)

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