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REVISION > Oral medicine > Flashcards

Oral medicine Flashcards

1
Q

What is albright’s disease

A

A genetic condition that affect bone growth, skin pigmentation and body hormonal balance, can be polystotic or monostotic

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2
Q

Clinical signs of albright’s disease

A
  • skin pigmentation
  • endocrine hyperfunction
  • facial asymmetry
  • polycystic fibrous dysplasia
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3
Q

Radiographic signs of Albright’s disease?

A
  • lesions with ground glass appearance
  • margins blend in with adjacent bone
  • bone fractures and deformities may occur
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4
Q

What is cherubism?

A

A genetic autosomal dominant disorder characterised with abnormal bone tissues, can have multolocular or multicystic cells

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5
Q

Clinical signs of cherubism

A
  • painless bilateral swelling of the jaw
  • swollen cheeks
  • dental malocclusions
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6
Q

Radiographic signs

A
  • multicystic lesions
  • multolocular lesions
  • facial sinuses appear obliterated
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7
Q

Name and describe the types of oro-facial pain syndromes

A

1 - Dental (odontogenic)
- usually gets better or worse over time
-can be acute and sub acute
2. non dental
- generally acute infective non dental pain that gets worse or chronic caused by non dental conditions

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8
Q

Examples of odontogenic facial pain syndromes

A
  • musculoskeletal: periodontal and tmjd
  • visceral structures: abscesses and caries
  • Atypical odontalgia - dental pain without detected pathology which follows a distinct pain pattern (episodic)
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9
Q

Examples of non dental pain syndromes (neuropathic)

A
  • constant burning and aching pain with a fixed location and intensity , can occur after injury or trauma or from herpes zoster virus , or destructive treatment
  • Such as : Trigeminal neuralgia, chronic regional pain syndrome, traumatic injury to facial nerve , surgical injury to nerves in the head and neck
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10
Q

Examples of non dental pain syndromes (psychogenic)

A
  • persistent idiopathic facial pain which poorly fits into the standard chronic pain syndromes and responds poorly to treatment
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11
Q

What is sjogren’s syndrome

A

It is an autoimmune disease where B-cell proliferation causes destruction of exocrine glands leading to dry mouth and dry eyes due to it affecting secretions

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12
Q

What are the types of Sjögren’s syndrome?

A

Primary : not associated with connected tissue disease
Secondary: associated with connective tissue disease such as (SLE, rheumatoid arthritis systemic sclerosis )
Partial Sjogren’s : Sicca Syndrome

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13
Q

Symptoms of Sjögren’s syndrome?

A

Dry eyes
dry mouth
fatigue
neuropathy

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14
Q

What antibodies are linked to Sjogrens syndrome?

A

Anti-La
Anti-Ro
Anti nuclear antibodies

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15
Q

investigations of Sjogrens according to the American European consensus criteria?

A

**ocular symptoms
**dry eyes for more than 3 months
recurrent sensation of sand in the eye
using tear substitutes more than 3 times a day
2) Oral symptoms
feeling of dry mouth daily for 3 months
swollen salivary glands
drinking liquids to aid swallowing
**3)Ocular signs *
Schrimer’s test (<5mm in 5 minutes)
Rose bengal test (>4)
4.histopathology
Biopsy
5. Salivary gland involvement
Ustimulated whole salivary test
Parotid Sialography
Salivary Sintigraphy
6. Autoantibodies
Serology
presence of anti-ro and anti-la antigens

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16
Q

What is the criteria rule of the european-american consensus

A

Any 4 criteria including criteria number 4 and 6

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17
Q

What does the ACR/EULAr 2016 for diagnosing sjogren’s syndrome?

A

-autoantibodies anti-ro or anti-la presence
- oral symptoms such as dry mouth
- occular symptoms
-objective salivary flow test
- Schrimer’s test
- unstimulated whole salivary flow test <1.5ml in 15mins

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18
Q

other investigations for Sjogren’s

A

MRI
labial gland biopsy
Anti-ro antibody test
Ultrasonography

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19
Q

What are the histopatholgical features of Sjogren’s syndrome?

A

Minor Glands :
- focal lymphocytic sialodentitis
-acinar loss
-fibrosis
- focal collection of lymphocytes (50+)
Major glands
- lymphocytic infiltrate
- Atrophy of acini
-myoepithelial islands
- duct epithelial hyperplasia

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20
Q

Oral complications due to sjogrens syndrome

A
  • oral infection: candida
  • increased caries rate and periodontal disease
    -poor denture retention
    -functional loss
    -salivary gland lymphoma ; non Hodgkin’s lymphoma
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21
Q

What drugs are used to manage Sjogren’s syndrome?

A
  • Pilocarpine which is a salivary stimulant
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22
Q

Other causes of xerostomia (than Sjogrens)

A
  • dehydration
    -medications
    -head and neck radiotherapy
    -chemotherapy
  • smoking
    -salivary gland tumours
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23
Q

What features in a parotid swelling would make you suspect a malignancy?

A

fast growing
unilateral
firm
fixed to underlying structures
asymmetry of the gland

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24
Q

Most common site of salivary neoplasm?

A

Parotid gland (80%)
Submandibular Gland (10%)
Sublingual gland (0.5%)
Minor glands (10%)

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25
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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26
Q

Signs and symptoms of ectodermal dysplasia

A

Hypodontia and peg shaped teeth
Poor functioning sweat glands
Abnormal nails
Cleft lip and palate
Decreased skin pigmentation (pallour)
Large forehead
learning disabilities
Thin hair

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27
Q

What is recurrent aphthous ulcers?

A

immunologically generated recurring oral ulcers that follow a pattern depending upon the ulcer type that may be caused by developmental or environmental factors

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28
Q

What is an ulcer?

A

Full thickness loss of epithelium where you can see underlying connective tissue and fibrin may be deposited on the surface - can only be diagnosed histopathologically

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29
Q

What is an erosion?

A

Partial thickness loss of epithelium - diagnosed histopathologically

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30
Q

What is behcet’s disease?

A

Severe form of apthous ulcers , 3 or more episodes of apthous ulcers affecting genitals, bowel and oral mucosa

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31
Q

Comparison between minor and major recurrent apthous ulcers

A

Minor
most common
less than 1cm
round or oval with red margins and yellow base
affects non keratinised mucosa
heals within 1-2 weeks
heals without scarring
children are most commonly affected
Major
more than 1cm in size
oval or irregular shape
can by multiple or single
heals within 6-12 weeks
heals with or without scarring
affects keratinised or non keratinised mucosa

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32
Q

What is the rarest type of apthous ulcers?

A

Herpetiform apthous ulcers
less than 0.5cm in size
round or oval often with large areas of ulceration
heals within 1-2 weeks
heals without scarring
1-200 per crop
affects non keratinised mucosa

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33
Q

what are the potential problems of recurrent apthous stomatitis (Canker sores)

A

infections
dehydration and malnutritionn
problems wearing dentures
affects speech and mastication

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34
Q

Causes of canker sores (recurrent apthous stomatitis)

A

Genetics : HLA type A2 and B1w
Stress
nutritional deficiencies - iron, folate, b12
hormone imbalance
Trauma
Systemic disease : Crohn’s mennorhagia, anaemia, OFG , coeliac disease (TTG test)
immunity - CD8 more than CD4

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35
Q

Special investigations for apthous ulcers?

A

blood tests
allergy tests (contact hypersensitibity)

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36
Q

how are apthous ulcers treated?

A

Correct nutritional deficiencies (B12 and folate)
treat if systemic disease is involved
remove trauma
Avoid dietary triggers
Use SLS free toothpaste

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37
Q

Medications use for apthous ulcers?

A

Antimicrobial mouthwashes (reduce secondary infection)
CHX and hydrogen peroxide
Doxycycline for recurrent apthous stomatitis
analgesics
benzydamine mouthwash or oromucosal gel
lidocaine ointment or spray
Topical corticosteroids
betamethasone mouthwash or inhaler
systemic immune modulation
Systemic steroids: Prednisolone
Immuno-suppressive : azathioprine
Immunomodulator : thalidomide

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38
Q

what would microcytic anaemia blood results show

A

MVC : LESS than 80fL
Hb, Hct and RBC less than mean value

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39
Q

What Gi conditions might cause microcytic anaemia?

A

Crohn’s
Coeliac
Ulcerative colitis
Gastric carcinoma

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40
Q

What common conditions cause microcytic anaemia but require further blood tests

A

Iron deficiency
Thalassaemia
Lead poisening
chronic disease such as Crohn’s

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41
Q

What oral conditions are associated with microcytic anaemia?

A

recurrent apthous ulcers
poor wound healing
increased candida infection
mucosal atrophy

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42
Q

Tx options for microcytic anaemia

A
  • Correct deficiencies : Iron tablets
  • if caused by menorrhagia - contraceptive pills and hormone therapy
  • Severe cases - blood tranfusion
  • Prevention - dietary and supplemental advice
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43
Q

Classification of denture induced stomatitis?

A

Newtons Classification
Type 1 -localised inflammation with no erythema
Type 2 - diffuse inflammation with erythema but no hyperplasia
Type 3 - granular inflammation with erythema and papillar hyperplasia

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44
Q

What is smokers keratosis

A

A premalignant pathological process as a result of smoking that presents in the mouth as white keratotic lesions

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45
Q

What epithelium is affected in smoker’s keratosis?

A

Stratified squamous cell keratinised epithelium mostly affecting the hard palate

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46
Q

What is the clinical presentation of smoker’s keratosis ?

A
  • thickened white area with brown/yellow/grey areas on tha palate
  • Painless
  • Other areas with tobacco related staining
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47
Q

What histological findings in smokers keratosis may indicate malignancy?

A

Hyperkeratosis
Atypia - abnormal cell
Dysplasia
Infiltrate of macrophages
Hyperchromatism (nucleus stains more)

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48
Q

What clinical presentation would indicate malignancy in smoker’s keratosis?

A

raised rolled margins
firm lesion
non-homogenous

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49
Q

describe desquamative gingivitis

A

A clinical descriptive form of non specific clinical expression in the gingivae (redness, burning, erosion, pain and plaque) of several dermatomucous disorders

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50
Q

Clinical presentation of desquamative gingivitis

A

can be seen as inflammed ginigva extending beyond the mucogingival margin with erythema and ulceration which involves the full width of the gingivae

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51
Q

What conditions are associated with desquamative gingivitis?

A
  • Liichen planus
  • pemphigoid
    -pemphigus
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52
Q

What local factors may exacerbate desquamative gingivitis?

A
  • smoking
    -poor oral hygiene
    -overhanging restorations
    -partial dentures
  • plaque buildup
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53
Q

How would you manage desquamative gingivitis?

A
  • confirm diagnosis and treat underlying cause if possible (blood tests and immunofluorescence)
  • Improve OH - give instructions
  • Topical steroid use - betamethasone inhaler or rinse or cream on gum shield
  • Tacrolimus - immune modulator
    Systemic immunosupressant
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54
Q

Name other gingival disease than desquamative gingivitis that may be painful on presentation

A
  • Erythema multiforme (related to steven-johnston syndrome
  • ANUG
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55
Q

What are local factors of oral pigmentation?

A

Restorations such as amalgam
vascular malformations (haemangioma - a brnign tumour that develops as a result of abnormal proliferation of endothelial cells)
naevus - melanocyte clusters - exophytic
macule - small flat area of discoloured skin or mucous

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56
Q

What are the general factors of oral pigmentation?

A

genetics
smoking - leakage of melanocytes and fibrosis
medications : iron tablets , antimalarials and contraceptive pills
Addison’s disease (reduced cortisol and aldosterone from adrenal glands cause brown patch due to increase in ACTH)

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57
Q

What is haemangioma?

A

A vascular malformation that can be described as a benign tumour made of extra blood vessels than can present as exophytic and erythmatous. It is due to abnormal proliferation of endothelial cells and it is part of the hamartoma family.

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58
Q

What are the types of haemangioma’s ?

A

Capillary
Small capillaries
lined by endothelial cells
Capillary haemangioma
Cavernous
Few large thin walled vessels
lined by epithelial cells
dilated vascular spaces

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59
Q

What herpes viruses are associated with intra-oral vesiculation?

A

herpes siimplex type 1 and type 2
Varicella-zoster
Epstein barr
Cytomeglo virus

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60
Q

What are diseases are caused by coxsackie virus?

A

hand-foot-mouth disease
herpangina

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61
Q

What oral diseases are caused by epstein barr

A

Oral hairy leukoplakia
infectious monomucleosis

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62
Q

What are the common trigger for reactivationn of herpes simplex virus?

A

Stress
infections
exposure to UV light
Fatigue
immunosuppression

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63
Q

What are the clinical signs on examination of TMD

A

E/O
limited range of mandibular movement
deviation on opening or closing
muscles of mastication
muscles of mastication tenderness and hypotrophy
TMJ clicking or crepitus on opening or closing
TMJ tenderness
I/O
Linea-alba, scalloping of the tongue
Wear facets, high occlusal points
Interincisal angle on opening (to see extent of opening)

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64
Q

What are the predisposing factors of TMD?

A

Females>males
Stress
Trauma
Occlusal abnormalities
Parafunctional habits - clenching, grinding, nail biting and bruxism

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65
Q

What is management for TMD?

A

Conservative advice
Re-assure
Stress management : relaxation, breathing, CBT
Limit jaw movement : soft diet and masticate laterally , support jaw while yawning
Stop parafunctional habits (use hot/cold packs)
Jaw exercising
Medication
NSAIDS
Antidepressants : tricyclics : amitryptyline
Splinting
soft bite guard
stabilisation splint
anterior bite plane

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66
Q

Any other conditions that might present with similar signs to TMD and how might it be differentiated from TMD?

A
  • Trimgeminal neuralgia - pain at night is more intense while TMD in the morning
  • Myofacial pain syndrome - no clicking of TMJ
    -Periocoronitis - no muscle hypotrophy and no clicking on TMJ
  • Salivary gland pathology - imaging
  • dental abscess - by clinical and radiographic assessment
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67
Q

How to describe how a stabilisation splint should be made to technician?

A
  • material : hard acrylic splint with full occlusal coverageg
  • requires to be ground in to achieve maximum intercuspation and sloping canine guidance line
  • upper and lower alginate + facebow registration is required for this splint to be made
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68
Q

What is bell’s palsy?

A

Unilateral facial nerve paralysis

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69
Q

Aetiology

A

unknown cause, but can be due to
inflammation around the facial nerve and this pressure causes facial paralysis (including the eyebrows)

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70
Q

How is it managed?

A
  • reassurance that paralysis will get better
    -prednisolone steroid given within 72 hours of onset reduce inflammation
  • Aciclovir used when suspected ramsay-huntn syndrome
  • protect affected eye with patch and eyedrops
    -Review - refer if not recovered within 3 months
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71
Q

how to differentiate between upper and lower motor neuron disease?

A

UMN (stroke)
Spaciticity (stiff muscle movements)
can wrinkle forehead and move eyebrows but cannot move lower portion of face
LMN
cannot wrinkle head or move eyebrows or move lower portion of face

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72
Q

How does the difference between upper and lower motor neuron occur?

A
  • upper motor disease occur in the supra-nuclear lesion whereas a lower motor neuron lesion affects the nucleus of the facial nerve
  • UNM interrupt neural pathways at a level above anterior horn cell
  • LNM interrupt spinal reflexes arc muscles
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73
Q

Give possible causes for LMN disease?

A

multiple sclerosis (chronic autoimmune disorder affecting the brain and nerves)
Bell’s palsy
Trauma
Parotid gland tumour
Misplaced LA
Reactivated HSV

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74
Q

Give possible causes of UNM disease

A

Stroke
multiple sclerosis
brain injury
cerebral palsy
spinal cord injury

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75
Q

How is LMN managed

A
  • distinguish and treat cause(history , x-ray, blood tests)
    -re-assure patient
  • prednisolone to reduce inflammation
  • eye protection if eyes are affected
  • referral if does not resolve
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76
Q

What conditions require patients to be on long term steroids

A

severe asthma
COPD
Addison’s disease
Lupus
Crohn’s disease
Rheumatoid Arthritis
Multiple sclerosis

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77
Q

Signs and symptoms of adrenal suppression

A

Dehydration
weight loss
weakness
disorientation
low blood pressure
oral pigmentation
postural hypotension

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78
Q

What emergency could be associated with adrenal insufficiency?

A

Adrenal crisis - insufficient levels of cortisol

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79
Q

Why asthmatics are more prone to erosion?

A

-due to inhaler use - results in less salivary protection against acid and xerostomia
-asthmatics are also more prone to GORD which cause dental erosion

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80
Q

What is syncope?

A

known as fainting, transient and self limiting loss of consciousness characterised by fast onset, short duration and fast recovery. The patient is also unable to maintain postural tone.

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81
Q

What is physiological aspect of a faint?

A

temporary malfunction in central nervous system due to a trigger resulting in a drop in blood pressure, reduction in oxygen and interruption of blood flow to the brain resulting in loss of consciousness

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82
Q

how to manage fainitng in general practice?

A
  • Assess patient through ABCDE
    lay the patient flat
    if the patient is not breathless, raise the patients feet
    loosen any tight fitting clothing around the neck
    Administer oxygen - 15L/min until consciousness is regained
    if no recovery phone 999
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83
Q

What is burning mouth syndrome?

A

A painful condition characterised by burning or scalding or tingling sensation in the mouth that is recurrent and the cause is not obvious.

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84
Q

What is the medical name of burning mouth syndrome?

A

Oral dysaesthesia

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85
Q

Who is more likely to be affected?

A

Females>males
menopausal women
age range 40-60

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86
Q

Causes

A

nutritional deficiencies
xerostomia
fungi infections
poorly fitting dentures
Stress and depression
Parafunctional habits
Diabetes and hypothyroidism

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87
Q

Signs and symptoms of burning mouth syndrome?

A

severe burning and tingling sensation in the mouth particularly the tongue
sensation of dry mouth
taste changes - metallic
loss of taste

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88
Q

Differential diagnosis of burning mouth syndrome

A

lichen planus
orofacial pain
xerostomia
diabetes

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89
Q

Investigations for burning mouth syndrome

A

Blood tests : FBC, UE, TFT , LFT hbA1c
Salivary flow rate for xerostomia assessment
intra/extra oral examination for parafunctional habits
denture assessment
psychiatric asssessment

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90
Q

management of burning mouth syndrome

A
  • reassurance
    -correct underlying cause
  • advice - stay hydrated , difflam mouthwash
  • pharmacotherapy - gabapentin and CBT
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91
Q

Which benign and malignant tumours affect the salivary glands? order them by incidence (PWAMA)

A

Pleomorphic Adenoma (mixed tumour, epithelial and myoepithelial origin) - 75%
Warthin’s Tumour - 10%
Adenoid cystic carcinoma - 5%
Mucoepidermoid carcinoma - <1%
Acinic cell carcinoma- 3%

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92
Q

histological features of pleomorphic adenoma

A
  • variable capsule
  • epithelium inducts and sheets
  • myoepthelial cells
  • myxoid
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93
Q

What histology feature is related to recurrence ?

A

poorly or non encapsulated

94
Q

histological features of warthin’s tumour?

A

cystic spaces
lymphoid tissue present
oncocytic epithelium

95
Q

histological features of adenoid cystic carcinoma?

A

cystic spaces
malignant cells with a cribiforom architecture
no capsule present

96
Q

how are salivary gland neoplasms diagnosed?

A

fine needle aspiration
core biopsy
incisional biopsy

97
Q

What is the mechanism of action of chlorhexidine?

A

diatonic action- positive charge on CHX react with phosphate negative charge on microorganism.
This destroys integrity of cell membrane allowing CHX to enter the cell resulting in percitipation of cytoplasmic components and leading to cell death.
- It can be bactericidal or bacteriostatic depending on its concentration

98
Q

what family of antiseptic do chlorhexidine belong to ?

A

bisbiguanides

99
Q

what is substantivity?

A

prolonged adherence of antiseptic to the oral cavity and its slow release of effective doses that guarantee the persistence of its antimicrobial effects (48h)

100
Q

CHX conc

A

0.2% or 0.12% mouthwash
use twice daily for 1 minute

101
Q

Side effects

A

mucosal irritation
brown staining
taste disturbance
burning sensation
hypersensitivity and anaphylaxis

102
Q

What are the indications of CHX

A

candidosis
cleaning dentures
post surgery
immunocompromised patients
management of ulcers, xerostomia, ANUG, mucositis
high risk caries patients

103
Q

Name stages in the formation of a clot

A

vasoconstriction
temporary blockage by a platelet plug
blood coagulation
fibrin clot

104
Q

How do aspirin affect clotting

A

it inhibits platelet agreggation by altering balance between thromboxane A2 and prosrtacyclin

105
Q

How does warfarin affect clotting?

A

inhibits synthesis of vitamin K which is important in the formation of clotting factors 2,7,9,10

106
Q

how does NOAC affect clotting?

A

Factor X inhibitor that inhibit conversion of prothromin to thrombin, stopping the formation of the fibrin clot

107
Q

Why is clopidegrol and aspirin used together?

A

It is used as a dual anti-platelet therapy can be used for acute coronary syndrome
Aspirin - reduce prostoglandins and inhibits COX-1
Clopedegrol - inhibits P2Y12 - leading to platelet inhibition due to it affecting fibrin cross linking

108
Q

What is the pattern of von willbrand’s disease?

A

Autosomal dominant
Type 1 - deficiency of vWF molecules
Type 2 - deficiency of vWF factor
Type 3 - deficieiincy in vWF molecules and factor

109
Q

How does vWD affect bleeding

A

vWF protein dtabilises clotting factor 8 which is important in clotting, vWD affect this protein quality and quantitiy resulting in interruption of clot formation

110
Q

What is a biofilm

A

aggregate of microorganisms that are adherent to each other and adherent to a surface. This adhered to the extracellular matrix EPS

111
Q

What are the stages of colonisation of a biofilm? ACACD

A

adhesion
colonisation
accumulation
complex community
Dispersal

112
Q

Methods of identifying organisms

A
  • microbiological culture (AGAR) through swab or rinse
  • molecular biology
    DNA probe
    PCR
    ELISA
113
Q

virulence factors of P.gingivalis (PATE)

A

proteases
adhesins - fimbrae
Tissue toxic metabolic byproducts - hydrogen sulphide and ammonia
endotoxins (LPS)

114
Q

Virulence factors of C.albicans ? (GAMES)

A

germ tube formation
adhesins
metabolic acids
Extracellular enzymes
Switching mechanisms

115
Q

Virulence factors for S.mutans (ASAP)

A

adhesins
sugar modified enzymes
acid tolerance and adaptation
polysaccharides

116
Q

What is lichen planus

A

a chronic autoimmune inflammatory disease than can affect the mucosa of the oral cavity

117
Q

What are the histological features of lichen planus?

A

hugging band of inflammatory cells
cell apoptosis
keratinisation, atrophy, hyperplasia of tissue
elongated rete pegs

118
Q

What are the types of lichen planus? (PPBread)

A

Papular - white plaque
Plaque - white
Bullous - exophyitic fluid filled vesicles
Reticular - lacy white lines
Erosive
Atrophic

119
Q

What is the aetiology of lichen planus

A
  • Autoimmune
  • Stress
  • Idiopathic
  • Hep C
  • Drug related : beta blockers, NSAIDS, hypoglycaemic and diuretics
    SLS allergy
    Amalgam restoration
120
Q

When to biopsy a lichen planus lesion?

A

Symptomatic
In a smoker
In high cancer risk area

121
Q

How is lichen planus managed?

A

** Asymptomatic : **
observe and monitor , CHX + OHI

** Symptomatic: **
remove cause . e.g. amalgam restoration
OHI
biopsy
Topical steroid use - betamethasone
Systemic steroid - prednisolone
Systemic immunomodulator - azathioprine

122
Q

What is anaemia

A

is is a condition caused by reduction in haemoglobin in the blood -> results in reduction inoxygen carrying capacity of of the blood

123
Q

What are the signs a symptoms of anaemia?

A

Dizziness
Weakness
Shortness of breath
Paleness
loss of consiousness
low blood pressure
palpations

124
Q

Oral signs of anaemia?

A

recurrent ulceration
candida infections
Glossitis or smooth tongue (iron deficiency)
beefy tongue
oral dysaesthesia
mucosal pallor

125
Q

Types of Anaemia

A
  1. Microcytic (80fl>)
    iron deficiency
    thalassaemia
  2. Normocytic (80-100fl)
    internal bleed
    pregnancy
    sickle cell anaemia
    chronic disease (RA, diabetes, kidney disease)
  3. Macrocytic (100+ fl)
    - b12 folate deficiency
    -liver disease ; hypothyroidism kidney disease
126
Q

What is the clinical appearance of plasma cell gingivitis?

A

generalised erythema and oedema which can extend from the free marginal gingivae to the attached (red ginigvae that bleed easily and can be accompanied by lip swellingn or golssitis)

127
Q

What is the aetiology of Plasma cell gingivitis?

A

hypersensitive reactions - SLS, pepper and cinammon
Idiopathic
Rare condition

128
Q

What may worsen plasma cell gingivitis?

A
  • not removing the causative agent form the oral cavity
  • Poor OH
  • plaque retentie factors
129
Q

What is the management of plasma cell gingivitis?

A
  • histological sampling for diagnosis
  • preventing exposure to causative agent (avoid cinammon, use SLS free toothpaste)
    Tacrolimus to heal lip swelling
130
Q

Wat are the local and systemic causes of xerostomia?

A

Local
mouth breathing
smoking
steroid inhaler
radiotherapy

Systemic
medications : SSRI, diuretics
Cancer therapy : chemotherapy
diabetes, addison’s disease
Sjogren’s syndrome
dehydration
Stress and anxiety

131
Q

How can you assess xerostomia intra orally?

A
  • measure unstimulated whole salivary flow over 15 mins should be more than 1.5 ml
  • Palpate salivary glands duct
  • Mirror stick test to cheek and tongue
  • check for saliva pooling
132
Q

What are the oral signs and symptoms?

A
  • difficulty swallowing
  • Speech problems and clicking
  • oral soreness and discomfort
  • problems with denture control
  • altered taste
  • increased caries rate
    increased candida infection
    halitosis
    tongue fissuring
    increased periodontal disease
133
Q

Management of xerostomia

A
  • Manage underlying cause
    treat systemic disease
    consider alternative medications
    stress management - CBT
    alcohol and smoking advice
  • Salivary substituents
    artificial saliva - gel oral spray and pastilles
    Orthana saliva spray
    Bioxtra gel
    Glandosane Spray
    Saliva stimulating tablets
134
Q

name 3 salivary substituents

A

Saliva orthana spray
Bioxtra gel
Glandosane gel

135
Q

Name 3 sugar substitiuents

A

Xylitol
aspartame
sucralose
sorbitol
manitol

136
Q

name 3 salivary proteins

A

Salivary IgA
histatin
mucins

137
Q

name 3 salivary enzymes

A

AMylase
lipase
lysozyme

138
Q

When are antibiotics indicated for dental treatment?

A
  • Signs of spread of infection?
  • Systemic involvement (malaise, fever)
  • Immunocompromised patients (diabetes)
  • ANUG if local measures are ineffective
  • when there is a risk of infective endocarditis
139
Q

Give 5 ways antibiotics work?

A
  • cell wall destruction
  • protein synthesis inhibition
  • DNA synthesis inhibition
  • DNA replication inhibition
  • cell membrane inhibition
140
Q

Disadvantages of ABS

A
  • antibiotic resistance
  • Gastrointestinal irritation
  • interaction with other medications
    -hyper sensitivity and anaphylaxis
141
Q

ABs used in dental treatment

A

Pen v
Metronidazole
Clindamycin

142
Q

Mechanism of antibiotic resistance?

A
  • enzymatic degredation of antibiotics
  • alteration of bacterial proteins
  • changes in membrane permeability
  • drug in activation
143
Q

What 2 kinds of asthmatic inhalers?

A

blue - salbutamol - beta agonist
brown - betamethasone - corticosteroid

144
Q

What is asthma

A

a reversible airway obstruction characterised by inflammation of the mucosa and excessive mucous secretion

145
Q

What are the signs and symptoms of asthma ?

A

shortness of breath
dizziness
wheezing and when exhaling
coughing
chest pain or tightness

146
Q

dental effects of inhalers + advice?

A
  • candida infections due to efffects of longevity of steroids in mouth (rinse after use)
    -increased erosion due to acidity (Fluoride use)
    -dry mouth due to decrease in saliva and caries risk
    use spacer
    rinse
    stay hydrated
147
Q

incidence of people treated with inhalers for asthma in scotland?

A

6.4%

148
Q

Histological signs in epithelial dysplasia

A

abnormal keratinisation
abnormal stratification
drop shaped rete pegs
basal cell hyperplasia
altered polarity of basal cell
hyperchromatism
Atypia
enlarged nuclei
pleomorphism
increased mitotic activity

149
Q

histological features of pemphigoid

A

sub-basal split
autoantibodies attack hemidesmosomes
linear IF pattern
increased fibrin
neutrophils in lamina propria

150
Q

histological features of pemphigus

A

suprabasal split
basket weave IF pattern
tzank cells present
autoantibodies attach desmosomes
acantholysis
epithelial cells separate from prickle cell layer

151
Q

how do pemphigus and pemphigoid differ clinically?

A

pemphigoid is a thick walled blisters affecting full epidermis usually filled with blood
Pemphigus is a superficial clear fluid filled blisters that burst then spread

152
Q

What investigations for permphigus and pemphigoid?

A
  • direct immunofluorescence using IgG antibodies
    biopsy taken from unaffected epithelium
  • indirect immunoflurescence tests for igG levels in serum
  • histopathological analysis
153
Q

Management of pemphigus and pemphigoid?

A

topical betamthasone
prednisolone
monocloncal antibody therapy
immune modulationn - azathioprine
refer if any severe symptoms or other areas are affected

154
Q

What are the high risk sites for cancer in the patient mouth?

A

floor of the mouth
lateral border of the tongue
soft palate

155
Q

how does cancer spread?

A

locally
through blood
through lymphatic spread

156
Q

What is the metastatic cascade? LSAEMM

A

local invasion and intravasation
survival in circulation
arrest in distant organs or tissues
extravasation
micrometastasis
macrometastatic growth

157
Q

What is Necrtotising Sialometaplasia

A

A benign inflammatory and ulcerative lesion affecting minor salivary glans causing blockage and may mimic squamous cell carcinoma

158
Q

What is the aetiology of necrotising sialometaplasia?

A

small vessels ischaemia and infraction due to smoking, trauma , LA, bulimia, radiation , infections
It is self healing and painless

159
Q

What is the histopathological appearance of necrotising sialometaplasia?

A

necrotic tissue
hyperplasia
squamous metaplasia of acini and ducts
necrosis of saliva acini

160
Q

what is the management of necrotising sialometaplasia?

A

it heals by itself in 6-10 weeks by secondary intention

161
Q

what is the differential diagnosis with necrotising sialometaplasia?

A

squamous cell carcinoma
salivary gland carcinoma

162
Q

What is the differential diagnosis of a swollen lip other than mucocele?

A

OFG
Trauma to lip
SCC
Fibrous overgrowth
Soft tissue abscess

163
Q

What is a mucocele?

A

a recurrent swelling (secretion retention) found most commonly in the lower lip due to a damaged or blocked minor salivary gland which can burst

164
Q

what is the histological appearance of a mucocele

A

macrophage lined cystic cavity
surrounded by granulation tissue
foam cells

165
Q

Management of mucocele

A

excision of mucocelel and gland

166
Q

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

A

Ranula

167
Q

What is orofacial granulomatosis

A

a condition where there is lymphatic obstruction form giant cell granulomas leading to accumulation of fluid in tissue causing oedema
- related to type IV hypersensitivity
- may be associated with crohns disease

168
Q

what is the aetiology of OFG

A
  • autoimmune condition
  • allergy to cinammon , chocolate, benzoates
  • linked to crohns disease and sarcodosis
169
Q

What is the histological features in OFG

A

Granulomas
increased tissue fluid
lymphatic obstruction
dilated lymph and blood vessels
Schaumann bodies

170
Q

what is the signs and symptoms of OFG

A
  • lip, cheek , gingivae swelling
  • skin changes
  • angular cheilitis
  • ulceration
  • buccal-cobble staining
  • mucosal tags
  • fistula formation
  • full thickness gingivae
  • stage horning of sublingual folds
171
Q

management of OFG

A
  • Dietary advice after patch test
  • tacrolimus for lip swelling
  • steroids - azathioprine
  • intralesion steroid injections
  • biological agents - adalimumab
172
Q

6 types of oral candida infections

A

pseudomembranous
erythema
hyperplastic
angular cheilitis
median rhomboid glossitis
denture induced stomatitis

173
Q

where does median rhomboid glossitis occur?

A

dorsum of the tongue -> central papillary atrophy anterior to sulcus terminals

174
Q

what are the histopathological features of median rhomboid glossitis?

A

candida hyphae infiltration
PMNL infiltration (polymorphonuclear)
Elongated and hyperplastic rete pegs

175
Q

methods of testing candida

A
  • Oral swab or rinse
  • biopsy
  • smear for microscopy
176
Q

what are the virulence factors of candida?

A

adhesins
switching mechanisms
hydrolytic enzymes> haemolysin(invasion), proteinase(adhesion),phospholipae (infiltration)
germ tube formation
acidic metabolites

177
Q

Antifungal agents examples?

A

miconazole
fluconazole
chlorhexidine
iatroconazole
nyastatin

178
Q

what medications are contraindicated with azoles?

A

warfarins and statins

179
Q

What information should be on a prescription?

A

Patient full name , address and CHI
age in number if under 12 years old
Date of prescription (vaild for 6 months)
name and address of prescriber
Status of prescriber
Signature of prescriber in ink
name of drug written clearly
for and strength of preparation
total quantitiy of drug (send)
instructions of how and when (label drug)
Residual space on form should be scored out
Stamp of practice

180
Q

Examples of prescription of 2 antibiotics

A

Amoxcillin capsules 500mg
for 5 days
Send : 15 capsules
Label : 1 Capsule 3 times daily
_______________________________________
Metronidazole tablets 200mg
Send : 15 tablets
Label : 1 tablet three times daily

181
Q

What is the rate of infection of HIC , HepC and Hep B

A

HIV - 0.3%
Hep C- 3%
Hep B - 30%

182
Q

Name 6 oral lesions associated with HIV ?

A

Candidosis lesions
hairy leukoplakia
Kaposi’s sarcoma
non- hodgkin sarcoma
periodontal disease

183
Q

How is HIV diagnosed

A

HIV RNA testing
Elisa antibody testing 6-12 weeks post infection

184
Q

How is HIV treated?

A

highly active anti-retroviral therapy which contains 3 or more drugs
2xnecleoside reverse transcriptase
1x non nucleoside reverse transcriptase

185
Q

What is fibrous epulis?

A

it is a reactive non-neoplastic condition affecting the gingiva as a result to chronic irrritation resulting in a localised fibrous enlargement

186
Q

What is the aetiology of fibrous epulis?

A

chronic local irritation -> restorations and calculus

187
Q

How does it appear histologically?

A

ulceration
granulation tissue
metaplastic bone tissue

188
Q

what is it known on sites other than gingivae?

A

fibro-epithelial polyp

189
Q

what is a pyogenic granuloma ?

A

it is granulation tissue that can be found in any mucosal site usually in a response to trauma - if found on gingivaw it is called vascular epulis

190
Q

how does it appear histologically?

A

granulation tissue with blood vessels

191
Q

name a heridiatry white patch

A

white spongy naevus is herdiatry condition characterised by increased production of keratin

192
Q

how does it appear histologically

A

intracellular oedema in keratin layer
present with parakeratosis

193
Q

how does smoker’s keratosis appear histologically?

A

hyper keratosis
areas of mild dysplasia
minimal infiltrate of macrophages and melonocytes in basal layer

194
Q

what are the differential diagnosis of denture induced hyperplasia?

A

pyogenic granuloma
giant cell granuloma
leaf fibroma

195
Q

What factors resulted in denture induced hyperplasia?

A
  • ill fitting dentures causing chronic trauma to tissues
196
Q

What is the management of denture induced hyperplasia?

A
  • LA then sugrical excision of the fibrous tissue overgrowth
  • address causative factors to prevent recurrence
  • Tissue conditioner temporarily
  • Replace denture
197
Q

What are the histological features of denture induced hyperplasia?

A
  • Psuedo epitheial dysplasia
  • hyperkeratosis
  • hyperplastic rete pegs
  • candida involvement
198
Q

what would the pathologist report of pemphigus vulgaris?

A

basket weave pattern on DI , on histopathology suprabasal split with tzank cells

199
Q

what is pemphigus vulgaris

A

It is an autoimmune blistering disease that usually begins in the mouth presents as clear fluid filled blisters that burst and spread which can also be on skin and it is fatal without treatment

200
Q

Why would pemphigus vulgaris occur?

A

it is an autoimmune disorder due to type II hepersensitivity where antibodies attack desmosomes (Dsg1 and Dsg3)

201
Q

what conditions may have same appearance as pemphigus vulgaris?

A

drug induced pemphigus
bullous pemphigoid

202
Q

what is the treatment of pemphigoid vulgaris?

A

immunomodulators - azathioprine
topical steroids - betamethasone
systemic steroids - prednisolone
monoclonal antibody therapy

203
Q

What are the risk factors of squamous cell carcinoma?

A

Tobbaco use
betelquid chewing habits
alcohol
viruses - HPV,HSV,EBV,HHV-8
poor diet and nutrition
poor OH
immunodeficiency
Socioeconomic factors

204
Q

What is the TNM system

A

It is a system for classifying malignancy according to tumour , nodular involvement and metastasis

205
Q

What is TNM breakout?

A

Tumour
Tx- cannot be assessed
T0 - no evidence of tumour present
T1 - <2 cm
T2 - 2-4 cm
T3 - >4
Nodular involvement
Nx - cannot be assessed
N0- no evidence of tumour present
N1 - ipsilateral node metastasis - <3
N2a - ipsilateral node metastasis - 3-6
N2b - multiple epsilateral - less than 6 cm
N2c - bilateral or contralateral
N3 - more than 6 cm
M (metastasis)
M0 - no distant metastasis
M1 - distant metastasis present

206
Q

What is the WHO cancer of grading malignancy according to degree of differentation?

A

Grade 1 - well differentiated
Grade 2 - moderately differentiated ( most cases)
Grade 3 - poorly differentiated

207
Q

WHO grades of dysplasia histopathologically?

A

Hyperplasia - no atypia, increase in cell numbers and regular stratification
Dysplasia - hyperchrmatism and pleomorphism are also present here
- Mild - architectural changes in lower third of epithelium involved, mild cellular atypia
- Moderate - architectural changes up to middle third of epithelium involved with moderate atypia
- Severe - architectural changes extend to upper third of epithelium , severe cellular atypia
carcinoma in situ - architectural change involve the full thickness of epithelium with severe hyperchromatism and pleomorphism

208
Q

What interventions other than surgery could the patient have for cancer?

A
  • chemotherapy - alkylating agents
  • radiotherapy
  • immunotherapy
209
Q

After removal of lesion how would you restore the function of the tongue?

A

By soft tissue grafting to rebuild the tongue by taking tissue from somewhere else, skin on forearm, chest, thigh and transplanting it in the tongue area to replace lost tissue.

210
Q

What is angular cheilitis?

A

It is an inflammatory skin condition that can affect the commisure of the mouth presenting as an erythmatous lesion ,

211
Q

what micro-organisms are involved in this condition?

A
  • S.aureas
  • C.albicans
212
Q

What type of sample is taken?

A

Swab of the commisure of the mouth

213
Q

What diseases make a patient more susceptible to angular cheilits ?

A

HIV - weakens the immune system making it more prone to pathogens
Crohn’s disease - impairs nutrient absorption leading to immunosuppression and therefore infection

214
Q

Name one extraoral and one intraoral disease that can be associated with angular cheilitis?

A
  • I/O - denture induced stomatitis , candiosis
    -E/O - orofacial granulomatosis
215
Q

Why is miconazole prescribed when microbiological sampling is not avaialble?

A

because it has both antifungal and antibacterial effects

216
Q

What instructions would you give to this patient regarding denture wearing? (he has angular cheilitis)

A

Clean dentures after eating and before bed with soft brush and denture cleaning solution
Clean mouth with toothpaste and soft brush or rinse with CHX mouthwash
Do not wear the denture overnight

217
Q

What is Trigeminal neuralgia?

A

pain that is usually on one side of the face described as an electrical shock type of pain that is due to demyelination or compressing of the trigrminal nerve

218
Q

What are the causes of trigeminal neuralgia

A
  • demyelination of the trigeminal nerve
  • OPT to rule out any dental cause
  • MRI
  • CT if MRI is contraindicated
219
Q

What disorders could give rise to TN?

A

Tumour compressing on the trigeminal nerve in the brain
Multiple sclerosis

220
Q

What drugs are used to manage trigeminal neuralgia?

A

Carbamazepine
Oxcarbazepine

221
Q

What tests to take before screening for carbamazepine?

A
  • FBC
  • Liver function test
  • Urea and electrolytes test
222
Q

What are the side effects of carbamazepine?

A

vomiting
confusion
nausea
allergies
Ataxia (decreased muscle tone)
sedation
Dry mouth
nightmares
dizziness

223
Q

What are the indications for surgery for carbamazepine?

A
  • medical intervention is contraindicated
  • medication causes adverse side effects
  • if the symptoms are very severe that affects the patient daily life
224
Q

What types of surgery can be preformed

A
  • microvascular decompression
  • ballon compression of trigeminal nerve
  • neuroectomy
  • radiosurgery using gamme knife
225
Q

What are the clinical signs of paget’s disease

A

bony expansion
ill fitting dentures
pain and tenderness
facial asymmetry

226
Q

Radiographic signs of paget’s disease

A

osteoporotic or osteosclerotic bone that is well defined
radiopaque lesions due to hypercementosis
radiolucent areas resembling cysts (may also occur in fibrous dysplasia)

227
Q

Cauliflower shape on labial commisure, What is this?

A

condyloma acuminatum

228
Q

What is the cause of condyloma acuminatum?

A

HPV

229
Q

What tests do you carry out for condyloma acuminatum?

A

PCR to detect DNA of HPV

230
Q

Clinical signs for condyloma acuminatum malignancy?

A

gets bigger in size
usually asymptomatic but if it causes pain it may be malignant
transforming to a firm mass

231
Q

What are the histopathological features of condyloma acuminatum malignancy?

A

Dysplasia
Atypia
hyperchromatism
pleomorphism
and architectural changes

232
Q
A

REVISION (4 decks)

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