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BDS5 > Oral Med > Flashcards

Oral Med Flashcards

1
Q

What is pain

A

-Unpleasant sensory and emotional experience
-Associated with actual or potential tissue damage

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2
Q

What is chronic pain

A

-Pain that has outlived its usefulness
-More than 3 months

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3
Q

What are the risk factors for TMJ

A

-Stress
-Bruxism
-Multiple pain conditions
-Sleep problems
-Exogenous hormone usage
-Females
-Facial trauma

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4
Q

What are signs of degenerative change in TMJ

A

-Clicking
-Crepitus
-Limitation of movement
-Sudden inability to close

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5
Q

What is involved in ‘self-care’ for TMJ

A

-Warmth to joints
-Muscle relaxants
-Jaw exercise
-Jaw massage
-Analgesics
-Attention to grinding

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6
Q

What are pharmacological treatments in managing TMJ

A

-Anti-anxiolytics
-Anti-depressants
-Corticosteroids
-Analgesics
-Muscle relaxants

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7
Q

What are the risk factors for persistent idiopathic facial pain

A

-Stress
-Dental intervention
-Prolonged dental treatment
-Severe dental infection

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8
Q

What is burning mouth syndrome

A

-Idiopathic burning or discomfort in the mouth
-Clinically normal oral mucosa
-Absence of medical or dental problems

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9
Q

What are local factors that can cause burning mouth symptoms

A

-Mucosal infection
-Soft tissue infection
-Parafunction
-Ill fitting dentures
-Hypersensitivity reaction

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10
Q

What are systemic factors that can cause burning mouth symptoms?

A

-Medical conditions
-Hormone deficiency
-Vitamin deficiency
-Medication

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11
Q

What are the associated symptoms of burning mouth syndrome

A

-Altered taste
-Sense of oral dryness
-Tongue thrusting
-Burning sensation

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12
Q

What are the causes of burning mouth

A

-Menopause
-Stress

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13
Q

What is the management of burning mouth

A

-Treat the mood
-Symptomatic management of reduced saliva
-Reassure the patient
-CBT
-Exclude local causes

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14
Q

What is glossopharyngeal neuralgia and its aetiology

A

-Sharp, shooting pain in the ear, the angle of the jaw and the base of the tongue
-Primary: decompression of nerve
-Secondary: vascular anomaly or tumour

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15
Q

What is the trigeminal neuralgia, its aetiology and predisposing factors

A

-Unilateral sharp shooting pain
-Caused by aberrant cerebellar artery causing decompression at the root of entry zone
-Can be caused by a tumour
-Hypertension and MS are risk factors

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16
Q

What is the treatment for trigeminal neuralgia

A

-Carbamazepine
-If not treated the remission periods will become less frequent

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17
Q

What is giant cell arteritis

A

-Sudden onset of headaches in the elderly
-Associated with thickened temporal artery

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18
Q

What are the symptoms of giant cell arteritis

A

-Headaches
-Visual disturbances
-Jaw and tongue claudication
-Chronic fatigue

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19
Q

What is the management of giant cell arteritis

A

-Corticosteroids
-Vitamin D and calcium

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20
Q

What are cluster headaches

A

-Severe headaches affecting the frontal, temporal and orbital region in the night
-Causes lacrimation and nasal congestion
-Affects middle aged
-More than 2 occurrences every week for more than 1 year

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21
Q

What is the management of cluster headaches

A

-Avoid triggers such as alcohol
-O2
-Nasal decongestants
-Subcutaneous injections of sumatriptan
-Prophylaxis with lithium or corticosteroids

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22
Q

What is the definition of a vesicle and a bulla

A

-Vesicle is a small fluid-filled blister less than 5mm in diameter
-Bulla is a large fluid-filled blister more than 5mm in diameter

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23
Q

What is the etiological classification of blisters and give an example of each

A

-Infective: HSV, herpangina, hand foot and mouth
-Immunological: MMP, PV
-Idiopathic: Erythema multiforme, drugs
-Collagen defect: Epidermalysis bullosa

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24
Q

What are the investigations for blistering conditions

A

-Incisional biopsy with a H&E stain to see the level of the blister within the epithelium
-Direct immunofluorescence
-Indirect immunofluorescence using patient’s serum

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25
Q

What is pemphigus vulgaris

A

-Intra-epithelial blistering disorder
-IgG auto-antibodies target the attachment proteins of desmosomes
-Causes dissolution of cell-to-cell adhesion

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26
Q

What are some risk factors for pemphigus vulgaris

A

-Diet rich in leeks, garlics, onions
-Sulphydryl containing drugs (captopril)
-Non-thiol containing drugs (diclofenac, rifampicin)

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27
Q

What is the clinical presentation of pemphigus vulgaris

A

-Affects the buccal mucosa, gingiva, palate
-Positive nikolsky’s sign
-Desquamative gingivitis
-Mucosal and skin lesions
-If oesophageal involvement then dysphagia
-Slow healing erosions

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28
Q

Describe the histological findings associated with pemphigus vulgaris

A

-Direct IF shows fishnet appearance
-Histology shows acantholysis which is the epithelium splitting into single cells
-Intraepithelial clefting is where the blisters form between the splitting epithelial cells

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29
Q

What is the treatment for pemphigus vulgaris

A

-Topical corticosteroids
-Systemic corticosteroids
-Steroid-sparing agents (immunosuppressants) such as azathioprine
-IV immunoglobulins
-IV monoclonal antibodies

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30
Q

What is mucous membrane pemphigoid

A

-Sub-epithelial blistering disorder
-Chronic or unknown aetiology
-Circulating or bound antibodies targeting the basement membrane zone

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31
Q

What is the clinical presentation of mucous membrane pemphigoid

A

-Positive nikolsy’s sign
-Desquamative gingivitis
-No skin lesions
-Irregular painful erosions
-Occular pemphigoid

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32
Q

Explain the occular changes associated with mucous membrane pemphigoid

A

-Conjunctival scarring
-Irritation of the eyes, excessive tearing
-Entropion (inturning of the lower eyelid)

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33
Q

What is the treatment for mucous membrane pemphigoid

A

-Topical corticosteroids
-Systemic corticosteroids
-Azathioprine
-Anti-inflammatory antibiotics (doxycycline)
-Dapsone

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34
Q

What is bullous pemphigoid and what is the management

A

-Blistering condition of the skin only
-Treated with corticosteroids and dapsone

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35
Q

What is dermatitis herpetiformis

A

-Papulovesicular rash
-Associated with gluten sensitive enteropathy
-Clinical presentations as blisters on the elbows, buttocks and knees
-Transient oral ulceration

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36
Q

What is the treatment for dermatitis herpetiformis

A

-Dapsone
-Gluten free diet

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37
Q

What is erythema multiforme

A

-Chronic hypersensitive reaction
-Causes lip erosions which are painful and slow to heal
-Target/iris lesions of the skin

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38
Q

What are the causes of erythema multiforme

A

-Drugs
-Infections (HSV)
-Idiopathic
-Malignancy, SLE

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39
Q

What is angina bullosa hemorrhagica

A

-Single blood blisters on the junction of the hard and soft palate
-Usually rupture after one day and heal over one week
-Reoccurence may occur

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40
Q

What are the causes of angina bullosa hemorrhagica

A

-Use of inhaled steroids
-Diabetes (can cause vascular fragility)
-Hard/dry foods, dry mouth

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41
Q

What is the management of angina bullosa hemorrhagica

A

-FBC
-Difflam
-Chlorhexidine mouth wash
-Incision if causing respiratory depression

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42
Q

What is the definition of Xerostomia and hyposalivation

A

-Xerostomia is the feeling of dry mouth
-Hyposalivation is the objective reduction in salivary gland secretion due to reduced salivary gland function

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43
Q

What are the functions of saliva

A

-Antimicrobial properties
-Lavage and buffering
-Taste perception
-Digestion
-Lubrication for speech and swallowing

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44
Q

What are the complications of xerostomia

A

-Dryness of the GI tract
-Voice hoarseness
-Increased risk of soft tissue disease
-Dental problems
-Difficulty speaking and swallowing

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45
Q

What questions need to be asked in the diagnosis of xerostomia

A

-Have you had persistently swollen salivary glands for more than 3 months
-Do you feel dryness for more than 3 months
-Do you wake up at night needed to drink fluids
-Do you struggle to swallow dry foods without fluids

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46
Q

What is the aetiology of dry mouth

A

-Dehydration
-Age
-Idiopathic
-Medications
-Habits (mouth breathing)
-Systemic conditions
-Salivary gland disease

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47
Q

What are the classifications of salivary gland disease

A

-Infective (bacterial or viral siladenitis)
-Damage to salivary glands secondary to cancer therapy
-Tumour of salivary gland
-Obstruction (calculi)
-Degenerative disease (sjogrens)

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48
Q

What are some systemic diseases associated with dry mouth

A

-Diabetes
-HIV
-Liver disease
-Sjogrens syndrome
-Sarcoidosis

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49
Q

What is important to do when examining salivary glands

A

-Muscle weakness
-Parasthesia
-Facial nerve weakness
-Compressible mass
-Lymphadenopathy

50
Q

What is sialosis

A

-Bilateral, non-specific inflammation of salivary glands (usually parotid)
-Aetiology is unknown
-Associated with alcoholism, nutritional deficiencies, pregnancy, diabetes

51
Q

What is sialolithiasis

A

-Presence of stones or calculi in the submandibular gland
-Causes mealtime syndrome

52
Q

What is sialadenitis

A

-Enlargement of the parotid or submandibular gland due to infection, inflammation or obstruction
-Can be caused by mumps, sarcoidosis, sjogrens

53
Q

What is pleomorphic adenoma

A

-Benign epithelial salivary gland condition
-Affects parotid gland
-Diverse histological patterns
-Incomplete capsule can make excision difficult

54
Q

What is warthin’s tumour

A

-Benign epithelial salivary gland condition
-Smooth, soft parotid mass
-Low rate of reoccurence

55
Q

What is a haemangioma

A

-Benign non-epithelial vascular tumour
-Common in children
-Dark red, lobulated mass
-Common in parotid gland
-Fast growth from 0-6 months, slow growth till 12 years

56
Q

What is necrotising sialometaplasia

A

-Benign, self-healing condition affecting minor salivary gland
-Single unilateral lesion on the hard palate

57
Q

What is mucoepidermoid carcinoma

A

-Malignant salivary gland tumour affecting parotid gland
-Made of mucous and epidermoid cells
-Low grade is easy to treat
-High grade has regional metastases to the lymph nodes

58
Q

What is adenoid cystic carcinoma

A

-Malignant salivary gland tumour affecting submandibular gland
-Regional metastases less common, but can have distant metastases to the lungs

59
Q

What is carcinoma ex-pleomorphic adenoma

A

-Regional and distant metastases are common
-Sudden growth, aggressive

60
Q

What is sjogre’s syndrome

A

-Autoimmune condition
-Primary: dry eyes and dry mouth
-Secondary: dry eyes, dry mouth, connective tissue disorder such as rheumatoid arthritis

61
Q

What are the special investigations for sjogren’s syndrome

A

-Blood test to look for anti-Ro, anti-La antibodies
-Imaging (sialography, US)
-Saliva flow rate test

62
Q

What is the management for salivary gland disease

A

-Regular dental visits, good OH, fluoride
-Diet advice
-Sip water frequently
-Use sugar free gum
-Artificial saliva
-Treat candida
-Pilocarpine in severe cases

63
Q

Complications of sjogrens

A

-Lymphoma
-Heart block
-Eye damage

64
Q

What are the effects of changes in iron, folate and B12 on the oral environment

A

-Atrophy of the epithelium
-Depapilation of the tongue
-Changes to the filoform papilla which results in candida infection and soreness
-Glossitis (iron deficiency: smooth, B12 deficiency: raw beefy red)
-ROU
-Angular chelitis
-Burning mouth syndrome
-Patterson Kelly syndrome (kolinchyia, iron deficiency anaemia, post-cricoid webs, glossitis)
-Candida

65
Q

What are the oral features of alcoholism

A

-Sialosis
-Dental erosion
-Oral squamous cell carcinoma
-Liver cirrhosis

66
Q

What are the oral features of bulimia nervosa

A

-Maintain a consistent weight unlike anorexia
-Russel’s signs on the hands
-Erosion
-Sialosis
-Ulcers on the palate
-Angular chelitis

67
Q

What are the predisposing factors for ANUG

A

-Stress
-Immunocompromised
-Poor OH
-Smoking
-Malnutrition

68
Q

What is the clinical presentation of ANUG

A

-Punched out ulceration of the gingiva
-Halitosis (rotting hay smell)
-Pain
-Periodontal pockets
-Sloughing of the gingiva

69
Q

What is the treatment for ANUG

A

-Analgesics
-Antibiotics if systemic involvement
-Chlorhexidine mouthwash
-Periodontal assessment
-Good OH
-Smoking cessation

70
Q

What are the effects of vitamin C deficiency

A

-Proliferation of the blood vessels around the gingiva and the hair follicles
-Causes cork screw hairs
-Causes exfoliation of teeth
-Scurvy

71
Q

What are the effects of zinc deficiency

A

-Benign migratory glossitis
-Lethargy
-Growth retardation
-Poor wound healing
-Alopecia

72
Q

What is the treatment of benign migratory glossitis

A

-Difflam (benzydamine rinse)
-Treat associated candida infection
-Corticosteroids
-Exclude other sources of tongue soreness

73
Q

What is coeliac disease

A

-Inflammatory condition affecting the small intestine
-Induced by gluten

74
Q

What are the oral manifestatiosn of coeliac disease

A

-Enamel hypoplasia
-ROU
-Angular chelitis
-ROU
-Exacerbation of lichen planus
-Glossitis (burning mouth)

75
Q

What oral lesions are characteristic of crohn’s disease

A

-Mucosal tags
-Cobblestone mucosa
-Lip fissuring
-Deep linear ulceration

76
Q

What is orofacial granulomatosis and its management

A

-Labial swelling which is recurrent
-Associated with a granulomatous infection
-Can be associated with angular chelitis, mucosal tags, mucosal ulceration
-Avoid cinnamon, use corticosteroids

77
Q

Whats is peutz-jehghers

A

-Genetic condition resulting in perioral and vermillion freckles
-Risk of intestinal polyps

78
Q

What is lichen planus

A

-Immune-mediated
-Basal cell degeneration
-Caused by cytotoxic T-cells
-Skin and oral lesions

79
Q

What are the predisposing factors for lichen planus

A

-Diabetes
-Liver disease
-Stress
-Spicy/acidic foods

80
Q

What are the types of lichen planus

A

-Reticular
-Erosive
-Ulcerative
-Plaque-like
-Bullous
-Papular

81
Q

Where does lichen planus affect

A

-Skin and oral lesions
-Areas of high friction (kobener’s phenomenon)
-Buccal mucosa, gingiva, tongue (rarely hard palate)
-Hair, nails, genitals

82
Q

What are the key histopathological features for lichen planus

A

-Basal cell degeneration/liquefaction
-Hyperkeratosis
-Saw tooth rete ridges
-Lymphocyte-dominant sub-epithelial band

83
Q

Management of lichen planus

A

-Reassure patient and warn them of malignant transformation
-Eliminate traumatic factors of restorations
-Eliminate chemical irritation from spicy or acidic foods
-Good OH to reduce plaque
-Eliminate SLS products
-Alcohol and smoking cessation

84
Q

Pharmacological management of lichen planus

A

-Topical and systemic corticosteroids
-Calcineurin inhibitors (tacrolimus/pimecrolimus)

85
Q

What is lichenoid reaction and management

A

-Similar to lichen planus
-Response to drugs or dental materials
-Take a good drug history
-Removal of the drug or material under rubber dam will resolve the symptoms

86
Q

Describe the histology of lichenoid reaction

A

-Similar to lichen planus
-Increased eosinophils
-Considerable basal cell liquefaction

87
Q

What is the clinical presentation of DLE

A

-Scaly, well-demarcated, atrophic skin lesions
-Found in areas exposed to sunlight
-Oral lesions similar to lichen planus
-SLE found on palate unlike lichen planus

88
Q

What are the special investigations for DLE

A

-Biopsy
-Serum

89
Q

What are the histological features of DLE

A

-Parakeratosis or orthokeratosis
-Basal cell degeneration
-Chronic inflammatory cell infiltration of sub-epithelial layer
-Irregular pattern of acanthosis

90
Q

What is the management of DLE

A

-Oral lesions management is same as lichen planus
-Chloroquine or SPF for skin lesions

91
Q

What are the risk factors for GVHD

A

-Elderly donor or recipient
-Poorly matched grafts

92
Q

What are the features seen with GVHD

A

-Oral dryness
-Burning sensation
-Reduced oral opening if sclerotic form of GVHD

93
Q

What is the management of GVHD

A

-Topical analgesics
-Corticosteroids
-Tacrolimus
-Increased risk of OSCC developing so monitor regularly

94
Q

What is the management of GVHD

A

-Topical analgesics
-Corticosteroids
-Tacrolimus
-Increased risk of OSCC developing so monitor regularly

95
Q

What is the difference between an erosion and an ulcer

A

-An erosion is a partial loss of skin or mucous membrane
-An ulcer is a total loss of epithelium

96
Q

What is the relevant history we would take for an ulcer

A

-Age
-Smoking and alcohol
-Check for other malignancy

97
Q

What are the features we would consider in a ulcer history

A

-Size, site, shape
-Age of onset
-Duration and frequency of attack
-Ulcer-free periods
-Prodrome
-Coalesce?
-Smoking cessation/menstruation

98
Q

What is the classification of ulceration

A

-Single persistent: neoplastic
-Single episode: trauma, infective, drugs
-Recurrent: RAS, erythema multiforme
-Recurrent: secondary to systemic disease

99
Q

What are the characteristics of major RAS

A

->10mm diameter
-Oval
-Grey base, erythematous border
-All surfaces
-Heals after up to 3 months
-Scars on healing
-1-10 in a crop
-Occurs in first decade of life

100
Q

What are the characteristics of minor RAS

A

-<10mm diameter
-Oval
-Grey base, indurated border
-Non-keratinised, esp. buccal mucosa
-Heals after 1-2 weeks
-No scars
-1-5 in a crop
-Occurs in second decade of life

101
Q

What are the characteristics of herpetiform RAS

A

-0.5-3mm in diameter
-Round, coalesce
-Yellow base, erythematous border
-Non-keratinised, esp floor of mouth
-Heals after 1-2 weeks
-Up to 20 in a crop
-Occurs in third decade of life

102
Q

What are the special investigations for ulcers

A

-Blood tests
-Biopsy
-Imaging

103
Q

What is the treatment for ulcers

A

-Topical or systemic analgesics to relieve the pain
-Corticosteroids to promote healing
-CHX mouthwash to maintain health

104
Q

What is behcet’s disease

A

-Triad of oral ulceration, uveitis, and genital involvement

105
Q

What is Candida albicans sensitive to

A

-Temperature
-pH
-Availability of nutrients
-These can cause normal organisms to become pathogenic

106
Q

What are the histological findings associated with candida

A

-Gram stained smear
-Associated with tangled hyphae
-Detached epithelial cells
-Leucocytes

107
Q

What are the general factors affecting candida infection

A

-Broad spectrum antibiotics
-Nutritional deficiency
-Immunosuppression
-Diabetes
-Xerostomia

108
Q

What are the local factors affecting candida infection

A

-Poorly fitting dentures
-Smoking
-Carbohydrate rich diet

109
Q

How does drug therapy impact on candida infections

A

-Broad spectrum antibiotics will alter the microflora in the mouth
-Reduces competition for other substrates
-Xerogenic agents reduce salivary flushing capacity
-Saliva contains anti-fungal agents

110
Q

How does diabetes increase risk of candida infection

A

-Reduced pH
-Increased blood glucose concentration which acts as a substrate for candida

111
Q

How does immunodeficiency cause candida infection

A

-Cell mediate and humoral immunity is important in the prevention of fungal infections

112
Q

What is the presentation of acute pseudomembranous candida

A

-Creamy white plaques that rub off to reveal an erythematous, bleeding base

113
Q

What is the management of acute pseudomembranous candida

A

-Improve oral hygiene
-Investigate and treat systemic causes
-Nystatin suspension or miconazole
-Chlorhexidine mouthwash

114
Q

What is the presentation and risk factors for chronic hyperplastic candida

A

-White lesions found bilaterally at the buccal mucosa close to the lip commisures
-Do not rub off
-Common in smokers, middle aged males

115
Q

What is the management for chronic hyper plastic candida

A

-Biopsy is mandatory due to malignant transformation risk
-Remove predisposing factors such as smoking
-Check for iron, folate, B12 levels
-Oral fluconazole for 2-4 weeks

116
Q

What is denture stomatitis

A

-Associated with upper acrylic dentures
-Poor fit of denture excludes saliva from the supporting mucosa
-Associated with inadequate denture hygiene

117
Q

What is the newton’s classification

A

-Type 1: pinpoint erythema
-Type 2: diffuse erythema limited to fit surface of the denture
-Type 3: Nodular appearance of palatal mucosa

118
Q

What is the management of denture stomatitis

A

-Improve denture and oral hygiene
-Eliminate trauma with soft tissue conditioners
-Apply miconazole gel

119
Q

What is the management of angular chelitits

A

-Correct vertical dimension
-Improve denture hygiene
-Treat with trimovate cream to the corners of the lips
-Miconazole gel

120
Q

What is median rhomboid glossitis

A

-Localised candida infection
-Causes atrophy of the filiform papilla anterior to the circumvallate papilla
-Usually a smooth diamond shape
-Associated with smoking and corticosteroid use

121
Q

What are the possible sampling methods for candida infection and their advantages or disadvantages

A

-Saliva culture: not useful in xerostomia
-Swab: identifies the type of candida present, but does not quantify
-Smear: quantitative
-Biopsy: requires minor oral surgery

BDS5 (4 decks)

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