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BDS4 EXAM PREP > oral med > Flashcards

oral med Flashcards

1
Q

keratosis

A

keratin formation in non-keratined sites

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2
Q

acanthsosis

A

hyperplasia of stratum spinosum

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3
Q

elongated rete ridges
due to

A

basal cell hyperplasia

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4
Q

atrophy

A

thinning of normal epithelium
reduction in viable cell layers

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5
Q

erosion

A

partial thickness loss of epithelium

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6
Q

ulceration

A

full thickness loss of epithelium

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7
Q

oedema

A

fluid accumulation and swelling

intracellular or intercellular (spongiosis)

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8
Q

blister

A

localised accumulation of fluid

vesicle <5mm
bulla >5mm

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9
Q

causes of chemimcal burns

A

drug induced (aspirin burns)

ingestion of bleach/strong acid

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10
Q

differential dx for white patch

A

heriditary
frictional keratosis
chemical burn
smoking kertosis
systemic lupus erythematous
chronic hyperplastic candidosis
squamous cell carcinoma
leukoplakia
lichen planus

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11
Q

heridatary white patches

2

A

white sponge naevus
fordryces spots/granules

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12
Q

white sponge naevus

features

A

heridatrary
diffuse
asymptomatic
soft unevening thickening of surface epithelium
often on non-keratinised mucosa
widespread oedema

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13
Q

fordyce spots

A

visible inactive sebaceous glands
small, raised, white/pale pink spots/bumps 1-3mm in diameter

usually around vermillon border, buccal mucosa, gentials

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14
Q

management of heriditrary white spot lesions

A

reassurance that is it not cancer

if any symptoms (unlike) advice on relief

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15
Q

causes of frictional keratosis

A

response to chronic low grade trauma
e.g.
* sharp cusps/restorations
* ill fitting denture
* cheek biting (parafunction)

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16
Q

clinical appearnce of frictional keratosis

A

white patch surrounded by erythematous inflammation

caused by reactive thickining of mucosa

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17
Q

histology of frictional keratosis

A

epithelial hyperkeratosis
acanthosis - hyperplasia of stratum spinosum
variable dysplasia
minimal infiltrate

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18
Q

how to manage frictional keratosis

A

remove souce (adjust denture, trim cusp/restoration, provide splint)

review
if no sign of healing within 2 weeks - urgent biopsy required

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19
Q

smokers keratosis

A

low grade burn and chemical irritation
usually on palate

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20
Q

smokers keratosis clincial appearnance

A

painless white keratotic layer
presence of small red spots (blocked sebaceous glands)

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21
Q

histology of smokers keratosis

A

hyperkeratosis
variable dysplasia
minimal infiltrate
underlying melanin pigmentation

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22
Q

management of smokers keratosis

A

smoking cessation

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23
Q

leukoplakia defintion

A

white patch which cannot be rubbed off or attributed to other cause

dx of exclusion

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24
Q

lichen planus histology

A

hugging band of T lymphocytes (cell mediated)
change in surface epithelium (hyperkeratosis/atrophy)
civatte bodies (apoptosed intraepithelial cells)
basal cell liquefaction
saw tooth retet ridges

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25
Q

risk of malignant transformation of lichen planus

A

1-5%

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26
Q

types of lichen planus

6

A

Reticular
Atrophic
Ulcerative/Erosive
Bullous
Plaque
Papular

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27
Q

erythroleukoplakia

A

Mixed red and white paatch

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28
Q

erythoplakia management

A

urgent biopsy
high chance of malignant potential

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29
Q

erythroplakia

A

red patch which cannot be rubbed off or attributed to any other cause

needs urgen biopsy

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30
Q

causes of pigmentation
internal

A

racial pigmentation
reactive melanosis/melanotic macule (freckle)
melanoma
systemic conditions - haemosiderin; impetigo

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31
Q

causes of pigmentation
internal

A
  • racial pigmentation
  • reactive melanosis/melanotic macule (freckle)
  • melanoma
  • systemic conditions - haemosiderin; impetigo; ADDISONS; Peutz-jejgers syndrome
  • pigmentary incontinence
  • kaposis sarcoma
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32
Q

causes of pigmentation
extrinsic

A
  • tea,coffee,CHX
  • bacterial overgrowth
  • metals - amlagam
  • smoking
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33
Q

macule appearance

A

usually solitary
<1cm in diameter
well defined
flat border
commonly lower lip, freckle like

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34
Q

melanocytic naevus
appearance
management

A

common on vermillon border and palate
can be >1cm
no change in size or colour

monitor, biopsy if concerned
reassure and review

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35
Q

syndromes associated with multiple naevi

2

A

peutz-jehers syndrome
* benign polyps in GIT and multiple small peri-oral naevi

gorlin-goltz syndrome
* multiple odontogenic Keratocysts and basal cell carcinomas

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36
Q

kaposi sarcoma is linked to

A

HHV-8 and HIV2

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37
Q

clinical appearnce of kaposis sarcoma

A

red/purple
individual or groups
flat or raised, slow progression

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38
Q

risk factors for kaposi sarcoma

A

immunosuppression
chronic lympodema

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39
Q

management of kaposi sarcoma

A

biopsy
surgery
radio and chemotherapy
biologics
HAART

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40
Q

clinical red flags for malignant melanoma

A
  • change in size, shape, colour (very dark)
  • itchy
  • skin breakdown
  • bleeding
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41
Q

causes of oral malignant melanomas

A

unknown/idiopathic
UV on skin of lips

secondary melanosis
* smoking
* drug related
* inflammation
* addisons disease/adrenal insufficiency

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42
Q

drugs which can lead to infection

A
  • antifungals
  • steroids
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43
Q

drugs linked to licheniod reactions

A
  • ACE inhibitors
  • beta blockers
  • diuretics
  • nifidepine
  • NSAIDs
  • anticonvulsants
  • omeprazole
  • tetracycline
  • oral hypoglyceamics
  • antimalarias
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44
Q

drugs which can cause ginigval hyperplasia

A
  • phenytoin
  • cyclosporin A
  • nifidipine
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45
Q

drugs which can cause oral pigmentation

A

antimalaraias
phenothiazines
hydroxychloroquinone
CHX
OCP
cisplatin

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46
Q

drugs which can cause oral pigmentation

A

antimalaraias
phenothiazines
hydroxychloroquinone
CHX
OCP
cisplatin

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47
Q

drug which can cause characteristic oral ulceration

A

nicorandil - angina

large, deep, persistent ulcers that have punched out edges

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48
Q

haemagioma

A

benign vascular tumour derived from blood vessel cell types

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49
Q

types of haemangioma

A

cavernous
capilllary

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50
Q

cavernous haemangioma

A

larger
encapsulated
dilated vascular space

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51
Q

capillary haemangioma

A

not encapsulated
thin walled capillaries

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52
Q

sturge weber syndromes

A

associated with vascular malformation
port wine stain that runs in distribution of CNV

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53
Q

lymphangioma

A

malformation of lymphatic system characterised by thin walled cyst lesion
commonly <2yrs old

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54
Q

geographic tongue

A

common, benign, inflammatory condition
1-2% adults
unknown aetiology

rapid appearance and disappearance, can change

areas of atrophic (red) and white keratotic areas with demarcated borders on dorsal surfaces of tongue with temporary loss of filiform papullae (depapillation)

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55
Q

clinical appearnce of geographic tongue

A

areas of atrophic (red) and white keratotic areas with demarcated borders on dorsal surfaces of tongue with temporary loss of filiform papullae (depapillation)

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56
Q

management of geographic tongue

A

dietary avodiance (hot,spicy foods, SLS)
sytomatic relief - benzydamine mouthwash

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57
Q

histology of geographic tongue

A

central lesion erosion and hyperkeratosis
chronic inflmmatory cells underlying connective tissue

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58
Q

causes of glossitis

A

vitamin/nutritional deficiencies
haematological deficiencies

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59
Q

clinical appearance of glossitis

A

loss of papullae
smooth red shiny dorsal surface

lobulated if severe
beefy tongue if haemaotological cause

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60
Q

management of glossitis

A

correct any underlying def
symptomatic relief

s

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61
Q

coated tongue
causes
management

A

build up of normal cellular debris on dorsal surface

dehydration, illness, poor diet

removal with abrasive instruement
correct underlying cause

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62
Q

possible tissue conditions due to dentures

A

chronic erythematous candidosis
leaf fibroma
papullar hyperplasia

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63
Q

osteogenesis imperfecta

A

type 1 collagen defect

features: blue sclera; weak bones; multiple easy fractures; dentinogenesis imperfecta

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64
Q

pathophyisiology of osteoporosis

A

bone atrophy - resorption occurs more than formation leading to endosteal net loss (quantitis deficiency)

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65
Q

bone consequence of hyperparathyroidism

A

osteitis fibrosa cystic (brown tumour)

giant cell lesion within the bone (bone swelling)
will regress if hyperparathyroidism is appropriately treated

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66
Q

histological appearance of hyperparathryoid bone lesions

A

multinucleated giant cells
haemosiderin
cystic cavities

osteitis fibrosa cystica (brown’s tumour)

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67
Q

primary herpetic gingivostomatitis
clinical features

A

widespread shallow vesicles - burst to form ulcers
gingival erythema
fever, malaise, halitosis, enlarged tender lymph nodes

primary HSV infection

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68
Q

primary herpetic gingivostomatitis
clinical features

A

widespread shallow vesicles - burst to form ulcers
gingival erythema
fever, malaise, halitosis, enlarged tender lymph nodes

primary HSV infection

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69
Q

management of primary herpetic gingivostoomatisis

A

self limiting
benzydamine spray
bed rest
analgesia
fluids

if child unable to eat/drink - hospital

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70
Q

pathogenesis of recurrent HSV

A

reaactivation of primary infeciton which is belived to lie dormant in dorsal root of trigeminal ganglia CNV3

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71
Q

oral presentation of recurrent HSV

A

herpes labalis - crop of blisters on lip

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72
Q

causes of recurrent HSV activation

A

trauma
sunlight
stress
immunocompromised/illness

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73
Q

disease progression of HSV

A

prodromal phase - burning/tingling
3-4 days before cold sore appearnce

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74
Q

management of HSV

A

High dose acyclovir during periods of acute infection (cream during prodromal phase),
long term low-dose acyclovir (prophylactic)
fluids, analgesia

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75
Q

varicella zoster virus
what are clinical presentations

A

Varicella - primary infection (chicken pox)
Zoster - reactivation of latent virus from sensory ganglion (shingles)

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76
Q

clinical appearance of varicella

A

Centripetal rash, fully body cutaneous spots, itchy, prone to bleeding
chickn pox

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77
Q

clinical appearance of zoster

A

Confined to distribution of nerve it remains dormant in.
Unilateral lesion, never crossing midline, sometimes CN V.
Painful vesicles, rupture to ulcers, crusting, scarring, pigmentation

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78
Q

EBV causes
clinical appearance

A

infectious mononucleosis

sore throat, generalised lymphadenopathy, fever, headaches, malaise, maculopapular rash

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79
Q

group A coxsackie causes

2

A

herpangina
hand, foot and mouth disease

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80
Q

clinical appearance of herpangina

A

wide spread small (pinhead) ulcers on uvula, palate, fauces
fever
sore throat
conjunctivitis

coxsackie group A

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81
Q

clinical appearance of hand, foot and mouth disease

A

papular, vesicular rash on hands and feet
oral vesicles which rupture into superficial painful ulcers (widespread, pinhead)

like herpangina but hands and feet affected too

coxsackie group A

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82
Q

EBV herpes number

A

4

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83
Q

syphillis appearance

primary secondary tertiary

A

Chancre - painless ulcerated nodule at site of inoculation, cervical lymphadenopathy

Cutaneous rash, condylomata, sensitive sloughy mucosa, serpiginous ulceration, malaise, fever, weight loss

Gumma - necrotic granulomatous reaction, enlarges and ulcerates, multi system disorder

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84
Q

how does oral candidosis occur

A

disease of diseased

Altered regulation of oral microflora, some commensal organisms eradicated allow others to flourish, overgrow and become pathogenic

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85
Q

examples of candidal species

A

c.aureus
c.albicans
c.tropicalis
c.krusei
c.glabrata

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86
Q

virulence factors for candida

A

hyphae
adherence
extracellular enzymes

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87
Q

stain needed for candida

A

PAS

doesnt show up well on H&E

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88
Q

types of candidosis

5

A

acute pseudomembranous
chronic erythematous
chronic hyperplasia
chronic atrophic
chronic mucocutaneous

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89
Q

acute pseudomembranous candidiosis appearance

A

white plaques, lightly adherent, can be rubbed off, discomfort eating, burning sensation, bad taste

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90
Q

clinical appearance of erythematous candidosis

A

atrophic mucosa, shiny red appearance

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91
Q

causes of pt becoming suscpetible to candida infection

A

denture
antibiotic stomatitis
indwelling cather
dry mouth/smoking/polypharmacy
post surgery

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92
Q

clinical appearance of chronic hyperplastic candidiasisi

A

white, nodular patches
on buccal mucosa, dorsum of tongue or oral commisures

unilateral or bilateral

biopsy - PMD

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93
Q

denture induced stomatitis
term

A

chronic erythematous stomatitis

wide spread erythema on mucosal surfaces underlying denture fitting surface
asymp or burning sensation/bad taste

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94
Q

denture induced stomatitis
term

A

chronic erythematous stomatitis

wide spread erythema on mucosal surfaces underlying denture fitting surface
asymp or burning sensation/bad taste

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95
Q

tx of chronic erythematous stomatitis denture induced

A

denture hygiene advice

topical antifunglas - miconazole or nystatin
CHX Mouthwash
reline or remake denture

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96
Q

classification of chronic erythematous candidiasis

Newtons

3 types

A

type I - localised inflammation
type 2 - diffuse erythema
type 3 - granular inflammation

97
Q

example of chronic atrophic candidosis

A

median rhomboid glossitis on tongue

flat midline area on dorsal posterior area of tongue
nodular, red/pink depapillation

98
Q

pathogens involved in angular cheilitis

A

staphlycoccus aureus
candida albicans

99
Q

angular cheilitis appearnce

A

red cracked skin at angles of mouth

100
Q

causes of angular cheilitis

A

inadqequate denture vertical dimension
trauma
vitamin def (iron, B12)

101
Q

dx for candida by

A

oral swab for angular cheilitis
oral rinse for intra oral

102
Q

antifungal types

A

Polyenes - nystatin
Azoles - fluconazole

103
Q

polyene antifungal
mech of action

A

fungicidal
Directly target ergosterol in cell wall, causing perforation and leakage of intracellular contents

nystatin

104
Q

azole antifungal
mech of action

A

fungistatic.
Target ergosterol in cell wall by interrupting activity of enzyme involved in its production, 14a demethylase. risk of resistance (krusei and glabrata are naturally resistant)

micronazole, fluconazole

105
Q

how common in minor RAU

A

up to 25% population

106
Q

minor RAU characteristic

A

small <5mm
1-20 in crops of ulcers
non keratinised mucosa
red halo surrounding yellow fibrin base
heal within 1-2 weeks without scarring
commonly recur

107
Q

how common is major RAU

A

10% of all RAS

108
Q

characteristics of major RAU

A

> 10mm in diameter
oral or irregular, red halo with yellow fibrin base
<5 per crop
keratinised or non mucosa
scar on healing
take longer to heal (6-12 weeks)

109
Q

how common is herpetiform RAU

A

5% of all RAU

110
Q

clinical appearance of herpetiform RAS

A

<5mm
round or oral often coincide with larger ulcers
1-200 per crop
non- keratinising mucosa
heal in 1-2 weeks without scarring

111
Q

bechets ulcers

A

numerous oral uclers
part of multisystem ulceration/pathology auto immune

112
Q

managment of Bechets

A

MDT (derm, OM, rheum, ophth, etc.).
Symptomatic relief, sometimes anti-TNF therapies

113
Q

causes of RAU

A

genetic - Bechets, SLE, erythema multiforme
nutritional def - haem
systemic disease - GI, AIDs
endocrine imbalance - pregancy
immunocompromised - HSV recurrent
environmental
allergy

114
Q

4 types of hypersensitivity reaction

A

Type I - IgE mediated
Type II - cytotoxic
Type III - immune comple
Type IV - cell-mediated

115
Q

examples of local immunological oral diseases

A

recurrent aphthous stomatitis
lichen planus
OFG
SLE

116
Q

systemic immunological diseases with oral manifestation

A

erythema multiforme
sjoregns
SLE
systemic sclerosis
pemphigus
pemphigoid

117
Q

methods of dx immune mediated diseases

A

biopsy for histological analsysis
direct immunofluorescence

118
Q

vesicle

A

<5-10mm diameter

119
Q

bullae

A

> 5-10mm diameter

120
Q

dermatits herpetiformis is associated with

A

gluten sensitivity

121
Q

examples of vesiculobullous diseases

A

pemphigoid
pemphigus
angina bullos haemorrhagica
linear IgA disease
dermatitis herpetiformis
epidermolysis bullosa

122
Q

what is angina bullosa haemorrhagica

A

formation of blood blosers in the absene of trauma
palate

123
Q

desquamative gingivitis

A

clinical descriptive term for full thickness gingivitis
often with clear distincition between inflamed and non inflamed mucosa

124
Q

desquamative gingivitis
seen in

A

erosive lichen planys
mucous membrane pemphigoid
pemphigus vulgaris
erythema multiforme
SLE

125
Q

erythema multiforme
type of hypersensitivity reaction
aetiology

A

type III

idiopathic
50% have trigger - drugs (NSAIDs, carbmazepine, penicillin), infection, pregnancy, UV, chemicals

126
Q

erythema multiforme
appearance

A

target lesions - concentric erythemaotus rings on palms, legs, face, neck, lips, anterior mouth
crops of bullae, burst to ulcers
crust and heal in 2 weeks
fever often

127
Q

management of erythema multiforme

A

self limiting
steroids
aciclovir
fluids
analgesia

128
Q

erythema multiforme associated with

A

Stenven Johnson syndrome

129
Q

clinical appearnce of pemphigoid

A

thick walled blisters

can be fluid or blood filled

full epidermis (sub-epithelial split)

130
Q

types of pemphigoid

3

A

mucous membrane
cicatricial
bullous

131
Q

aetiology of pemphigoid

A

autoimmunity against hemidesmosomes in basal cell layer

132
Q

possible complications of cicatricial pemphigoid

A

scarring of eyes - can cause blindness or other ocular damage
(symblepharon)

133
Q

histopathology of pemphigoid

A

sub epithelial antibody attack
* demoglein destroyed by antibodies

HEMIDESMOSOMES targeted
* loss of attachment between basal cell layer and underlying lamina propria

space gets filled with fluid

full thickness separation of epithelium

134
Q

direct immunofluorence of pempigoid

A

linear
IgG and C3 often present in basement membrane

135
Q

tx for pemphigoid

A

refer
steroids and immunomodulators (azathioprine)

136
Q

pemphigus types

A

vulgaris
IgA
familia benign chronic
foliaceus

137
Q

pathogensis of pemphigus

A

formation of autoantibodies (IgG, C3) against DESMOSOMES involved in cell-cell adhesion (dsg-1, dsg-3)
causing intra-epithelial separation above basal cell layer

138
Q

clinical appearance of pemphigus

A

oedema
intra-epithelial blisters
rupture to leave white friable mucosa
red erosive areas

139
Q

histological features of pemphigus

A

desmosomes target at periphery of spinous cell layer - INTRA EPITHELIAL split (supra basal)

tzank cells

acanthosis

140
Q

direct immunofluorescence appearnce of pemphigus

A

basket weave appearnce

141
Q

tx for pemphigus

A

refer

systemic steroids
azathriopine
ritzimab (biologics)

142
Q

risk of maligannt transformation with leukoplakia

A

under 5%

143
Q

hsitological predictors/features of mlaignant change

3

A

epithelial dysplasia
architectural changes - abnormal maturation and stratification
cytological abnormalities - cellular atypia

144
Q

hsitological predictors/features of mlaignant change

3

A

epithelial dysplasia
architectural changes - abnormal maturation and stratification
cytological abnormalities - cellular atypia

145
Q

dysplasia

A

disordered maturation of tissue (growth)

146
Q

grades of dysplasia

A

epithelial hyperplasia
mild
moderate
servere
carcinoma in situ

WHO 2005

147
Q

mild dysplasia features

A

chnages in lower third of epithelium
mild celllular atypia

148
Q

moderate dysplasia features

A

changes in middle third of epithelium
moderate cellular atypica

149
Q

severe dysplasia

A

changes in upper third of epithelium
severe cellular atypia

150
Q

signs of cellular atypia

A

hyperchromatism
pleomorphism
change in size/number
mitotic bodies in epithelium, not just in basal layer

151
Q

features of carcinoma in situ

A

malignant but not invasive - abnormal architecture, pronounced cytological atypia

152
Q

histological features of dysplasia

7

A
  • increased and abnormal mitotic bodies (higher position, abnormal form)
  • nuclear and cellular pleomorphism (different size and shape),
  • abnormal keratinisation (below normal keratin layer, keratin pearls),
  • nuclear hyperchromatism - prominent and enlarged nuclei
  • basal cell hyperplasia - elongated/drop shaped rete ridges
  • distrubed basal cell polarity/loss of cellular orientation
  • irregular epithelial startification or distrubed maturation
  • reduced/lost intercellular adhesion
153
Q

high risk sites for oral cancer

A

lateral border of tongue
FoM
retromolar areas
soft palate

154
Q

risk factors for oral cancer

A
  • smoking - cigarette, betel quid
  • alcohol (synergistic with smoking)
  • previous SCC
  • first degree relative with OSCC
  • poor diet
  • low socioeconomic status
  • viruses - HPV 16+18, EBV
  • poor OH
155
Q

6 hallmarks for carcinogenesis

A

Self-sufficient in growth signals
Limitless replication potential
Insensitivity to anti-growth signals
Tissue invasion and metastasis
Evading apoptosis
Sustained angiogenesis

STILES

156
Q

cancer genetics

A

Molecular basis of cancer
* damage - inactivated, useless or over/under express
* altered gene expression - Gene responsible for protein which has a function
* altered cell function - if gene expression is changed and target for protein (function) is changed causes alteration in cell function

Oncogenes e.g. tumour suppressor genes (p53 mutation/inactivation)
* aneuploidy, translocation, amplifications
dysregulation of apoptosis and DNA repair

field change theory for tissue - not just PML

157
Q

red flags for OSCC

A
  • persistent (>2wk) ulcer despite removal of obvious cause,
  • rolled margins,
  • necrotic (firm) centre (indurated, inflamed, granular base, raised edges),
  • speckled leukoplakia/non-homogenous
  • weight loss,
  • dysphagia,
  • worsening pain (neuropathic, dysaesthesia, paraesthesia),
  • referred pain (ear, throat, jaw),
  • cervical lymphadenopathy (enlarged >1cm, firm, fixed, tethered, non-tender)
158
Q

histological patterns for OSCC invasive front

4 types; 2 fronts

A
  • Local,
  • perineurial,
  • lymphatics,
  • haematogenous (lungs, spine, bone).

Cohesive or non-cohesive front (linked with nodal spread)

159
Q

factors for OSCC prognosis

7

A
  • Site,
  • size,
  • depth of invasion,
  • disease spread,
  • comorbidities,
  • neck metastasis (contralateral and unilateral),
  • extra capular spread
160
Q

TMN staging

A

T - tumour
M- metastasis
N - nodes

161
Q

T stages

A

T1 - <2cm
T2 - 2-4cm
T3 - >4cm

162
Q

N stages

A

N0 - no clinically positive nodes
N1 - single ipsilateral node <3cm
N2 - single ipsilateral node 3-6cm or multiple nodes <6cm
N3 - any node >6cm

163
Q

M stages

A

M0 - no distant mesatasis
M1 - distantn mesatasisi

164
Q

OSCC management options

A

Resective surgery,
radiotherapy,
chemotherapy,
radiochemothearpy
immunotherapy

Curative intent, palliative, best-supportive care

165
Q

possible causes of neck lumps

6

A
  • head and neck cancer
  • infection/reactive - abscess, pericoronitis, tonsilitis, glandular fever
  • lymphoma
  • skin swellings
  • arterial (carotid aneurysm)
  • bone issue
166
Q

clinical presentation of reactive lymph nodes

A

large (diffuse)
tender
inflammed
erythematous surface
soft
mobile
hot

167
Q

clinical presentation of metastatic nodal disease

A

large
firm
fixed/tethered to underlying tissue

168
Q

clinical presentation of lymphoma nodes

A

large
rubbery
tethered

169
Q

aetiology of lichen planus

A

Chronic immunological, cell-mediated (type IV) reaction.
Autoimmune condition mediated by a T lymphocyte attack on stratified squamous epithelium

170
Q

commonly affected intra oral sites for lichen planus

A

buccal mucosa
gingivae
tongue (dorsal/ventral)
lips

171
Q

skin lichen plnaus

A

itchy lesions (shiny red/purple papules)
interlaced by wickham’s straie (white lacy lines) on flexor surfaces

172
Q

lichenoid reaction

A

known cause

e.g. amalgam, medications (ACE inhibitors, b-blockers, NSAID, diuretics, nifedipine)

173
Q

reticular lichen planus

A

bilateral on buccal mucosa
white lacy like lines, spider web appearance

174
Q

erosive (ulcerative) lichen planus

A

oral ulcers,
presistent irrgeular areas of erythema

assoc with desquamative gingivitis

175
Q

papular lichen planus

A

small white asymptomatic pinpoint papules

176
Q

palque lichen planus

A

large homogenous white pathces
resembles leukplaksia

common in smokers

177
Q

palque lichen planus

A

large homogenous white pathces
resembles leukplaksia

common in smokers

178
Q

atrophic lichen planus

A

common to erosive

atrophic lesions on backgound of eythema with radiating white striae at margins

179
Q

bullous lichen planus

A

rarer.
Fluid-filled vesicles (white or grey/purple, fluctuant) that rupture easily, leave ulcerated surface.
Fluid is usually clear but may be haemorrhage or purulent

180
Q

histology of lichen planus

5

A
  • Keratinisation/keratosis of surface epithelium (hyperkeratosis - usually orthokeratosis),
  • acanthosis (hyperplasia of underlying epithelium, especially spinous cells) - elongated rete ridges with saw-tooth appearance,
  • thick sub epithelial ‘hugging’ band of T lymphocytes (blue band of chronic inflammatory cells under epithelium and following contour),
  • occasionally epitheliotropism (inflammatory cells drawn up into epithelial layer),
  • apoptosis (of basal cell layer - cells surrounded by clear halo),
  • destruction of basal cell layer
181
Q

lupus
what is it
types

A

connective tissue autoimmune disease

SLE (mutisystem), chronic discoid (limited to skin and mucosa)

182
Q

clinical appearance of SLE

A

skin leasiosn - butterfly zygomatic rash
oral mucosal lesions (palate - ulcers, purport, red/white striae)
antinuclear antibodies
arthritis
anaemia

may have disc like white plaues intra orally

need topical steroids and disease modifying drugs

183
Q

OFG hypersensitivty reaction

A

Type IV (sometimes type I) hypersensitivity to food additives; unknown aetiology.

184
Q

pathogensis of OFG

A

Characterised by non-caseating granulomatous inflammation.
Lymphatic obstruction from giant cell granulomas, accumulation of tissue fluid

185
Q

difference between OFG and Crohns

A

if systemic symptoms more likely to be crohns

186
Q

clinical fearures of OFG

7

A
  • Angular cheilitis,
  • buccal mucosa cobblestoning,
  • mucosal tags,
  • aphthous-pattern ulceration (or other types) - esp linear in depth of buccal sulcus
  • swollen lips, cheeks and gingivae (full-width gingivitis),
  • gingival erythema,
  • FoM oedema - stag horning
187
Q

histology of OFG

4

A
  • non caseating granuloma formation
  • giant cell formation
  • inc tissue fluid production between Connective tissue - causing separation of connective tissue
  • lymphatic obstruction and oedema fluid build up
188
Q

dx and managment of OFG

A

dx of exclusion
* allergy past test
* test for coelic - blood tests transglutaminase, faecal calprotectin

try dietary exlusion - cinnamon aldehyde, SLS, benzoates
steroids, disease modifying drugs, biologics, anti-TNF therapies

189
Q

types and pathogenesis of Pagets disease

A

monostotic or polystotic

maxilla in pagets disease due to over activation of osteoclasts and osteoblasts
* Paget’s disease 3% of routine autopsies
* Mainly inc age and male

replacement of normal bone by remodelling by a chaotic alteraion of resorption and deposition
* causes inc bone

190
Q

symptoms of paget’s disease

A

often asyptomatic
frontal bossing (dentures and hat no longer fit)
headaches
hearing disturbance

191
Q

radiographic appearance of pagets disease

A

Cotton wool appearance
hypercementosis of teeth

192
Q

histology of pagets

A

increased bone turnover so osteoclastic and osteoblastic activity

193
Q

fibrous dysplasia
what it is
symptoms

A

slow growing asymptomatic swelling
active in those <20years
area of bone replaced by fibrous connective tissue

mono or polystotic

194
Q

radiographic appearance of fibrous dysplasia

A

orange peel/ground glass appearance
ill defined margins between affected and unaffected bone

195
Q

histology of fibrous dysplasia

A

bone appears metaplastic or woven but will remodel and inc in density

196
Q

fibrous dysplasia associated with

A

Albright syndrome
- melanotic navi
- odontogenic keratocysts
- fibrous dyplias
- early puberty

197
Q

causes of dry mouth

A

Polypharmacy/drugs, alcohol, smoking, radiotherapy, chemotherapy, poorly controlled diabetes, Sjogren’s, psychogenic

198
Q

dx of dry mouth

A

unstimulated salivary flow rate <1.5ml in 15mins

199
Q

issues dur to dry mouth

A

swallowing issues
issues in speech
dyseasethesia/pain or brunding mouth
alteraed taste
non retentive dentures
inc dental disease - caries, perio
halitosis

200
Q

mucocele

A

swelling, bluish translucent colour, soft/fluctuant

can be mucous extracastaion or retention cyst
due to trauma to duct or minor salivar gland

201
Q

common sites for mucoceles

A

lower lip
palate
buccal mucosa
tongue
FoM - ranula

202
Q

histology of mucocele

A

cystic cavity containing saliva, wall of granulation tissue, macrophage lining

203
Q

tx for mucocele

A

excision with damaged gland and duct

204
Q

types of sjogrens

A

primary - no associated CT disease
secondary - associated with CT disease (e.g. SLE, RA, systemic sclerosis)

205
Q

dx criteria for sjorgrens

A

modified european - 4+ crieteria (inc 5 or 6)

1 and 2. Dry eyes subjective/objective - dry for >3mths, recurrent sensation of gravel in eyes, tear substitutes >3 times/day
3 and 4. Dry mouth subjective/objective - for >3mths, reduced unstimulated flow rate, liquid to swallow dry food
5-Anti-Ro, anti-La autoantibodies (bloods)
6- Positive labial gland biops

206
Q

histological features of sjorgrens

A
  • more than one duct with 50+ lymphocytes (llymphocytic foci)

lymphotcytes cause
* acinic atrophy
* hyperplastic ductal epithelial

207
Q

consequences of sjogrens

A

caries
oral infection
poor Oral healthy QoL

208
Q

management of sjorgrens

A

sugar free gum
regular sips water
high F toothpaste
salivary substituties - biotene oral balance

209
Q

sicca syndrome

A

dry mouth only
partial sjogrens

210
Q

subacute obstruction

A

swelling associated with meals, slowly progressive and then eventually fixed and paiful

due to sialoliths or muccous plugs

211
Q

causes of hypersalivation

A

stroke, MS , Parkinsonos, perceived

212
Q

sialenditis

A

inflammation of major salivary gland

due to obstruction (stone, stricture) or bacterial (s.aureus)

removal obstruction, FNA and ABX, gland removal

213
Q

sialenditis

A

inflammation of major salivary gland

due to obstruction (stone, stricture) or bacterial (s.aureus)

removal obstruction, FNA and ABX, gland removal

214
Q

parotiditis

A

Bacterial infection, common in children, resolves by puberty

215
Q

Freye’s syndrome
tx

A

syndrome involving duct and gland fistula (EO saliva leakage)

Botox, excision of duct, gland removal, propantheline before food (reduce salivary flow), scolopaline patches

216
Q

sjorgen
sialograpy
US

A

snowstrom due to destruction of acini

leopard spot on US

US as no radiation

217
Q

salivar gland most likely to get neoplasma
and % malignant

A

parotid 80% (15% malignant)

218
Q

neoplasma in salivary gland
likelihood of location

A

parotid 80% (15% malignant)
submandibular 10% (30% malignant)
minor 10% (45% malignant)
sublingual 0.5% (80% malignant)

219
Q

salivary gland neoplasma symptoms

A

localised swelling, painless
slow growing
well defined
neuro changes (CNVII involved)

220
Q

most common neoplasm is salivary gland

A

pleomorphic salivary adenoma (75%)

221
Q

histological features of pleomorphic salivary adenoma

2

A

incomplete capsule
foam cells (macrophages that have engulfed mucin)
mixed

222
Q

management of PSA nad issues

A

wide local excision

high recurrnece - due to incompleted capsule
5% risk of maligannt

223
Q

Warthin tumour

A

most commonly parotid
15%
can be multiple or bilateral - unsual features

have cystic spaces, distincitive epithelium, lymphoid tissue, complete capusle

tx by excision

224
Q

salivary gland carcinomas
how common
2 most common types
sites

A

15% of all salivary neoplasms

adenoid cystic carcinoma
mucoepidermoid

**minor salivary glands **

225
Q

mucoepidemoid carcinomas

A

3-5%
minor glands

have 2 cell types
* squmous - epidermoid
* glandular - glandular

unpredictable behaviour and spread

226
Q

adenoid cystic carcinoma

A

slow growing, painless, can ulcerate - pain

varied patterns
* cribiform - swiss cheese
* tubular
* solid

local spread - blood and nerves

difficult to tx - close to vital structures and recurrence; poor long term prognosis

227
Q

trigeminal neuralgia symptoms

A

*(Associated with MS and Brain Tumour) - MRI needed esp young *

severe sudden onset pain (paroxysmal),
* electric shock
* lasts for a few seconds,
* may be associated with lacrimation;
* Trigger spots in 1/3 of pts.

follows unilateral side of trigeminal nerve branch(es), Very rarely bilateral.

228
Q

trigemenial neuralgia casues

3

A
  • idiopathic
  • classical - vascular compression of CNV (MRI)
  • secondary - MS; space occupying lesion
  • others - skull base defomity, CT disease, atreriovenous malformation
229
Q

aetiology of trigeminal neuralgia

A

damage or irritation to nerve
* CNV ischaemia, distoration of myelin sheath so interrupt or altered electrical conductivitvity

230
Q

invesigation for trigeminal neuraligia

A

rule out odonogenic source of pain

MRI - assess focal demyelination on peripheral nerve and/or abberant intra craniall artery

FBC - carbmazepine has blood side effects so will need baseline

231
Q

TN ref flags

3

A

young pt (>40years)
sensory deficit in facial region - hearling loss
other cranial nerve lesions

ALWAYS TEST CRANIAL NERVES
ALL PTS NOW GET MRI

232
Q

management of TN

A

medications
* 1st line: carbmazepine/oxcarbazepine/lamotrigine
* 2nd line: gabapentin/ pregablin/phenytoin

surgery
* only if pt not managing on medications (side effects too much)
* younger pt - will need to be on drugs for long time

233
Q

surgical otpions for TN

A

**microvascular decompression **

destructive central procedures
sterotactic radiosurgery
destructive peripheral nerectomies

234
Q

medication for TN

A

should be responsive to carbmazepine (if tolerated)
* alter dosing regime to maximise efficacy with minimial side effects
* pain diary helpful

235
Q

carbazepine side effects

A

Blood dyscrasias
* Thrombocytopenia
* Neutropenia
* Pancytopenia

Electrolyte imbalances (hyponatreamia) – careful if pt on diuretic, PPI (omeprazole)

Neurological deficits
* Paraesthaesia
* Vestibular problems

Liver toxicity

Skin reactions (including potentially life threatening)

236
Q

cluster headache

A

attack
* restless, agitated - diff from migraine
* rapid onset and cessation of pain
* mainly oribital and temporal pain
* sharp throbbing
* 1-6 per day

bout
* attacks cluster into bouts with periods of remission
* attack circadian rhythm

abortive= sumatriptan; prevntative=topiramate

237
Q

paroxysmal hemicrania

A

10% can be precipitated by bending or rotating head
80% chronic, 20% episodic

sharp throbbing
duration 2-30mins
2-40attacks per day (no circadian rhythm)

absolute response to indomethacin (prophylaxis)

alt med - COXII inhibiotrs, topiramate

238
Q

fibrous dysplasia
what it is
symptoms

A

slow growing asymptomatic swelling
active in those <20years
area of bone replaced by fibrous connective tissue

mono or polystotic

239
Q

polyene antifungal
mech of action

A

Directly target ergosterol in cell wall, causing perforation and leakage of intracellular contents

nystatin

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