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BDS4 Exam Perp > 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 Reconstructive surgery
* By taking tissue from somewhere elase in the body , for example thighs or foreaerm
* this is then transplanted in the tongue area to replace lost tissue (blood vessels connected to new tissue)

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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 due to low levels of CD4 + T cells

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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 a broad spectrum antifungal with antibacterial properties so can work 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
  • compression of the trigeminal nerve leading to demylination of the trigeminal nerve
  • Can also be attributed to other causes such as multiple sclerosis , tumours, infections and trauma
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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
  • Thrombocytopenia
  • Paraesthesia
  • Electrolyte imbalance
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32
Q

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

A
  • Reaching the maximum dose of the drug treatment
  • Very young patients on many drugs
  • If medication is contraindicated with the medical history
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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 bilateral growth of 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
  • Nociceptive
  • Neuropathic
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44
Q

What is sjogren’s syndrome?

A
  • It is a chronic autoimmune disease where immune cells attack 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 - not 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
* Atrophy of acini
* 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?

A
  • Recurrent apthous ulcers
  • Lichen planus
  • Oral dysaesthesia
  • Angular cheilitis
  • Candidiasis
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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
  • Infections : HIV , candida
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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 single layer of thin endothelial cells
  • Cavernous
    Large vessels - less in number
    Lined by a thicker wall of endothelial 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
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121
Q

Which HHV virus is related to kaposi’s sarcoma?

A

HHV-8

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122
Q

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

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

What does Crepitus indicate in TMJ?

A

Late degenerative disease

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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 a the peripheral nervous system 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
  • Incomplete connective tissue capsule
  • Myoepithelial islands
  • Cystic spaces
  • Chondroid and myxoid tissues
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
  • Positive charge of CHX molecules interact with negative charge of microorganisms surface molecules (phosphate)
  • 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?

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

299
Q

What is your differential diagnosis?

A
  • Squamous cell carcinoma
  • Condyloma acuminatum
  • Verruca vulgaris
  • Verrucous carcinoma
300
Q

Three different clinical presentations of oral squamous cell carcinoma?

A
  • Raised rolled border
  • Indurated
  • Ulceration
301
Q

Patient is elderly presenting with a high alkaline phosphate level with expansion in their maxilla , what disease may have caused this?

A

Paget’s disease

302
Q

patient has raised calcium level with expansion in their maxilla , what disease may have caused this?

A

hyperparathyroidism

303
Q

15 year old with bilateral maxillary expansion , what may have caused this?

304
Q

The patient has pigmented spots on their skin and has precocious puberty with maxillary expansion, what might have caused this?

A

Albright’s syndrome

305
Q

What is the most common salivary gland tumour in the parotid gland?

A

Pleomorphic adenoma

306
Q

What is the most common salivary gland tumours in the upper lip?

A

Acinic cell adenocarcinoma

307
Q

What is the most common salivary gland tumour in the soft palate?

A

Mucoepidermoid carcinoma

BDS4 Exam Perp (72 decks)

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