Oral Med Flashcards

(121 cards)

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
What is pemphigus vulgaris
-Intra-epithelial blistering disorder -IgG auto-antibodies target the attachment proteins of desmosomes -Causes dissolution of cell-to-cell adhesion
26
What are some risk factors for pemphigus vulgaris
-Diet rich in leeks, garlics, onions -Sulphydryl containing drugs (captopril) -Non-thiol containing drugs (diclofenac, rifampicin)
27
What is the clinical presentation of pemphigus vulgaris
-Affects the buccal mucosa, gingiva, palate -Positive nikolsky's sign -Desquamative gingivitis -Mucosal and skin lesions -If oesophageal involvement then dysphagia -Slow healing erosions
28
Describe the histological findings associated with pemphigus vulgaris
-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
29
What is the treatment for pemphigus vulgaris
-Topical corticosteroids -Systemic corticosteroids -Steroid-sparing agents (immunosuppressants) such as azathioprine -IV immunoglobulins -IV monoclonal antibodies
30
What is mucous membrane pemphigoid
-Sub-epithelial blistering disorder -Chronic or unknown aetiology -Circulating or bound antibodies targeting the basement membrane zone
31
What is the clinical presentation of mucous membrane pemphigoid
-Positive nikolsy's sign -Desquamative gingivitis -No skin lesions -Irregular painful erosions -Occular pemphigoid
32
Explain the occular changes associated with mucous membrane pemphigoid
-Conjunctival scarring -Irritation of the eyes, excessive tearing -Entropion (inturning of the lower eyelid)
33
What is the treatment for mucous membrane pemphigoid
-Topical corticosteroids -Systemic corticosteroids -Azathioprine -Anti-inflammatory antibiotics (doxycycline) -Dapsone
34
What is bullous pemphigoid and what is the management
-Blistering condition of the skin only -Treated with corticosteroids and dapsone
35
What is dermatitis herpetiformis
-Papulovesicular rash -Associated with gluten sensitive enteropathy -Clinical presentations as blisters on the elbows, buttocks and knees -Transient oral ulceration
36
What is the treatment for dermatitis herpetiformis
-Dapsone -Gluten free diet
37
What is erythema multiforme
-Chronic hypersensitive reaction -Causes lip erosions which are painful and slow to heal -Target/iris lesions of the skin
38
What are the causes of erythema multiforme
-Drugs -Infections (HSV) -Idiopathic -Malignancy, SLE
39
What is angina bullosa hemorrhagica
-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
40
What are the causes of angina bullosa hemorrhagica
-Use of inhaled steroids -Diabetes (can cause vascular fragility) -Hard/dry foods, dry mouth
41
What is the management of angina bullosa hemorrhagica
-FBC -Difflam -Chlorhexidine mouth wash -Incision if causing respiratory depression
42
What is the definition of Xerostomia and hyposalivation
-Xerostomia is the feeling of dry mouth -Hyposalivation is the objective reduction in salivary gland secretion due to reduced salivary gland function
43
What are the functions of saliva
-Antimicrobial properties -Lavage and buffering -Taste perception -Digestion -Lubrication for speech and swallowing
44
What are the complications of xerostomia
-Dryness of the GI tract -Voice hoarseness -Increased risk of soft tissue disease -Dental problems -Difficulty speaking and swallowing
45
What questions need to be asked in the diagnosis of xerostomia
-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
46
What is the aetiology of dry mouth
-Dehydration -Age -Idiopathic -Medications -Habits (mouth breathing) -Systemic conditions -Salivary gland disease
47
What are the classifications of salivary gland disease
-Infective (bacterial or viral siladenitis) -Damage to salivary glands secondary to cancer therapy -Tumour of salivary gland -Obstruction (calculi) -Degenerative disease (sjogrens)
48
What are some systemic diseases associated with dry mouth
-Diabetes -HIV -Liver disease -Sjogrens syndrome -Sarcoidosis
49
What is important to do when examining salivary glands
-Muscle weakness -Parasthesia -Facial nerve weakness -Compressible mass -Lymphadenopathy
50
What is sialosis
-Bilateral, non-specific inflammation of salivary glands (usually parotid) -Aetiology is unknown -Associated with alcoholism, nutritional deficiencies, pregnancy, diabetes
51
What is sialolithiasis
-Presence of stones or calculi in the submandibular gland -Causes mealtime syndrome
52
What is sialadenitis
-Enlargement of the parotid or submandibular gland due to infection, inflammation or obstruction -Can be caused by mumps, sarcoidosis, sjogrens
53
What is pleomorphic adenoma
-Benign epithelial salivary gland condition -Affects parotid gland -Diverse histological patterns -Incomplete capsule can make excision difficult
54
What is warthin's tumour
-Benign epithelial salivary gland condition -Smooth, soft parotid mass -Low rate of reoccurence
55
What is a haemangioma
-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
What is necrotising sialometaplasia
-Benign, self-healing condition affecting minor salivary gland -Single unilateral lesion on the hard palate
57
What is mucoepidermoid carcinoma
-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
What is adenoid cystic carcinoma
-Malignant salivary gland tumour affecting submandibular gland -Regional metastases less common, but can have distant metastases to the lungs
59
What is carcinoma ex-pleomorphic adenoma
-Regional and distant metastases are common -Sudden growth, aggressive
60
What is sjogre's syndrome
-Autoimmune condition -Primary: dry eyes and dry mouth -Secondary: dry eyes, dry mouth, connective tissue disorder such as rheumatoid arthritis
61
What are the special investigations for sjogren's syndrome
-Blood test to look for anti-Ro, anti-La antibodies -Imaging (sialography, US) -Saliva flow rate test
62
What is the management for salivary gland disease
-Regular dental visits, good OH, fluoride -Diet advice -Sip water frequently -Use sugar free gum -Artificial saliva -Treat candida -Pilocarpine in severe cases
63
Complications of sjogrens
-Lymphoma -Heart block -Eye damage
64
What are the effects of changes in iron, folate and B12 on the oral environment
-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
What are the oral features of alcoholism
-Sialosis -Dental erosion -Oral squamous cell carcinoma -Liver cirrhosis
66
What are the oral features of bulimia nervosa
-Maintain a consistent weight unlike anorexia -Russel’s signs on the hands -Erosion -Sialosis -Ulcers on the palate -Angular chelitis
67
What are the predisposing factors for ANUG
-Stress -Immunocompromised -Poor OH -Smoking -Malnutrition
68
What is the clinical presentation of ANUG
-Punched out ulceration of the gingiva -Halitosis (rotting hay smell) -Pain -Periodontal pockets -Sloughing of the gingiva
69
What is the treatment for ANUG
-Analgesics -Antibiotics if systemic involvement -Chlorhexidine mouthwash -Periodontal assessment -Good OH -Smoking cessation
70
What are the effects of vitamin C deficiency
-Proliferation of the blood vessels around the gingiva and the hair follicles -Causes cork screw hairs -Causes exfoliation of teeth -Scurvy
71
What are the effects of zinc deficiency
-Benign migratory glossitis -Lethargy -Growth retardation -Poor wound healing -Alopecia
72
What is the treatment of benign migratory glossitis
-Difflam (benzydamine rinse) -Treat associated candida infection -Corticosteroids -Exclude other sources of tongue soreness
73
What is coeliac disease
-Inflammatory condition affecting the small intestine -Induced by gluten
74
What are the oral manifestatiosn of coeliac disease
-Enamel hypoplasia -ROU -Angular chelitis -ROU -Exacerbation of lichen planus -Glossitis (burning mouth)
75
What oral lesions are characteristic of crohn’s disease
-Mucosal tags -Cobblestone mucosa -Lip fissuring -Deep linear ulceration
76
What is orofacial granulomatosis and its management
-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
Whats is peutz-jehghers
-Genetic condition resulting in perioral and vermillion freckles -Risk of intestinal polyps
78
What is lichen planus
-Immune-mediated -Basal cell degeneration -Caused by cytotoxic T-cells -Skin and oral lesions
79
What are the predisposing factors for lichen planus
-Diabetes -Liver disease -Stress -Spicy/acidic foods
80
What are the types of lichen planus
-Reticular -Erosive -Ulcerative -Plaque-like -Bullous -Papular
81
Where does lichen planus affect
-Skin and oral lesions -Areas of high friction (kobener's phenomenon) -Buccal mucosa, gingiva, tongue (rarely hard palate) -Hair, nails, genitals
82
What are the key histopathological features for lichen planus
-Basal cell degeneration/liquefaction -Hyperkeratosis -Saw tooth rete ridges -Lymphocyte-dominant sub-epithelial band
83
Management of lichen planus
-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
Pharmacological management of lichen planus
-Topical and systemic corticosteroids -Calcineurin inhibitors (tacrolimus/pimecrolimus)
85
What is lichenoid reaction and management
-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
Describe the histology of lichenoid reaction
-Similar to lichen planus -Increased eosinophils -Considerable basal cell liquefaction
87
What is the clinical presentation of DLE
-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
What are the special investigations for DLE
-Biopsy -Serum
89
What are the histological features of DLE
-Parakeratosis or orthokeratosis -Basal cell degeneration -Chronic inflammatory cell infiltration of sub-epithelial layer -Irregular pattern of acanthosis
90
What is the management of DLE
-Oral lesions management is same as lichen planus -Chloroquine or SPF for skin lesions
91
What are the risk factors for GVHD
-Elderly donor or recipient -Poorly matched grafts
92
What are the features seen with GVHD
-Oral dryness -Burning sensation -Reduced oral opening if sclerotic form of GVHD
93
What is the management of GVHD
-Topical analgesics -Corticosteroids -Tacrolimus -Increased risk of OSCC developing so monitor regularly
94
What is the management of GVHD
-Topical analgesics -Corticosteroids -Tacrolimus -Increased risk of OSCC developing so monitor regularly
95
What is the difference between an erosion and an ulcer
-An erosion is a partial loss of skin or mucous membrane -An ulcer is a total loss of epithelium
96
What is the relevant history we would take for an ulcer
-Age -Smoking and alcohol -Check for other malignancy
97
What are the features we would consider in a ulcer history
-Size, site, shape -Age of onset -Duration and frequency of attack -Ulcer-free periods -Prodrome -Coalesce? -Smoking cessation/menstruation
98
What is the classification of ulceration
-Single persistent: neoplastic -Single episode: trauma, infective, drugs -Recurrent: RAS, erythema multiforme -Recurrent: secondary to systemic disease
99
What are the characteristics of major RAS
->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
What are the characteristics of minor RAS
-<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
What are the characteristics of herpetiform RAS
-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
What are the special investigations for ulcers
-Blood tests -Biopsy -Imaging
103
What is the treatment for ulcers
-Topical or systemic analgesics to relieve the pain -Corticosteroids to promote healing -CHX mouthwash to maintain health
104
What is behcet's disease
-Triad of oral ulceration, uveitis, and genital involvement
105
What is Candida albicans sensitive to
-Temperature -pH -Availability of nutrients -These can cause normal organisms to become pathogenic
106
What are the histological findings associated with candida
-Gram stained smear -Associated with tangled hyphae -Detached epithelial cells -Leucocytes
107
What are the general factors affecting candida infection
-Broad spectrum antibiotics -Nutritional deficiency -Immunosuppression -Diabetes -Xerostomia
108
What are the local factors affecting candida infection
-Poorly fitting dentures -Smoking -Carbohydrate rich diet
109
How does drug therapy impact on candida infections
-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
How does diabetes increase risk of candida infection
-Reduced pH -Increased blood glucose concentration which acts as a substrate for candida
111
How does immunodeficiency cause candida infection
-Cell mediate and humoral immunity is important in the prevention of fungal infections
112
What is the presentation of acute pseudomembranous candida
-Creamy white plaques that rub off to reveal an erythematous, bleeding base
113
What is the management of acute pseudomembranous candida
-Improve oral hygiene -Investigate and treat systemic causes -Nystatin suspension or miconazole -Chlorhexidine mouthwash
114
What is the presentation and risk factors for chronic hyperplastic candida
-White lesions found bilaterally at the buccal mucosa close to the lip commisures -Do not rub off -Common in smokers, middle aged males
115
What is the management for chronic hyper plastic candida
-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
What is denture stomatitis
-Associated with upper acrylic dentures -Poor fit of denture excludes saliva from the supporting mucosa -Associated with inadequate denture hygiene
117
What is the newton's classification
-Type 1: pinpoint erythema -Type 2: diffuse erythema limited to fit surface of the denture -Type 3: Nodular appearance of palatal mucosa
118
What is the management of denture stomatitis
-Improve denture and oral hygiene -Eliminate trauma with soft tissue conditioners -Apply miconazole gel
119
What is the management of angular chelitits
-Correct vertical dimension -Improve denture hygiene -Treat with trimovate cream to the corners of the lips -Miconazole gel
120
What is median rhomboid glossitis
-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
What are the possible sampling methods for candida infection and their advantages or disadvantages
-Saliva culture: not useful in xerostomia -Swab: identifies the type of candida present, but does not quantify -Smear: quantitative -Biopsy: requires minor oral surgery