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BDS4 > Oral medicine questions > Flashcards

Oral medicine questions Flashcards

1
Q

What is this method of analysis?

A
  • Direct immunofluorescence
  • basket weave pattern
  • this is pemphigus vulgaris
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2
Q

What would the pathologist report of IF of pemphigus vulgaris?

A
  • Basket weave pattern on IF
  • C3 and IGg antibodies
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3
Q

What are the main histopathological features of pemphigus vulgaris? (3)

A
  • supra-basal split
  • Tzank cells present
  • acantholysis ( loss of coherence between epidermal cells due to the breakdown of intercellular bridges)
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4
Q

what is pemphigus vulgaris ?

A
  • it is an autoimmune blistering disease that begins in the mouth
  • seen as clear-fluid fill blisters that burst and then spread
  • it is fatal without treatment
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5
Q

Why would pemphigus vulgaris occur?

A
  • autoimmune conditions
  • Type 2 hypersensitivity reaction causing antibodies to form against desmosomes
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6
Q

What is similar to pemphigus clinically but have different histopathology?

A
  • Bullous pemphigoid - sub basal split
  • Drug induced pemphigus
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7
Q

What is the clinical appearance/features of pemphigus?

A
  • superficial clear fluid filled blisters
  • burst and spread
  • can affect skin
  • fatal
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8
Q

What medications is used to treat pemphigus vulgaris? (3)

A
  • immune modulators - azathioprine
  • topical steroids - betamethasone
  • systemic steroids - prednisolone
  • monoclonal antibody therapy
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9
Q

List risk factors for oral squamous cell carcinoma? (8)

A
  • tobbaco use - smoking or smokeless
  • betel quid - chewing habit
  • alcohol use
  • Viruses - HPV, HSV , EBV , HHV-8
  • Poor diet and nutrition
  • Poor oral hygiene
  • immunodeficiency
  • socioeconomic factors
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10
Q

How would you grade dysplasia histopathologically ?

A

Hyperplasia
Mild
moderate
severe
carcinoma in situ
* based on cytological and architectural changes

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11
Q

How does hyperplasia appear histopathologically?

A

*Increase in cell numbers; no cellular atypia
* regular stratification
* basement compartment is larger

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12
Q

How does carcinoma in situ appears?

A
  • malignant but not invasive
  • abnromal architecture involving full thickness of epithelium
  • Severe atypia and mitosis
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13
Q

What intervention for cancer other than surgery?

A
  • chemotherapy ± radiotherapy
  • immunotherapy medication
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14
Q

After removal of a malignant lesion in the tongue, how would you restore its function?

A

Using a soft tissue graft to rebuild the tongue
* By taking tissue from somewhere else in the body such as skin on forearm, chest, thigh or gingival or mucous membranes
* this is then transplanted in the tongue area to replace lost tissue , blood supply is also checked

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15
Q

If the tumour invades bone and muscles what grade would this be?

A

High grade or Stage IV

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16
Q

Patient attends with redness at the corner of their mouth, what is your diagnosis?

A

Angular cheilitis

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17
Q

What is angular cheilitis?

A

inflammatory skin condition of variable aetiology (bacterial or fungal) occurring at the angle of the mouth which can be present as redness

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18
Q

What microorganisms are involved in angular cheilitis?

A
  • candida albicans
  • staphylococcus aureus
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19
Q

What type of sample should be taken for angular cheilitis ?

A

swab the commissure of the mouth

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20
Q

Name an immunological disease that can increase risk of candida infections? and why?

A

HIV
* patient is immunocompromised which allows harmless organisms to become pathogenic and cause infection
* impaired immune function

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21
Q

Name one GI disease that increase candida infections?

A

Crohn’s disease
* impaired nutrient absorption
* also due to immunosuppressive therapy making the body more suceptible to pathogens

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22
Q

Name other diseases that can be associated with angular cheilitis ?

A
  • intra oral - oral candidiasis and denture induced stomatitis
  • extra-oral - OFG orofacial granulomatosis
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23
Q

Why is miconazole is prescribed to a patient with angular cheilitis when histological sampling is not available?

A
  • Because it is effective against both caninda and gram positive cocci species bacteria such S. aureus
  • to confirm diagnosis as if this treats the condition then it is angular cheilitis
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24
Q

What 2 instructions should be given to a patient who wears a denture and have angular cheilitis?

A
  • do not wear denture overnight
  • denture hygiene instructions
    • clean dentures after eating , before bed and in the morning with soft brush and soapy warm water
    • clean with denture cleaning solutions according to manufacturer guidelines
    • clean mouth with softbrush and toothpaste or CHX mouthwash
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25
Q

What is trigeminal neuralgia?

A

A condition that cause pain usually on one side of the face characterised by stabbing sharp pain due to irritation of the trigeminal nerve

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26
Q

How does trigeminal neuralgia occur?

A
  • demyelination of the trigeminal nerve
  • compression of the trigeminal nerve
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27
Q

What special investigations would you do for trigeminal nerve?

A
  • Trigeminal nerve reflex testing - clenching
  • OPT to rule out dental cause then MRI
  • Use CT if MRI is contraindicated
  • Blood tests - FBC, U&E’s , blood glucose and liver function test ( in case of confirmed diagnosis and tx with carbamazepine)
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28
Q

What neurological disorders can cause trigeminal neuralgia?

A
  • multiple sclerosis
  • brain tumour compressing on the trigeminal nerve
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29
Q

What is the first line drug management for trigeminal neuralgia?

A

Carbamazepine 100mg
send 20 tablets
1 x twice daily

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30
Q

What blood tests should be done before starting carbamazepine?

A
  • liver function test
  • Urea and electrolytes test
  • Full blood count - haematinics
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31
Q

What are the side effects of carbamazepine? (7)

A
  • liver dysfunction
  • Allergies
  • Ataxia
  • Nausea , vomiting
  • Dizziness
  • Sedation
  • nightmares
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32
Q

What are the indications for surgery for treating trigeminal neuralgia? (4)

A
  • if the medical intervention is not effective
  • if the medical intervention is contraindicated
  • if the medication have severe side effects
  • if the condition is seriously affecting the quality of life of the patient
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33
Q

Name types of surgical interventions that can be carried out for trigeminal neuralgia?

A
  • Peripheral neurectomy
  • Trigeminal nerve balloon comression
  • Microvascular decompression
  • Radio-surgery gamma knife
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34
Q

What is paget’s disease?

A

a chronic (long-lasting) disorder that causes bones to grow larger and become weaker than normal

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35
Q

What are the clinical signs of paget’s disease (6)

A
  • localised pain and tenderness
  • focal temperature due to hyperaemia and hypervascularity
  • bilateral Increased bone size
  • bowing deformities
  • decreased range of motion
  • denture become ill fitting
  • facial asymmetry
  • nerve compression
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36
Q

What are the radiographic signs of Paget’s disease? (5)

A
  • Hypercementosis
  • loss of lamina dura
  • osteoporotic circumscripta
  • radiolucent regions resembling cysts
  • cotton wool appearance due to sclerotic and lytic lesions
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37
Q

What is albrights disease?

A

a genetic condition that affects bone growth, skin pigmentation and the body’s hormone balance can be polystotic or monostotic

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38
Q

What are the clinical signs of Albright’s disease? (7)

A
  • skin pigmentation
  • bone hard tissue expanding around teeth
  • facial asymmetry
  • endocrine hyperfunction
  • slow growing
  • Asymptomatic
  • early puberty

determined at timing of gene mutation

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39
Q

What are the radiographic signs of albright’s disease? (3)

A
  • regular bone fractures
  • bone deformities
  • craniofacial fibrous dysplasia
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40
Q

What is Cherubism?

A

a disorder characterized by abnormal bone tissue in the jaw caused by a genetic condition (autosomal dominant)

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41
Q

What are the clinical signs of Cherubism? (4)

A
  • painless bilateral enlargement of the bone
  • round face and swollen cheeks
  • dental malocclusion
  • grow until the age of 7 then regress after puberty
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42
Q

What are the radiographic signs of cherubism?

A
  • Multicystic and Multilocular lesions ( posterior of mandible and maxilla)
  • mandible or maxilla is replaced by fibrous tissue
  • obliterated facial sinuses

Histopathology include vascular giant cell lesions

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43
Q

What are the types of orofacial pain?

A
  • odontogenic ( acute and sub-acute)
    periodontal , abscess , caries
  • non-odontogenic ( acute or chronic)
    trigeminal neuralgia, chronic regional pain synfrome , traumatic injury to facial nerve , surgical injury to nerves of the head and neck
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44
Q

What is sjogren’s syndrome?

A
  • It is a chronic inflammatory and autoimmune disease where b-cell proliferation causes destruction of the exocrine glands causing dry mouth and dry eyes
  • it affects secretion production at the mucous membranes
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45
Q

What are the three types of Sjogren’s syndrome?

A
  • Partial Sjogren’s - sicca syndrome - dry eyes and mouth
  • Primary Sjogrens - associated with CT disease
  • Secondary Sjogren’s - Associated with CT disease
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46
Q

Which connective tissue disease can be associated with Sjogren’s syndrome? (3)

A
  • Systemic lupus erythematosus
  • Rheumatoid arthritis
  • Scleroderma
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47
Q

What antibodies are linked with Sjogren’s syndrome?

A

Anti-la and Anti-ro

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48
Q

What investigations do you carry out for Sjogren’s syndrome?

A
  • Schrimer’s test
  • Fluorescein tear film test
  • unstimulated whole salivary flow test
  • Salivary ultrasound scan
  • MRI for major salivary gland’s
  • labial gland biopsy
  • Radio-neucleotide assessment
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49
Q

What oral symptoms are gained subjectively from the patient regarding sjogren’s syndrome according to AECG?

A
  • daily feeling of dry mouth for more than 3 months
  • recurrent swelling in salivary gland as an adult
  • frequently drink liquid to aid swallowing dry food
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50
Q

What ocular symptoms are mentioned in AECG regarding sjogren’s syndrome?

A
  • Persistent troublesome of dry eyes for more than 3 months
  • Tear substitute used more than 3 times a day
  • Recurrent sensation of sand in the eyes
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51
Q

What is an abnormal result for UWS test?

A

less than 1.5ml in 15 minutes

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52
Q

What is abnormal schrimer’s test result?

A

less than 5mm in 5 minutes

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53
Q

How many positive criteria should there be AECG to confirm sjogren’s ?

A

4 or more positive criteria including number 5 and 6

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54
Q

Describe preventative measures for Sjogren’s syndrome?

A
  • Lialise with rheumatologist - multi-system disease
  • consider immune modulating treatment
    hydroxychloroquine and methotrexate
  • Diet advice , F toothpaste 5000ppm , OHI advice
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55
Q

Symptomatic management of Sjogren’s ?

A
  • Salivary stimulants - pilocarpine
  • Salivary substitutes - biotene gel , saliva orthana
  • Artificial tears
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56
Q

What are the histopathological features of sjogren’s syndrome?

A

Minor
* Focal lymphocytic sialodentitis
* Focal collection of lymphocytes 50+ in each collection
Major
* lymphocytic infiltrate extending to whole lobules
* Atrophy of acini
* Duct epithelial hyperplasia
* myoepithelial islands

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57
Q

What is the most diagnostic feature in the ACR-EULAR criteria for Sjogren’s ?

A

Positive labial gland biopsy

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58
Q

Name oral complications associated with sjogren’s syndrome? (5)

A
  • Caries
  • Poor denture retention
  • Infection risk - candida
  • loss of function - speech and swallowing
  • Salivary lymphoma risk - non hodgkin lymphoma - unilateral
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59
Q

What are the causes of xerostomia other than sjogren’s syndrome? (5)

A
  • dehydration
  • medications
  • head and neck radiotherapy ± chemotherapy
  • Smoking
  • Salivary gland tumours
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60
Q

What features in a parotid gland swelling makes you suspect a malignancy? (6)

A
  • Localised and firm
  • Painless
  • Unilateral
  • Fixed to underlying structures
  • Fast growing
  • Causes obstruction of the gland

Late stage will have pain and possible facial palsy

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61
Q

Where would you most commonly find a salivary gland neoplasm?

A
  • Parotid gland 80% of all tumours - 15% malignant
  • Submandibular 10% of all tumours - 30% malignant
  • Sublingual 0.5% of all tumours - 80% malignant
  • Minor salivary 10% of all tumours - 45% malignant

Most tumours in parotid and most malignancy rate is in sublingual

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62
Q

What is ectodermal dysplasia?

A
  • A group of conditions where there is abnormal development of the skin, hair, nails, teeth or sweat glands
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63
Q

What are the symptoms of ectodermal dysplasia? (9)

A
  • hypodontia and peg shaped teeth
  • large forehead
  • low nasal bridge
  • thin hair
  • abnormal nails
  • poor functioning sweat glands
  • cleft lip ± palate
  • learning difficulties
  • decreased skin pigmentation
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64
Q

What is an ulcer?

A
  • it is the loss of the full thickness of epithelium
  • where you can see underlying connective tissue and fibrin may be deposited on the surface
  • can only be diagnosed histologically
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65
Q

What is an erosion?

A
  • It is the partial thickness loss of epithelium
  • can be diagnosed histologically
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66
Q

How would you differ between recurrent major and minor aphthous ulcers?

A
  • Minor
    Size = less than 10mm
    Shape = round or oval with a red margin and yellow base
    Number = 1-20 per crop
    Histology = non-keratinised mucosa
    Heals without scarring with 1-2 weeks
    Commonly affects children
  • Major
    Size = more than 10mm
    Shape - oval or irregular
    Number = less than 5 at a time
    may affect keratinised or non keratinised mucosa
    may take up to months to heal (6-12 weeks) and may heal with scarring
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67
Q

What is herptiform aphous ulcers?

A
  • rarest form of apthous ulcers
  • multiple small ulcers on non keratinised mucosa
  • heal within 2 weeks without scarring
  • Affect non keratinised mucosa
  • not associated with HSV but look similar to primary herpatic gingivostomatitis in the early stages
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68
Q

What are the potential problems associated with recurrent aphthous stomatitis? (6)

A
  • infections
  • dehydration
  • malnutrition
  • problems with wearing dentures
  • may affect speech and mastication
  • painful
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69
Q

What are the causes of recurrent apthous stomatitis? (9)

A

Multifactorial including
* nutritional deficiencies - B12, iron, folate
* Stress - smoking - infections
* Systemic diseases - Crohn’s , ceoliac disease
* Hormonal imbalance : more in females
* Immune dysfunction : CD8 > CD4 at ulcer stage
* Genetics - HLA type A2 and B1w
* Trauma
* Allergies - SLS toothpaste
* metabolic such as growth in teenagers and children

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70
Q

What systemic diseases might be associated with apthous ulcers? (7)

A
  • Coeliac
  • Crohn’s disease
  • Ulcerative colitis
  • orofacial granulomatosis
  • Menorrhagia
  • Chornic GI blood loss
  • pernicious anaemia - B12 deficiency
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71
Q

How is recurrent apthous stomatitis treated?

A
  • Correct underlying cause
    Blood tests
    nutritional deficiencies
    remove traumatic cause
    SLS free toothpaste if allergic and dietary avoidance
    Treat systemic disease
  • Medications
    Topical : Benzydamine gel (pain) , betamethasone MW , beclomethasone inhaler , doxycylcline MW, CHX mouthwash, hydrocotisone pallets
    Systemic :
    Systemic steroids - prednisolone
    immunosuppressants - azathioprine
    DMARD - adalimumab
    immune modulation - thalidomide
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72
Q

What medications might cause oral ulceration? (4)

A
  • potassium chanel blockers
  • NSAIDs
  • DMARDS (disease modifying anti-rheumatic drugs)
  • Bisphosphonates
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73
Q

What would microcytic blood tests show?

A
  • MCV less than 80Fl
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74
Q

What 3 GI conditions might cause microcytic anaemia?

A
  • coeliac disease
  • Crohn’s
  • ulcerative colitis
  • gastric or colonic carcinoma
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75
Q

What common conditions cause microcytic anaemia but require further blood tests? (5)

A
  • iron deficiency
  • thalassaemia
  • lead poisoning
  • anaemia of chronic disease
  • congenital sideroblastic anaemia
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76
Q

What oral conditions can be associated with microcyctic anaemia? (5)

A
  • Recurrent apthous ulcers
  • poor wound healing
  • increased candida infection
  • atrophic glossitis
  • mucosal atrophy
  • burning mouth syndrome
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77
Q

What are the treatment options for microcytic anaemia?

A
  • Correct underlying cause
    Further blood tests to correct deficiencies - Fe supplement
    diagnose and treat cause of blood loss (acute or chronic)
    Mennorhagia - contraceptive pills or hormone therapy
  • Severe cases - blood transfusion of RBC
  • Prevention - Diet advice and supplement advice
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78
Q

Generalised white plaques that scrape off easily leaving an erthmatous base , what is your diagnosis?

A

Pseudomembranous candidosis

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79
Q

What local conditions might cause pseudomembranous candidosis? (5)

A
  • Steroid inhaler use
  • broad spectrum antibiotic use
  • Poor OH
  • Xerostomia
  • Dentures
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80
Q

What medical conditions might contribute to pseudomembranous candidosis?

A
  • Diabetes
  • HIV
  • Hypothyroidism - weaken the immune system
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81
Q

What are the advantages and disadvantages of oral swab for microbiology testing?

A
  • Simple and site specific
  • Can be easily contaminated and uncomfortable
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82
Q

What are the advantages and disadvantages of oral rinse?

A
  • Comfortable and records the whole mouth
  • Not site specific , difficult to standardise , some patients find the rinse process hard to do
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83
Q

With what drugs does fluconazole interact with and describe the interaction?

A
  • Warfarin - increases the anticoagulant effect of warfarin , and increase the likelihood of a catastrophic bleed - increase INR
  • Statins (simvastatin) - increase the exposure to statins leading to an increased risk of hepatotoxicity

Classed as severe interaction

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84
Q

What information is required on a lab sheet for sampling? (9)

A
  • patient details
  • GDP , GMP details
  • Patient history (MH DH SH)
  • Clinical prescription of the problem
  • Provisional diagnosis
  • Test previously done and test required to be done
  • Antibiotic use - previous, current , resistant
  • Date and time of sample
  • referring clinician name and signature
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85
Q

Patient attends with denture stomatitis
What features do you notice about the palatal tissues?

A
  • Eythmatous denture bearing area
  • Inflammation - swelling , oedema
  • Papillary hyperplasia
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86
Q

What are the classifications of denture induced stomatotitis?

A
  • Newton type 1 = localised inflammation and erythema
  • Newton type 2 = diffuse inflammation with erythema at denture bearing area without hyperplasia
  • Newton type 3 = granular inflammation, erythema and papillary hyperplasia
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87
Q

What might be the causes of denture stomatitis? (6)

A
  • xerostomia
  • poor oral/denture hygiene
  • wearing denture overnight
  • immunosuppression
  • steroid inhaler use
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88
Q

What is denture induced stomatitis?

A

It is a condition characterised by inflammation in the oral mucosa on the denture bearing area caused by candida (fungal) overgrowth.

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89
Q

What is your first line management of denture induced stomatitis? (4)

A
  • Denture hygiene advice
  • Denture wearing advice
  • Tissue conditioner on denture bearing area to allow healing
  • Adjust dentures if they are causing problems
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90
Q

What denture hygiene/wearing advice would you give to a patient presenting with denture induced stomatitis? (5)

A
  • Brush palate daily with soft brush
  • Clean denture by soaking CHX mouthwash or sodium hypochlorite for 15 mins twice daily
  • Leave denture out of the mouth as much as possible
  • Apply tissue conditioner to the area to allow tissue to heal when wearing the denture
  • Rinse mouth after inhaler use
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91
Q

What is the second line treatment for denture induced stomatitis?

A
  • Antifungal medication
    Fluconazole capsules 50mg - 7 days
    Miconazole 20mg for 7 days after lesions heal
    Nyastatin oral suspension (in warfarin and statin pts)
    1ml after food 4 times daily continue for 48 hours after lesion heals
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92
Q

keratin on a histology slide

A
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93
Q

melanin on a histology slide

A
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94
Q

What epithelium is affected in smoker

A

Keratinised squamous epithelium of the hard palate

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95
Q

What is the clinical presentation of smoker’s keratosis? (3)

A
  • thickened white area on the hard palate with dark brown or grey areas
  • Other areas in the mouth can be present with tobacco staining
  • Painless
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96
Q

What factors can cause smoker’s keratosis? (4)

A
  • Smoking tobbaco + pipe smoking
  • long term drinking of very hot beverges
  • Poor oral hygiene
  • Chronic inflammation
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97
Q

What histological presentation of smoking keratosis could indicate malignancy? (4)

A
  • Hyperchromatism
  • Cellular Atypia
  • Dysplasia
  • loss of basement membrane integrity
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98
Q

What is the histological features of smoker’s keratosis?

A
  • hyperkeratosis
  • Keratinised stratified squamous epithelium
  • melanin or melonocytes in basal layer
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99
Q

What clinical presentation of smoker’s keratosis would indicate malignancy? (6)

A
  • Raised rolled border
  • Hard (endurated) lesion
  • Non-homogenous - exophytic and flat areas
  • Ulceration
  • Pain or discomofort
  • If the lesion grows quickly
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100
Q

What is desquamative gingivitis?

A

It is a descriptive term of non specific clinical expression in the gingiva such as erythema, ulceration, pain and plaque **as a result of several dermato-mucous disorders. **
* presents as erythmatous, desquamating and painfull gingiva
* may involve the full thickness of the gingivae

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101
Q

What local factors may exacerbate desquamative gingivitis ? (5)

A
  • Smoking
  • Plaque build up
  • Restorations overhangs
  • Partial dentures
  • SLS toothpaste
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102
Q

How would you manage desquamative gingivitis?

A
  • Confirm diagnosis and any underlying conditions and manage these appropriately (blood tests , immunofluorescence assay)
  • Treat underlying cause - allergy or SLS toothpaste
  • Improve oral hygiene as plaque may worsen the condition
  • Topical steroid use : betamethasone - can use gum sheild
  • Topical tacrolimus immune modulator cream or mouthwash
  • Systemic immunosuppressant
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103
Q

What is erythema multiforme?

A
  • It is a spectrum disorder of immunogenic origin skin and mucosa ulceration
  • ulcer crops that are very painful affecting eating and drinking
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104
Q

Which disorder is related to erythema multiforme?

A

Stevens-johnson

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105
Q

What is your treatment options for erythema multiform

A

Systemic steroids
Systemic aciclovir
Encourage fluid intake - may require IV fluid if cannot eat or drink

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106
Q

What might cause erythema multiforme? (3)

A
  • drugs
  • herpes simplex
  • mycoplasma
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107
Q

Management options for recurrent erythema multiforme symptoms?

A
  • prophylactic aciclovir daily
  • do allergy test to find out trigger
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108
Q

Name local pigmented lesions in oral mucosa? (6)

A
  • Amalgam tattoo - macrophages (melanin) and granulation tissue surrounding amalgam tattoo
  • Macule (flat) - increased melanocytes
  • Naevus (raised) - increased melanocytes
  • vascular malformation (haemangioma)
  • mucosal melanoma secondary to metastatic cancers
  • pigmented incontinence associated with chronic inflammation
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109
Q

Name general causes of pigmentation in the oral mucosa?

A
  • Race
  • medications - contraceptive pills , iron tablets , antimalarials (hydroxychloroquine)
  • addison’s disease - increased ACTH causes brown patch
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110
Q

Describe how Addison’s disease may cause oral pigmentation?

A
  • reduced cortisol and aldosterone from adrenal glands causes brown patch due to increased ACTH
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111
Q

What is a vascular malformation?

A

A benign tumour due abnormal development of blood vessels

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112
Q

What is haemangioma?

A
  • It is part of the hamartoma family which is benign tumour as a result of abnormal formation of blood vessels (endothelial cells) that can be present at birth
  • can grow during normal growth and stops when patient stops growing
  • 60% are found in the head and neck
  • known as strawberry haemangioma
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113
Q

Name 2 types of haemangioma and give 2 histological differences?

A
  • Capillary -
    Small vessels (capillaries) - more in number
    lined by endothelial cells
  • Cavernous
    Large thin walled vessels - less in number
    Lined by epithelial cells
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114
Q

Herpes group viruses associates with oral vesiculation?

A
  • Human Herpes simplex virus (HHS)
  • Epstein Barr virus (EBV)
  • Varicella zoster virus
  • Cytomegalovirus
  • Group A coxsackie virus
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115
Q

Name oral mucosal disease caused by coxsackie virus? (RNA virus)

A
  • Hand Foot and Mouth disease
  • Herpangina
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116
Q

What oral diseases are caused by Epstein Barr viruses?

A
  • Infectious mononucleosis
  • Oral hairy leukoplakia
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117
Q

Which cranial nerve does herpes simplex become resident to on lower lip? (Nerve and branch)

A

mandibular division of the trigeminal nerve

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118
Q

What can trigger the reactivation of herpes simplex virus? (6)

A
  • Stress
  • Infections
  • Exposure for ultraviolet light
  • hormonal changes during menstruation
  • Fatigue
  • Immunosuppression
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119
Q

What might cause a pigmented tongue (local) ?

A
  • Smoking
  • food colouring
  • chromogenic bacteria - black hairy tongue
  • medications - hydroxyquinone
  • macule
  • melanoma
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120
Q

What are the general causes of pigmented tongue? (5)

A
  • Chemotherapy
  • Race
  • Addison’s disease
  • Lead poisoning
  • kaposi’s sarcoma
121
Q

Which HHV virus is related to kaposi’s sarcoma?

A

HHV-8

122
Q

What information could you get from clinical examination when you suspect TMD to confirm diagnosis?

A
  • TMJ tenderness
  • limited mouth opening
  • Deviation on opening or closing
  • Limited range of movements
  • Mom tenderness
  • Mom hypertrophy
  • Signs of parafunctional habits - wear facets , linea alba , scalloped tongue , cheek biting
  • inter-incisal opening is also measured (35-55mm)
123
Q

What does Crepitus indicate in TMJ?

A

Late degenerative disease

124
Q

What are the predisposing factors in TMD?

A
  • Stress
  • Female > male
  • Occlusal abnormalities
  • age 18-30
  • Psychogenic response
  • Parafunctional habits
125
Q

What parafunctional habits could contribute to TMD?

A
  • Chewing habits
  • nail biting
  • grinding
  • clenching
  • bruxism
126
Q

What might cause TMD?

A
  • Myofascial pain
  • Disc displacement - anterior ± reduction
  • Degenerative disease - SLE , RH, fibromyalgia ,osteoarthritis
  • Recurrent dislocation
  • Ankylosis
  • Hyperplasia
  • Neoplasia ( osteochondroma, osteoma , sarcoma)
    infection
127
Q

reversible management of TMD?

A

By conservative advice including
* Reassurance
* Stress management : relaxation , massage, mindfulness, counselling
* Stop parafunctional habits : CBT, splints
* Limiting jaw movement - soft diet, masticate bilaterally, limit wide opening , no chewing gum, no biting nails , support jaw while yawning,
* Jaw exercises - side to side movement
* Splinting - bite raising appliances , anterior repositioning splint
*Medications - tricyclic antidepressants , NSAIDs , botox , steroids

128
Q

Irreversible management of TMD?

A
  • Occlusal adjustment
  • TMJ surgery
    ^ arthrocentesis
    ^ arthroscopy
    ^ Disc repositioning surgery
    ^ Disc repair or removal
    ^ high condylar shave
    ^ total joint removal
129
Q

Are there any conditions that might have similar symptoms to TMD and how to exclude them?

A
  • Atypical facial pain - no clicking/crepitus of TMJ
  • Trigeminal neuralgia - pain at night while TMD worst at morning + no clicking + MRI to confirm
  • Dental pain - OPT or PA to confirm
  • Sinusitis - radiograph the sinuses
  • Salivary gland pathology - radiograph salivary glands
130
Q

You decide to construct a stabilisation splint , how would you describe how this splint should be made to the technician? (6)

A
  • Hard acrylic splint
  • full occlusal coverage
  • Use impressions and bite registration to produce occlusion
  • Include even centric stops
  • include canine rise which provide disclusion in eccentric mandibular movement (canine guidance)
  • require to achieve maximum intercuspation
131
Q

What is bell’s palsy?

A

unilateral facial nerve paralysis of full side (eyebrows, eyes , lower part)

132
Q

What is the aetiology of Bell’s palsy?

A
  • Unknown cause
  • May be caused by inflammation around the facial nerve which causes pressure leading to paralysis of the affected side
  • May be caused by viral infections (HSV, EBV, VSV)
  • May be caused by an autoimmune reaction
  • commonest cause of facial palsy
  • ages 15-60
133
Q

How is Bell’s palsy managed? (6)

A
  • Distinguish cause if possible - history, x-ray, blood tests
  • Reassure patient it will get better
  • Prednisolone given within 72h of symptoms, may reduce inflammation of the facial nerve
  • Aciclovir if suspected viral infection (ramsay-hunt syndrome)
  • Protect affected eye with eye patch
  • Give patient eye drops to manage dry eyes
  • Review and refer if not recovered within 3 months
134
Q

How can you differentiate between an upper and lower motor neuron disease?

A
  • UMN (stroke) -
    1. can wrinkle forehead and move eyebrows but cannot move lower portion of face (smile)
    2. Spastic paralysis
  • LMN (facial palsy) -
    1. cannot wrinkle forehead and move eyebrows and cannot smile
    2. flaccid paralysis
135
Q

How does this difference occur?

A

The damage in upper motor neuron to the nerves occur at the level of the brain whereas in lower motor neuron it occurs at the brainstem or spinal cord to nerves innervating the muscles and glands

136
Q

Give possible causes to LMN diseases? (5)

A
  • Trauma
  • Parotid gland tumour
  • Multiple sclerosis
  • Misplaced LA in the parotid gland
  • Reactivated HSV causing bell’s palsy
137
Q

Give possible causes of UMN disease?

A
  • Stroke
  • Multiple sclerosis
  • Traumatic brain injury
  • Cerebral palsy
  • Spinal cord injury
138
Q

What conditions might require a patient to be on long term steroids? (7)

A
  • Severe asthma
  • COPD
  • Addison’s disease
  • Arthritis
  • Crohn’s disease
  • Lupus
  • Multiple sclerosis
139
Q

What are the signs and symptoms of adrenal suppression? (7)

A
  • Hypoglycaemia
  • Dehydration
  • Weight loss
  • low bp
  • Disorientation
  • Weakness, dizziness, low blood pressure
  • Postural hypotension
  • Oral pigmentation on buccal mucosa
140
Q

What emergency can be associated with adrenal insufficiency ?

A
  • Adrenal crisis
  • caused by insufficiency level of the hormone cortisol
141
Q

Why are asthmatics more prone to erosio?

A
  • due to the use of steroid inhalers which lead to xerostomia causing reduced protection against acids
  • asthmatic patients are more prone to Gastro-oesophageal reflux disease (GORD) which can cause erosion
142
Q

What is a syncope?

A
  • It is known as fainting which is defined as a transient, self limiting loss of consciousness with an unability to maintain postural tone which is followed by spontaneous recovery
  • characterised by fast onset, short duration and spontaneous recovery
143
Q

What is the physiological aspect of a faint?

A
  • temporary malfunction in the autonomic nervous system
  • results in drop in blood pressure and oxygen levels
  • interrupetion of blood flow to the brain
  • leadinig to loss of consiousness
144
Q

How to manage a syncope in the dental practice?

A
  • Assess the patient through ABCDE
  • lay the patient flat, raise patient feet and loosen any tight clothes around the neck
  • Administer 100% oxygen 15l/min until gain of consciousness
145
Q

What is burning mouth syndrome?

A

A painful condition associated with burning, scalding or tingling sensation in the mouth that is recurrent with no obvious cause.
* most likely to be associated with haematinincs deficiencies

146
Q

What is the proper name for burning mouth syndrome?

A
  • Oral Dysaesthesia
147
Q

Who is most likely to affected by burning mouth syndrome?

A
  • Females - mostly menopausal women
  • Aged 40-60
148
Q

What might be the causes of burning mouth syndrome? (8)

A
  • Nutritional deficiencies: B1, B6 , haematinics, zinc
  • Xerostomia
  • Parafunctional habits
  • Poorly fitting dentures
  • Allergies
  • Endocrine disorders : diabetes and hypothyroidism
  • Physiological factors : stress, anxiety , depression
  • Infections
149
Q

What are the signs and symptoms of burning mouth syndrome? (4)

A
  • paraesthesia
  • dysgeusia (abnormal taste = metallic)
  • dry mouth feeling
  • painful burning feeling
150
Q

What might be the cause if the affected area by dysaesthesia is the lips and tongue tip or margin?

A
  • Parafunctional habits
151
Q

What are the differential diagnosis of oral dysaesthesia? (6)

A
  • Lichen planus
  • Dental pain
  • Xerostomia
  • Diabetes
  • undiagnosed systemic condition
  • Orofacial pain
152
Q

What investigation you might carry out for oral dysaesthesia?

A
  • Blood tests : FBC , U&E , TFT , LFT, HbA1c
  • Unstimulated whole salivary flow test for xerostomia assessment
  • Examine parafunctional habits intra and extra
  • Denture assessment
  • Psychiatric assessment
153
Q

Management options for burning mouth syndrome?

A
  • reassure pt and Correct underlying cause
    ^ nutruent replacement therapy
    ^ Diabetes management
    ^ correct poorly fitting dentures
    ^ management of parafunctional habits
  • Stay hydrated
  • CBT
  • Use Difflam (benzydamine) mouthwash
  • Medication : Gabapentin (anticonvulsant)
154
Q

Which benign and malignant tumours affect the salivary glands and order by incidence?

A
  • Pleomorphic adenoma (75%) - benign - affect parotid
  • Warthin’s tumour (10%)
  • Adenoid cystic carcinoma (5%) - malignant
  • Mucoepidermoid carcinoma (3%) - malignant
  • Acinic cell carcinoma (<1%) - malignant

PWAMA

155
Q

What are the histological features of pleomorphic adenoma?

A
  • Epithelial ductal cells
  • Myoepithelial islands
  • well defined borders
  • chondromyxoid stroma
156
Q

What are the histological feature is related to recurrence?

A
  • poorly encapsulated or non encapsulated tumour
157
Q

What are the histological signs of Warthin’s tumour?

A
  • Oncocytic epithelium
  • Lymphoid stroma
  • Cystic spaces
158
Q

What is the histological sign of an adenoid cystic carcinoma?

A

Cribiform pattern of basaloid cells
* no capsule present and can be solid or tubular in nature

159
Q

What signs of a tumour indicated it is benign? (4) (imaging)

A
  • well defined
  • encapsulated
  • Peripheral vascularity
  • No lymphadenopathy
  • low grade malignancy can mimics benign lesions
160
Q

What signs may indicate malignancy in a tumour? (4)(imaging)

A
  • irregular margins
  • poorly defined
  • lymphadenopathy
  • increased internal vascularity
161
Q

How are salivary gland neoplasms diagnosed? (4)

A
  • Fine needle aspiration - cytopathological examination
  • Core biopsy - histopathological examination
  • Incisional biopsy - partial removal
  • Excisional biopsy - to remove entire tumour
162
Q

What is the mechanism of action of CHX?

A
  • Diatonic antimicrobial action
    • charge of CHX molecules interact with - charge of microorganisms surface molecules
  • This damages the microbial cell envelope allowing for permeability
  • prevents replication of bacteria and can result in cell death through interfering with intracellular activity
163
Q

What family of antiseptics does CHX belong to?

A

Bisbiguanides antiseptics

bisbaguanide is the active ingredient in CHX

164
Q

What is substantivity ?

A
  • The prolonged adherence of the antiseptics to the oral cavity and its slow release in effective doses
  • Ensure persistence of antimicrobial activity
165
Q

What is CHX substantivity time?

A

About 12 hours
*meaning it is retained in the mouth for a prolonged time with a slow and sustained release of bisbaguanide

166
Q

What solution of CHX is given to patients?

A

0.12% or 0.2% CHX mouthwash 10ml x2 daily rinse for 1 min

167
Q

What are the side effects of chlorhexidine? (7)

A
  • Staining (brown) - can be reversed - on tooth and restorations
  • Mucosal irritation
  • Parotid gland swelling
  • Taste disturbance
  • Tongue discolouration
  • Burning of mouth
  • Hypersensitivity and anaphylaxis
168
Q

What are the indications for using CHX? (9)

A
  • short term use for candidosis
  • Cleaning dentures
  • In immunocompromised patients
  • In patients with disabilities to prevent infection when oral hygiene is difficult to maintain
  • Management of ANUG, aphthous ulcers and mucositis
  • As irrigant during RCT
  • Pre ± post oral and periodontal therapy
  • In high risk caries patients
  • When jaw fixation is present (IMF;ORIF)
169
Q

What are the 3 stages of clot formation?

A
  • Vasoconstriction
  • Platelet plug forms in break
  • Formation of fibrin clot ( blood coagulation)
170
Q

How does Aspirin affect clotting and at what stage?

A
  • Inhibit platelet aggregation ( enzyme COX)
  • by altering balance between thromboxane A2 and prostacyclin
  • inhibiting the formation of thrombi
171
Q

How does Warfarin affect clotting and at what stage?

A
  • Inhibits the synthesis vitamin K-dependent clotting factors
  • Factors 2,7,9,10
  • prolonging clotting time and inhibits the formation of thrombi
172
Q

How does NAOC affect clotting and at what stage?

A
  • Inhibit factor 10
  • Inhibit conversion of prothrombin to thrombin
  • Stop the production of the fibrin clot
173
Q

Why are aspirin and clopidogrel used in conjunction?

A
  • ** Dual anti-platelet therapy for management of acute coronary syndrome **
  • Decreases platelet aggregation and inhibits thrombus formation in arterial circulation
  • Aspirin - reduce production of prostaglandin - inhibit COX-1
  • Clopidegrol - inhibit P2Y12 subtype of the ADP resceptor

** meaning platelet inhibition and fibrin clot production is reduced **

Better prevention of a stroke

174
Q

What is the pattern of Von Willebrand’s disease?

A

Autosomal dominant condition with different inheritance patterns
Type 1 = autosomal dominant - quantitative deficiency in vWF factor
Type 2 = autosomal dominant - qualitative deficiency in vWF factor
Type 3 = autosomal recessive - quantitative and qualitative deficiency in vWF factor

175
Q

How does von willebrand’s disease affect bleeding?

A
  • impaired platelet adhesion to blood vessel walls and reduced levels of factor 8
  • leading to high risk of haemorrhage
176
Q

What is a biofilm?

A
  • An aggregate of microorganisms
  • in which cells adhere to one another
  • these adherend cells get embedded within the extracellular matrix EPS (extracellular polymeric substances)
177
Q

What are the stages of colorisation of a biofilm? (5)

A
  • Adhesion
  • Colonisation
  • Accummulation
  • Complex complexity
  • Dispersal

AC AC D

178
Q

Methods of identifying organisms? (4)

A
  • Agar microbiological culture - through swab / rinse
    molecular biology
  • PCR
  • DNA probes
  • ELISA
179
Q

What are the virulence factors of P.gingivalis? (4)

A
  • Proteases - MMPs , collagenase , fibrinolysin
  • Adhesins - fimbriae
  • Tissue-toxis metabolic products - hydrogen sulphide and ammonia
  • Endotoxins (LPS)

P A T E

180
Q

What are the virulence factors in C.albicans? (5)

A
  • Germ tube formation
  • Adhesins
  • Metabolic acids
  • Extracellular enzymes
  • Switching mechanisms

GAMES

181
Q

What are the viruelence factors of S.mutans? (4)

A
  • adhesins
  • sugar modifying enzymes
  • acid tolerance and adaptation
  • polysaccharides

ASAP

182
Q

What is lichen planus?

A
  • A chronic autoimmune inflammatory disease that can affect the oral mucosa
  • CD8+ cell-mediated destruction of basal keratinocytes
  • affect mainly females aged 30-50
  • 1% increased risk of malignancy over 10 years in severe cases
183
Q

Histological features of lichen planus (6)

A
  • Hugging band of lymphocytes
  • Basal cell layer liquefaction
  • Acantholysis - less of cell to cell adhesion
  • Saw tooth rete pegs (elongated)
  • Apoptosis (death of cells) - civatte bodies (dead keratinocytes)
  • Orthokeratosis
184
Q

What are the 6 types of lichen planus (appearance)
BRE APP

A

Papular - white
Plaque - plaque arranged in lines
Bullous - vesicles
Reticular - variant of Wickham’s striae - spider web like
Erosive - ulceration
Atrophic - white-bluish with central superficial atrophy

185
Q

What are the types of lichenoid lesions (aetiology)

A
  • Amalgam restoration OLL
  • Drug related OLL
  • Chronic graft verses host disease
  • Lichen planus-like lesions that lack one or more clinical characteristics of LP
186
Q

What can be the cause of lichen planus? (8)

A
  • Stress
  • Autoimmune dysfunction
  • idiopathic
  • Amalgam
  • Hepatitis C - high incidence
  • Drug related
  • Plaque build-up in desquamative gingivitis
  • SLS toothpaste
187
Q

What medications can contribute to lichen planus? (5)

A
  • Beta blockers
  • DMARDS - end with ine
  • Ace inhibitors
  • NSAIDS end with in
  • Diuretics - end with - ide
188
Q

When do you biopsy a lichen planus lesion?

A
  • Symptomatic
  • When it appears in a smoker
  • When the lesion is in a high risk area
189
Q

What are high risk areas when considering lichen planus?

A
  • floor of the mouth
  • lateral border of the tongue
190
Q

How is lichen planus manages if it is Asymptomatic?

A
  • Observe and monitor
  • OHI
  • CHX mouthwash
  • SLS-free toothpaste
191
Q

How is lichen planus managed if it is symptomatic?

A
  • Identify and remove causative agent where possible - e.g. amalgam, consider switching medicines if they are the cause
  • OHI
  • Biopsy white patches
  • Topical steroid use - betamethasone
  • Systemic steroid use - Prednisolone
  • Immune modulator - Azathioprine
192
Q

What can you switch ace inhibitors with?

A

AT2 blocker

193
Q

What is anaemia?

A
  • A condition in which there is lower red blood cells or lower haemoglobin within them than normal
  • Leading to reduced oxygen carrying capacity of the blood
194
Q

What are the general signs and symptoms of anaemia? (7)

A
  • Irritation and dizziness
  • Weakness
  • Shortness of breath
  • Paleness and coldness
  • Loss of consciousness
  • Low blood pressure
  • Palpations and rapid heart rate
195
Q

What are the oral signs of anaemia? (7)

A
  • Recurrent oral ulceration
  • Candida infections
  • Glossitis or smooth tongue ( iron def)
  • Beefy tongue ( b12/folate def)
  • Oral dysaesthesia
  • Mucosal pallor
  • increased risk of candida infections
196
Q

Types of anaemia

A
  • Microcytic - small RBC , MCV <80 fl
  • Macrocytic - Large RBC MCV >100 fl
  • Normocytic - normal RBCC MCV 80-100
197
Q

Examples of Microcytic anaemia causes

A
  • Iron deficiency
  • Thalassaemia
198
Q

Examples of Normocytic anaemia causes

A
  • Internal bleed
  • Pregnancy
  • Sickle cell anaemia
  • Chronic disease ( RA, diabetes or kidney disease)
199
Q

Examples of macrocytic anaemia causes ?

A
  • B12/folate def
  • Liver disease
  • hypothyroidism
200
Q

What clinical appearances might mimic lichen planus? (4)

A
  • Plasma cell gingivitis
  • Pemphigoid
  • Pemphigus
  • Oral lupus erythmatosus
201
Q

What is plasma cell gingivitis?

A

It is a rare gingival inflammatory condition where there is a dense infiltrate of plasma cells in the connective tissue leading to inflammation and enlargement of the gingivae

202
Q

What is the clinical appearance of plasma cell gingivitis? (5)

A
  • Generalised erythema and oedema that can extend from the free gingiva to the attached gingivae
  • Normal gingival stippling is lost
  • Friable gingivae
  • Bleed easily
  • Accompanied by cheilitis or glossitis
203
Q

What is the aetiology of Plasma cell gingivitis? (3)

A
  • Hypersensitivity reactions - SLS, pepper, cinnamon
  • Idiopathic

It is a rare condition

204
Q

What may worsen the plasma cell gingivitis ? (5)

A
  • Poor OH
  • Immunosuppression
  • infections
  • Plaque retentive factors
  • smoking
205
Q

What is the histological features of plasma cell gingivitis?

A

Dense plasma cell infiltrate in the connective tissue

206
Q

How is plasma cell gingivitis managed? (4)

A
  • Histological sampling to diagnose
  • Dietary avoidance advice : pepper,cinammon
  • OHI ; SLS free toothpaste
  • Tacrolimus for lip swelling
207
Q

What might be the local causes of xerostomia? (6)

A
  • mouth breathing
  • alcohol
  • smoking
  • candidosis
  • steroid inhalers
  • Radiotherapy for oral cancer
208
Q

What are the systemic causes of xerostomia? (7)

A
  • Medications
  • Cancer therapy - chemotherapy
  • Chronic syndrome - diabetes, addison’s
  • Dehydration
  • Stress/anxiety
  • Sjogren’s syndrome
  • Eating disorders due to vomitting
209
Q

List medications that can cause xerostomia? (5)

A
  • Antihistamines
  • Antidepressants
  • Antipsychotics
  • Diuretics
  • Beta blockers
210
Q

How can you assess xerostomia intra-orally? (4)

A
  • Unstimulated salivary flow test
  • Palpate and assess ducts for salivary gland secretions
  • Mirror stick test to cheek and tongue
  • Check for saliva pooling in the FoM
211
Q

What might the oral signs and symptoms of xerostomia? (11)

A
  • Dysphagia
  • Difficulty speaking (clicking speech)
  • Altered taste
  • Problems with denture control
  • Increased cervical caries
  • Oral soreness and discomfort
  • Halitosis
  • Glossy appearance of gingiva
  • Tongue fissuring
  • increased periodontal disease
  • increased candida infections
212
Q

How can you manage xerostomia?

A
  • manage underlying cause
  • Salivary substitutes -
  • Medications - pilocarpine
  • Monitor bacterial fungal load
213
Q

Examples of management of underlying cause of xerostomia? (6)

A
  • Alternative medication - discuss with GP
  • Identify and control diet, medical conditions , blood sugar
  • Moderate alcohol use and smoking cessation
  • Change to SLS free toothpaste
  • Assess mouth breathing including sleep apnea (refer)
  • Moderate caffeine intake and increased water intake
214
Q

Name 3 saliva substitutes?

A
  • Spray - saliva orthana
  • lozenges - salivax
  • Oral care system - biotene
215
Q

Name sugar substitutes? (5)

A
  • Xylitol
  • Aspartame
  • Sucralose
  • Sorbitol
    *Manitol
216
Q

Name salivary proteins

A
  • IgA
  • Mucins
  • histatin
  • Proline
217
Q

Salivary enzymes (3)

A
  • Lysozyme
  • Amylase
  • Lipase
218
Q

When are antibiotics indicated for dental treatment?

A
  • Signs of spread of oral infections ( cellulitis) and **systemic involvement ** (fever)
  • In case of ANUG or pericoronitis where there is persistent swelling despite local treatment or systemic involvement
  • In case of **severe sinusitis ** or persistent symptoms
  • In cases of antibiotic prophylaxis to prevent infective endocarditis in patients with cardiac conditions according to NICE guidelines (consult cardiologist)
  • immunocompromised patients (diabetes)
  • OAC/OAF
219
Q

Give 5 ways antibiotics work

A
  • Cell wall destruction
  • Protein synthesis inhibition
  • DNA synthesis inhibition
  • DNA replication inhibition
  • Cell membrane inhibition
220
Q

Possible antiobiotics disadvantages?

A
  • Antibiotic resistance
  • Gastointenstinal irritation
  • Interaction with other medications - blood thinners/antifungals
  • Hypersensitivity/anaphylaxis
221
Q

What is regime of Amoxicillin ?

A

Amoxicillin capsules 500mg for 5 days
Send : 15 capsules
Label : one capsule three times daily

Used for dental abscess and systemic involvement

222
Q

Metronidazole regimen

A

200 mg for 3 days
Send : 9 tablets
Label : one tablet 3 times daily

ANUG , Pericoronitis
or allergic penicillin in dental abscess (5 days)

223
Q

Clindamycin capsules Regimen

A

150 mg for 5 days
Send : 20 capsules
Label : one capsule 4 times daily swallowed with water

This is used in spreading cellulitis or
if not affective for abscess

224
Q

What are the mechanisms of antibiotic resistance? (3)

A
  • Enzymatic degradation of antibacterial drugs
  • Alteration of bacterial proteins that are antibacterial target
  • Changes in membrane permeability to antibiotics
225
Q

Name 2 types of inhalers asthmatics use

A
  • Beta-agonist salbutamol inhaler - blue
  • Corticosteroid betamethasone inhaler - brown
226
Q

What is asthma?

A
  • A condition where there is reversible airway obstruction
    Characterised by
  • inflammation and swelling of airway mucosa
  • Excessive mucous secretion
  • Smooth muscle contraction
227
Q

What are the signs and symptoms of asthma? (5)

A
  • Shortness of breath
  • Wheezing
  • Coughing
  • Chest tightness and pain
  • Fatigue
228
Q

What are the dental effects of inhalers and what advice should be given?

A
  • Increased candida infections due to steroid inhalers - Rinse mouth after using
  • Increased erosion due to acidity - Fluoride use and OHI
  • Xerostomia - keep hydrated and use spacer
229
Q

What considerations regarding treating a child with asthma?

A
  • Colophony allergy in FV
  • FV contraindicated with asthmatic patients who have been hospitalised in the past 3 years
  • Medical emergency for asthmatic attack
  • Best to keep appointments short for pts with severe asthma ± cold/flu
230
Q

What percentage of people in scotland are being treated for asthma?

A

7%

231
Q

List 11 histological features signs of epithelial dysplasia

A
  • Abnormal keratinisation
  • Abnormal stratification
  • Drop shaped rete pegs
  • Basal cell hyperplasia
  • Altered polarity of basal cell
  • hyperchromatism
  • atypia
  • pleomorphism
  • increased mitotic activity
  • acantholysis
  • enlarged nuclei
232
Q

What is the histological difference between pemphigus and pemphigoid?

A

** Pemphigus**
* Supra-basal split
* tzank cells in clefts
* autoantibodies attack desmosomes
* Basket weave IF pattern
** Pemphigoid**
* Sub-basal split
* lots of fibrin
* autoantibodies attack hemidesmosomes
* Linear IF pattern

233
Q

How pemphigus and pemphigoid differ clinically?

A

** Pemphigus **
* Thick walled blisters
* Affecting full depth of epidermis
* Filled with blood
** Pemphigoid **
* blisters burst and spread easily
* Superficial
* Filled with clear fluid

234
Q

How might you investigate Pemphigus and Pemphigoid?

A
  • Direct immunofluorescence using IgG antibodies
  • Biopsy taken for unaffected area for histological analysis
  • Indirect immunofluorescence using patient serum testing for IgG levels (circulating autoantibodies)
  • Clinically using nikolskys sign
235
Q

What is nikolsky’s sign ?

A

the separation of the epidermis when probing (shedding)

236
Q

What high risk sites of oral cancer?

A
  • FoM
  • lateral border of the tongue
  • Soft palate
237
Q

Treatment options for pemphigoid and pemphigus?

A
  • Betamethasone MW
  • Systemic prednisolone
  • Monoclonal antibody therapy
  • Immune modulation - azathioprine
  • Pemphigus can be fatal
238
Q

What areas can pemphigoid affect other than the mouth?

A
  • Eyes
  • Genitals
239
Q

What does symptoms oral cancer in the mouth? (4)

A
  • numbness or pain
  • exophytic
  • ulcers with rolled border and indurated
  • Bleeding
240
Q

How does cancer spread? (routes)

A
  • locally
  • lymphatic spread
  • through the blood
241
Q

What is the metastatic cascade?

A
  • Invasion ,migration and intravasation
  • survival in the circulation - immune evasion, CTC clusters, platelet binding
  • Arrest in distant organs - trapping , adhesion
  • Extravasation - through physical barriers (seeding)
  • Micro metastasis - survival on arrival, proliferation (dormancy - survival without growth)
  • Macro metastatic growth

CTC = circulating tumour cells clusters

242
Q

TNM staging

A
  • A staging used to describe the amount and spread of cancer in the patient body
  • T = tumour
  • N = node
  • M - Metastasis
  • Scores then combined to give overall stage of cancer 1-4
243
Q

T in TNM

A

Tx - no available info for assessment
T0 - no evidence of primary tumour
T1 - less than 2 cm
T2 - 2-4 cm
T3 - more than 4 cm
T4 - more than 4cm involving :
Pterygoind muscle
Antrum
Base of tongue
Skin

244
Q

N in TNM

A

Nx - cannot be assessed
N0 - no clinical positive nodes
N1 - single, ipsilateral <3 cm
N2a - single, ipsilateral 3-6 cm
N2b - multiple ipsilateral >6 cm
N2c - bilateral or contralateral >6 cm
N3 - metastasis in lymph node more than 6cm

245
Q

M in TNM

A

Mx - cannot be assessed
M0 - no distant metastasis
M1 - distant mitastasis present

246
Q

What is sialometaplasia?

A
  • It is a benign inflammatory condition that affects the salivary glands , primarily the minor salivary glands in the hard palate
  • Usually caused by blocked blood supply to the glands leading to tissue death
  • It can mimic a malignancy
247
Q

What is the aetiology of sialometaplasia? (5)

A
  • As a result ischaemia of small blood vessels to the salivary glands leading to infraction (death of tissue)
  • Smoking
  • Trauma
  • LA injection
  • Bulimia
  • Infection
  • iodising radiation
  • Self healing and painless
248
Q

How does sialometaplasia appear histologically? (3)

A
  • surface slough of necrotic tissue (can be clinical sign)
  • Hyperplasia
  • Squamous metaplasia of the ducts + acini
  • Necrosis of salivary acini
249
Q

How is sialometaplasia managed?

A
  • Heal on its own - ulcers heal by secondary intention in 6-10 weeks
250
Q

What can be the differential diagnosis of sialometaplasia?

A
  • Oral squamous cell carcinoma
  • Salivary gland carcinoma
251
Q

Patient present with a lip swelling
Give differential diagnosis other than a mucocele?

A
  • OFG
  • Trauma to lip
  • Benign fibrous overgrowth
  • Soft tissue abscess
  • Squamous cell carcinoma
  • Schwannoma
  • Oral lymphangioma
252
Q

What is a mucocele?

A
  • Recurrent swelling found mostly in the lower lip
  • due to a damaged or blocked salivary gland
  • can burst and recur
  • can be superficial or deep
  • Types : extravasation and retention

swellings in upper lip are usually neoplastic rather than simple mucocoeles

253
Q

How does a mucocele appear histologically? (3)

A
  • Macrophage lined cystic cavity
  • Surrounded by granulation tissue
  • Foam cells present
  • Inflammatory cells present
254
Q

How is a mucocele managed?

A
  • Excision of the mucocele and gland
255
Q

What is a mucocele called in the floor of the mouth?

A

Ranula
* Usually sublingual extravasation type

256
Q

What is orofacial granuloma?

A
  • Swelling or Oedema in the oral and facial tissue due to lymphatic obstruction due to an immune reaction
  • Associated with type 4 hypersensitivity reaction to certain food
  • Linked with Crohn’s (15%), sarcoidosis disease, tuberculosis
257
Q

What is the aetiology of OFG?

A

** Autoimmune reaction ( type 4 hypersensitivity reaction) **
** Allergy to **
* Benzoic
* Sorbic acid
* Cinnamon
* Chocolate

258
Q

What the histological appearance of OFG?

A
  • Increased tissue fluid produced due to inflammation
  • Granulomas - cluster of white cells
  • Multinucleated giant cells
  • Lymphocytes

Dilated lymph and blood vessels due to obstruction

259
Q

What is the difference between angio-oedema and OFG swelling?

A
  • Angio-oedema is caused by increased fluid exuadate from the capillaries but with lymphatic drainage whereas in OFG there is lymphatic obstruction
  • Angio-oedema comes and settles quickly (24-48h) whereas OFG comes quickly but settles very slowly
  • OFG have continuous growth which changes intensity from days to days or weeks to weeks
260
Q

What are the signs and symptoms of OFG? (7)

A
  • Lip , cheeck and gingivae swelling
  • Angular cheilitis
  • Skin Changes
  • Apthous ulceration
  • Mucosal tags
  • Erythmatous gingivae
  • Stag-horning of sublingual folds
261
Q

Management options for OFG (5)

A
  • 3 months dietary exclusion (benzoate/cinammon/chocolate/ E210-219) then provide diet advice
  • Topical treatment to angular cheilitis - miconazole, hydrocortisone
  • Topical treatment to lip swelling or facial erythema - Tacrolimus ointment
  • intralesional steroid injection (areas of swelling) - triamcinolone
  • Syetemic immude modulation -
    Short term - prednisolone
    Azathioprine
    Mycophenolate
262
Q

What is your initial management (before diagnosis) (3)

A
  • Consider whether this is oro-facial or part of Crohn’s disease
    GI symptoms
    Faecal calprotein
    Start sequential growth monitoring
  • Take diet history and identify allergens
  • Discuss of a complete diet exclusion trial
263
Q

Give 6 types of oral candida infections?

A
  • Denture induced stomatitis
  • Angular cheilitis
  • Pseudomembranous candidosis
  • Erythmatous
  • Hyperplastic
  • Median rhomboid glossitis
264
Q

Where does median rhomboid glossitis occur?

A
  • Central papillary atrophy of the tongue
  • Affecting the dorsum of the tongue at the midline region
  • Anterior to circumvallate papillae
265
Q

Histological features of median rhomboid papillae

A
  • Caninda hyphae infiltration
  • Hyperplastic rete pegs (bulbous)
  • Elongated rete pegs
  • PMNLs (leukocytes) infiltration
266
Q

Methods for testing for candida? (3)

A

Swab , oral rinse , foam pad = culture
Biopsy - histology
Smear - microscopy

267
Q

What are the virulence factors of candida?

A
  • Adhesins
  • Hydrolytic enzymes (haemolysin, proteinase, phospholipase)
  • Switching mechanisms
  • Germ tube formation
  • Extracellular enzymes
  • Acidic metabolites
268
Q

Name antifungal agents

A
  • Miconazole
  • Fluconazole
  • Chlorhexidine
  • Nyastatin
  • Itraconazole
  • Amphotericin B
269
Q

What information should be on a prescription? (10)

A
  • Patient details
  • Age in number if under 12
  • Date of prescription (valid for 6 months)
  • Name and address of prescriber
  • Signature of prescriber in ink
  • Name of drug written clearly
  • Duration of treatment
  • Total quantity of drug
  • instruction of how and when
  • Residual space should be scored out
270
Q

What is the rate of infection for HIV , Hep C and Hep B?

A

HIV 0.3%
Hep C 3%
Hep B 30%

271
Q

Name 6 lesions that can be associated with HIV? (5)

A
  • Candidosis lesions - angular cheilitis
  • Hairy leukoplakia
  • Kaposi’s sarcoma (GI tract skin or mucous membranes)
  • Non-hodgkin lymphoma
  • Periodontal disease (NUP/NUG)
272
Q

How can HIV be diagnosed

A
  • ELISA antibody test 6-12 week post extraction
  • HIV RNA testing
273
Q

How is HIV treated?

A
  • Highly active anti-retroviral therapy which consist of 3 or more drugs
    2xNRTIs
    1xNNRTI
    Protein inhibitor
274
Q

What is a fibrous epulis?

A

It is a localised swelling arising in the gingivae caused by chronic irritation

275
Q

What is the aetiology’s of a fibrous Epulis?

A
  • Hyper-plastic response to irritation such as overhanging restorations or calculus
276
Q

How does fibrous epulis appear clinically? (4)

A
  • smooth surface
  • rounded swelling
  • pink
  • pedunculated
277
Q

How does fibrous epulis appear histologically ?

A
  • Granulation tissue
  • Metaplastic bone formation
  • Ulceration
278
Q

What is a fibrous Epulis named on other sites other than the gingiva ?

A

Fibro-epithelial polyp
* most common in buccal mucosa and inner surface of the lip

279
Q

What is pyogenic granuloma?

A
  • Overgrowth of granulation tissue
  • may be related to extraction sockets or traumatic soft tissue injuries due to failure of normal healing
280
Q

How does pyogenic granuloma appear clinically?

A
  • red with defined margins
281
Q

How does pyogenic granuloma appear histologically?

A
  • Granulation tissue
  • Mixed inflammatory infiltrate on fibrovascular background
  • Ulceration
  • Endothelial cells proliferation
282
Q

How can you manage pyogenic granuloma?

A
  • Surgical excision
  • Curettage of base
283
Q

What do you call a pyogenic granuloma in a preganant women?

A
  • Pregnancy epulis
284
Q

What do you call a pyogenic granuloma on the gingivae?

A
  • Vascular epulis
285
Q

When to refer a swelling such as a fibrous epulis or a pyogenic granuloma?

A
  • rubbery in consistency
  • abnormally overlying the mucosa
  • Increases in size
  • abnormal appearance
  • fixed to underlying structures
  • Symptomatic (a sign of salivary gland infection)
286
Q

Give an example of a heriditary white patch?

A
  • white spongy naevus ( increased production of keratin)
287
Q

How does white spongy naevus appear histologically?

A
  • Intracellular oedema in keratin layer
  • Parakeratosis
288
Q

How does smoker’s keratosis appear histologically?

A
  • Hyperkeratosis
  • Areas of mild/variable dysplasia
  • Melanocytes and macrophages in basal layer

Smoker’s are 6 times more likely to develop leukoplakia

289
Q

Give differential diagnosis for denture induced hyperplasia? (4)

A
  • leaf fibroma
  • papillary hyperplasia of the palate
  • Giant cell granuloma
  • Pyogenic granuloma
290
Q

What factors have resulted in denture induced hyperplasia?

A
  • ill fitting dentures causing trauma to tissues
  • Fibrous reaction of the gingivae caused by pressure from the denture flange
291
Q

How would you manage denture induced hyperplasia ?

A
  • LA then surgical excision of the fibrous tissue overgrowth
  • Address causative factors - adjust denture or remake
  • Use tissue conditioner under denture while making a new one
292
Q

What histological features can be seen in denture induced hyperplasia?

A
  • Pseudoepitheliomatous hyperplasia
  • Hyperplastic rete pegs
  • Candida involvement
  • irregular hyperkeratotic epithelial cells

Same as leaf fibroma - papillary hyperplasia

293
Q

What is this?

A

Condyloma Acuminatum which is a benign growth usually appears in mucosal surfaces and mostly affects the genitals , mostly transmitted through sexual activity

294
Q

What causes condyloma acuminatum?

A

HPV virus esp. type 6 and 11

295
Q

Histopathological features of condyloma acuminatum? (5)

A
  • Koilocytosis - hallmark of HPV infection
  • Papillamatosis ; Elongated rete pegs
  • Inflammatory infiltrate
  • Hyperganulosis - hyperplasia of granular layer of epidermis
  • Hyperkeratosis - increased keratin
296
Q

Clinical signs of malignancy? (5)

A
  • Lymphadenopathy
  • Changes in size
  • Changes in appearance
  • Becomes symptomatic
  • Irregular borders
297
Q

How to test for HPV?

A
  • PCR
  • HPV DNA testing
298
Q

How to manage condyloma Acuminatum?

A
  • Topical antiviral cream
  • Surgical excision
  • Cryotherapy - freeze and remove
  • Laser therapy

Make sure of diagnosis first with PCR and histopathology analysis

BDS4 (63 decks)

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