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Oral medicine > Oral mucosa and histology > Flashcards

Oral mucosa and histology Flashcards

1
Q

Important details to get when doing a history and why

A

Pre-exisiting/underlying conditions, medical history, medications, family history, chronic illnesses - all can affect oral presentations and management options

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2
Q

Special tests/investigations for oral medicine

A 
Biopsy
Imaging
Sialometry (saliva)
Shirmers (eye)
Blood tests
Swabs/smears/oral rinses
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3
Q

Different types of oral samples

A

Biopsy
Aspirate
Plain swab
Rinse

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4
Q

What is an aspirate sample/how do you take it

A

Inject into an abscess/something similar and get some pus - better because keeps the bacteria in the natural environment.

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5
Q

Different types of biopsies and details

A

Fine needle aspirate
Core needle biopsy - similar to FNA but a bigger tissue sample
Incisional - when you don’t have clear margins, don’t know how to manage, large diffuse lesions.
Excisional - small, clear margins.
Punch biopsy - but gives you a circular sample which is hard to orientate

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6
Q

How to take a plain swab sample

A

If on dry tissue - moisten with saline solution

If on abscess/wet tissue - use dry

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7
Q

What kind of samples would you take of a pus lesion

A

Plain swab sample or fine needle aspirate

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8
Q

What kind of samples would you take for mucosal/skin lesions

A

Biopsy
Plain swab
Smear/rinse

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9
Q

What kind of biopsies are GDPs NOT meant to do

A

If malignant or pre-malignant lesion, bone biopsies

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10
Q

What is an abscess/how to diagnose

A

Pus filled cavity
Fluctuant swelling, painful.
No Xrays needed usually bc takes 7-10 days for it to show on xray. Can sometimes be shown as widening of PDL space and loss of lamina dura

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11
Q

Treatment of acute infections/abscesses - general/systemic

A

Drainage
antibiotics. IV for systemically unwell/septic patients.
Broad range -> narrow when you’ve done cultures
Usually amoxicillin/metronidazole combo
NSAIDs, analgesics

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12
Q

Local measures for abscesses

A 
Drainage;
- LA not into the abscess but on the mucosa overlying
- horizontal incision
- open and drain
Warm saltwater rinses for 24h after
Antibiotics to stop spread of infection
Remove cause
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13
Q

Microbial aetiology:

Dento-alveolar abscess

A

Black pigmented anaerobes/ anaerobic cocci e.g. Prevotella, Pepto-streptococcus
Eurobacteria
Fusobacteria
Spirochaetes e.g. treponema/ T. denticola

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14
Q

Periodontal abscess and Microbial aetiology

A

Periodontal pockets become occluded and infected/secondary infection of lateral periodontal cyst.

Xray will show radiolucency on lateral aspect of root

Tx = Drainage and debridement

Same bacteria as chronic periodontitis + candida

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15
Q

Streptococcal gingivostomatitis and Microbial aetiology:

A

Inflammation and pain of gingiva
Can cause fasciitis, rheumatic heart failure and tissue destruction
Treat w penicillin
Bacteria = Strep. pyogenes, viral and drug causes so needs lab sampling.

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16
Q

Acute ulcerative gingivitis and Microbial aetiology:

A

Ulceration, pain and destruction of interdental papilla. Halitosis, malaise, lymphadenopathy.

Microbes:
Anaerobic cocci, black pigmented anaerobes (prevotella) spirochaetes (treponema) fusobacteria. Worsened by smoking, stress, poor OH.
Needs debridement and antibiotics

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17
Q

Cancrum oris/Noma and Microbial aetiology:

A

South african and south asian. High mortality rate.
Usually preceded by ANUG, or previous illness/parasitic infection (measles, malaria, TB), malnutrition, immuno-suppression.

Prevotella, T. denticola, fusobacterium

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18
Q

TB in oral cavity and Microbial aetiology and investigations

A

cough, lymphadenopathy, ulcers on tongue, delayed healing after XLA and can have osteomyelitis.
Investigations = Zeil Neilson stain of biopsy, Lowenstein Jenson culture, PCR/T cells serology and look at histology - giant cells, caseation, epithelioid granulomas.

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19
Q

Syphillis stages and effects on oral cavity

A

Caused by treponema pallidum spirochaetes.

Primary = ulcers, painless oedema, lymphadenopathy, lesions on lip or tongue.

Secondary = rashes on palm of hands and feet, lymphadenopathy, snail track ulcers on lip. 6 weeks after initial lesions heal

Tertiary = firm necrotic centre surrounded by inflammation on tongue, tonsils and palate. Leukoplakia on tongue which increases chance of oral cancer.

Congenital = concave incisor edge, multi-crowned molars.

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20
Q

Gonorrhoea in oral cavity

A

Neisseria gonorrhea.
Can affect any part of oral mucosa and pharynx.
Lymphadenopathy, ulcers, pseudo-membranes, pain, oedema.

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21
Q

Acintomycosis and Microbial aetiology:

A

Large lump under angle of mandible. Can be secondary to trauma e.g. broken jaw. Slow growing and walled off so needs drainage, debridement and antibiotics.

Caused by Acintomyces Oris and A. Isreali.

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22
Q

Acute bacterial sialadenitis - what it is, symptoms, microbial aetiology and treatment

A

ascending infection of parotid/Wharton’s (submandibular) duct. Can be due to blockage, or Sjogrens, drugs or infection.

Causes trismus, red painful swelling, pus released by duct. Unilateral.

Treat w antibiotics e.g. amoxicillin.

Bacteria = anaerobic strep, staph aureus.

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23
Q

Angular chelitis - what is it, treatment, causes

A

Fungal/bacterial infection at lip commissures (candida or opportunistic staph. aureus)

Caused by loss of vertical height, Vit B12/folate/iron deficiencies.

Treat using antifungals (miconazole, nystatin, fusidic acid) and treating underlying causes.

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24
Q

Complications of oro-facial infections - cavernous sinus thrombosis

A

Infection can drain into sinus surrounding pituitary gland and make the blood here thrombose.
Presents as chemosis (red eye), ptosis (dropping upper eyelid), proptosis (bulging eye) and no eye movement (opthalmoplegia)

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25
Q

When would orofacial infections need antibiotics

A

If systemic sign/spreading infection e.g. throat pain, lymphadenopathy. If chronic infection that is persistent despite drainage e.g ANUG, acintomycosis.

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26
Q

Why can broad spectrum antibiotics be bad

A

Kills all the bacteria and lets C. diff infect.

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27
Q

Why can antibiotics fail

A
  • Not enough blood supply to the area/access to the area if it’s been walled off or something blocking the area
  • Poor patient compliance
  • Antibiotic resistance or wrong antibiotic used.
  • Too low dose
  • Bacteriocidal in immunosuppressed patients instead of bacteriostatic.
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28
Q

HHV 1

A

Herpes simplex virus 1

neuronal/epidermal

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29
Q

HHV 2

A

Herpes simplex virus 2

neuronal/epidermal

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30
Q

HHV 3

A

Varicella-zoster virus/chicken pox (neuronal/epidermal)

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31
Q

HHV 4

A

Epstein-Barr virus (B-cells)

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32
Q

Oral viral infections/viruses

A

Herpes virus
Paramyxovirus (measles)
HPV
Coxsakia virus

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33
Q

Herpes virus

A

Binds to cells, unsheds and inserts dsDNA and then gets translated into lots of new herpes viruses.

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34
Q

Paramyxovirus

A

Measles, mumps

Koplik’s spots - white papules on buccal and palatal mucosa, skin rashes and long term complications

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35
Q

HPV forms/presentations

A

Different forms:

  • Oropharyngeal carcinogenesis
  • Warts
  • Focal epithelial hyperplasia
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36
Q

HPV related oropharyngeal carcinogenesis

A

Most common form is squamous cell papilloma.

Can also get genital/anal cancer

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37
Q

Life cycle of HPV

A

Infects keratinocytes so needs broken skin to get in.
When keratinocytes differentiate, it gets released from the surface (contageous).
Sometimes it get’s integrated into chromosomes of the keratinocytes and becomes carcinogenic.

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38
Q

Coxsackia A virus types

A 
Herpangina form (vesicles and ulcers on soft palate of young people) and hand/foot/mouth disease form (vesicles and rash on hands, feet and mouth).
Both mild illnesses and self-limiting
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39
Q

Types of candida infections

A

Acute atrophic candidosis
Acute psuedomembranous candidosis (thrush)
Chronic hyperplastic
Chronic atrophic/denture stomatitis

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40
Q

Risk factors for candida infection

A

Abnormal exfoliation
Immunosuppressed (HIV, steroids, diabetes, age)
Xerostomia
Broad range antibiotics (kill the good bacteria = commensals infect)
Poor OH

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41
Q

About the candida fungus

A 
Candida albicans (yeast and hyphae forms, candidalysin punches holes in cells and cause damage)
Candidia auris (systemic infections)
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42
Q

Investigations for candida

A

Swab, rinse

Biopsy

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43
Q

Treating fungal infections

A

Topical antifungals = Nystatin, miconazole gel

Systemic = fluconazole

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44
Q

Acute pseudomembranous candidosis

A

can be wiped off to leave a bleeding base.

Thick white plaques.

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45
Q

Acute atrophic candidosis

A

Red areas on dorsum of tongue.

Prolonged use of antibiotics or corticosteroids

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46
Q

Chronic hyperplastic candidosis

A

White lesions near lip connoisseurs or lateral tongue that can’t be wiped off.
Biopsy bc risk of malignant change to leukoplakia.

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47
Q

Chronic atrophic candidosis

A

/denture stomatitis

Poor denture hygiene and area isn’t kept clean e.g. wearing denture at night.

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48
Q

Candida associated infections/lesions

A

Angular chelitis
HIV-related candidosis
Median rhomboid glossitis

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49
Q

Angular chelitits

A

Immunosuppressed, reduced OVD, Vit B12/folate/iron deficiencies

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50
Q

HIV-related candidosis

A

Prolonged forms e.g. Acute pseudomembranous candidosis that doesn’t go away or erthyematous form of acute atrophic candidosis

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51
Q

Median rhomboid glossitis

A

erythematous area on dorsum of tongue.

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52
Q

What counts as oral cancer

A

Head and neck - above the clavicle and not the brain or salivary gland. Oropharynx is included

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53
Q

Aetiology of oral cancer

A 
Smoking
Alcohol
Infections
Diet and nutrition
Sunlight
Hereditary e.g. P53 faulty tumour suppressor gene
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54
Q

Infections that can contribute to oral cancer

A 
HPV
- Focal epithelial hyperplasia (benign)
- Squamous cell papilloma (benign)
Candida
- Chronic hyperplastic candidosis
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55
Q

Oral lesions that predispose to cancer

A 
Leukoplakia
Erythroplakia
Lichen Planus - erosive/ulcerative versions
Chronic hyperplastic candidosis
Actinin keratosis
Oral submucous fibrosis
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56
Q

Leukoplakia

A

A white lesion that can’t be rubbed off and clinically/histologically isn’t caused by anything. No chemical or traumatic causes other than smoking. Idiopathic

Non-homogeneous = speckled, veroccous, nodules. More likely to be more dysplastic.
Homogenous = smooth, even surface.

Dysplasia in the histological sample can be mild (basal third), moderate (basal and middle third) or severe (full thickness of epithelium, basically a cancer in situ that hasn’t become invasive yet)

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57
Q

Erythroplakia

A

A red oral lesion that isn’t caused by anything - no histological or clinical cause. Idiopathic

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58
Q

Histological features of leukoplakia/erythroplakia

A

Hyperkeratosis +/- dysplasia
Architectural features = loss of stratification, basal cells not aligned/polar, drop-shaped rete pegs.
Cytological features = nuclear and cellular pleomorphism, hyperchromatosis/increased DNA, more mitosis.

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59
Q

Actinin keratosis

A

Lesion on lip
Crusting, red
Easy to spot, hard to manage

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60
Q

Oral submucous fibrosis

A

Especially in people that chew tobacco products
Lots of fibrous tissue under the epithelium
Presents as fixing of tissues, white lesion

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61
Q

Malignant oral cancers- signs and symptoms

A 
Fixation to underlying tissues
Dysphagia 
Paraesthesia or numbness
Bone loss and mobile teeth
Swellings
Non-healing lesion
Systemic signs
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62
Q

Grading and staging of cancers

A

Grading = well-differentiated, moderately or poorly differentiated. Poorly differentiated is the worst.

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63
Q

TNM info

A 
Determines prognosis - N is the most important. Stage 4c if any M1. 
T = tumour size and depth of invasion
- T0 = can't detect the primary cancer
- T1 = <2mm diametre, <5mm invasion
- T2 = 2-4mm, <5mm or <2mm, 5-10mm
- T3 = >4mm, >10mm 
- T4 = deep structures involved e.g. muscle, bone
N = nodes involved
- N0 = No local nodes involved
- N1 = 1x <3cm, ipsilateral
- N2a = 1x 3-6cm, ipsilateral
- N2b = 1+ <6cm, ipsilateral
- N2c = bilateral or contralateral
- N3a = any >6cm
- N3b = extracapsular spread
M = metastasis
- M0 = no metastasis
- M1 = distant metastasis
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64
Q

MDT involved in the management of oral cancers

A 
Radiologist
Oncologist
Max fac surgeon
Restorative dentist
GDP/GMP
Speech and language therapist
Nutritionist
Pathologist
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65
Q

The role of the radiologist in oral cancer management

A 
Diagnosing
US-guided biopsy
CT/MRI
Planning for surgery or radiotherapy
Monitoring after treatment
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66
Q

The role of the restorative dentist in oral cancer management

A

Pre-op assessment to determine which teeth have poor prognosis and to extract them/stabilise the mouth before any radiotherapy to the area.
Warn patient of side effects and plan for them e.g. xerostomia, trismus.
Improve OH and prevention e.g. duraphat

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67
Q

Radiotherapy side effects

A

Short term =

Long term = ORN, trismus, xerostomia, radiation-related caries (radio tx damages the ADJ), slower healing, immunosuppression, mucositis

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68
Q

Localised swellings of gingival tissues - differentials

A

Fibroepithelial polyp - mucosa coloured
Pyogenic granuloma - red and fluctuant
Peripheral giant cell granuloma - red, big, trauma
Ulcer
Pregnancy/hormone-induced epulis - plaque related
Bohn’s nodules
Gingival cyst

69
Q

Generalised swellings of gingival tissues - differentials

A 
Gingival fibromatosis
Gingival hyperplasia - hormone or medication-induced
Crohn's/Oro-facial granulomatosis
Leukaemic infiltrate
Chronic hyperplastic gingivitis
70
Q

Peripheral giant cell granuloma

A

Vascular granulation tissue with lots of giant cells.
Can erode through cortical bone - needs debridement
Peripheral means it starts from mucosa - need Xray to determine the extent
Can be trauma related
Anterior teeth and young people = common

71
Q

Gingival fibromatosis

A

Overgrowth of fibrous tissue - genetic and hereditary

72
Q

Gingival hyperplasia

A

Overgrowth of gingival tissue - needs gingivectomy but can grow back.
Can be medication-related, leukaemic infiltrate (red, bleeding gums), hormone-related, or due to lack of collagen, like in Scurvy

73
Q

Medication induced gingival hyperplasia

A

Cyclosporins - immunosuppressant
Anti-convusltant - phenytoin
Anti-hypertensive - Nifedipine

74
Q

Crohn’s signs and symptoms

A

Swollen lips and cracking
Cobblestone mucosa, tags on mucosa
Ulcers
Gingival hyperplasia

75
Q

Benign swellings affecting the oral mucosa

A 
focal epithelial hyperplasia/Heck's disease
Lipoma
Neuroma
Haemangioma
Squamous cell papilloma
Mucocele
76
Q

Heck’s disease/focal epithelial hyperplasia

A

HPV related
lots of small flat viral warts on the lip
Can resolve on their own/excise

77
Q

Traumatic neuroma

A

Overgrowth of nerves due to trauma

Can be painful so excise

78
Q

Haemangioma

A

Overgrowth of blood vessels - red/purple lesion

Careful excision - don’t let it bleed out

79
Q

Lipoma

A

Overgrowth of fat tissue - yellow/pink with a smooth surface

80
Q

Taking tissue samples for testing considerations

A

Need to stop contamination w other organisms and use a transport medium to preserve sample until it can be processed/tested.

81
Q

Transport medium for tissue samples

A
  • Needs to have no growth support medium to stop the sample changing or commensals growing.
  • Aerobic or anaerobic
  • Reducing agent can be added to preserve anaerobes
  • Charcoal/gelatin added to absorb toxic metabolic products of host microbes
82
Q

Sending a sample to the lab

A
  1. Need to fill in a specimen request form
  2. Needs special labeling for the post (A or B if it will cause life-threatening illness if exposed e.g. hep-B, HIV)
  3. Leak-proof rigid container w absorbent material
83
Q

Sources of pigmentation in oral mucosa pigmented lesions [4]

A

Intrinsic

  • Melanin = is made by clear melanocytes in the basal third of the epithelium and then taken up by neighbouring basal cells
  • Haemosiderin = breakdown product of RBC (iron)

Extrinsic

  • Heavy metals e.g. from amalgam, lead, gold. From restorations, medications (antimalaria, amiodarone) or from occupation
  • Chromogenic bacteria e.g. actinomyces in a hairy black tongue
84
Q

Endogenous developmental causes of oral mucosa pigmented lesions [4]

A

Physiological = people with darker skin have more melanin
Peutz Jehger’s
Haemochromatosis
Melanocytic naevus

85
Q

Endogenous acquired causes of oral mucosa pigmented lesions [5]

A

Addison’s
Melanotic macule
Post-inflammatory
Smokers melanosis

86
Q

Neoplastic oral mucosa pigmented lesions [2]

A

Melanoma

  • malignant melanocytes proliferate along epithelium/CT junction and into CT
  • V aggressive
  • On the palate a lot
  • Can be pigmented or not. Slow growing or fast/ulcerated/painful/bony infiltration

Kaposi’s sarcoma

  • HHV8/HIV
  • On palate usually
  • Blue/black growth due to haemosiderin.
87
Q

Exogenous causes of oral mucosa pigmented lesions [2]

A

Chromogenic bacteria

Heavy metals

88
Q

oral mucosa pigmented lesions - Addison’s

A

Adrenal gland disorder - autoimmune
Less adrencorticol hormone = more ACTH from pituitary = melanocytes stimulated = more melanin = pigmented areas on skin
Don’t need to treat

89
Q

Melanotic macule

A

More melanin in the basal third

90
Q

Smoker’s melanosis

A

Smoking stimulates melanocytes = more melanin

Melanin drops into lamina propria and gets picked up by macrophages

91
Q

Post-inflammatory oral mucosa pigmented lesions

A

Inflammation damages or stimulates melanocytes = more melanin.
Called melanocytes incompetence.
E.g. After leukoplakia

92
Q

Peutz Jehger’s

A
  • melanin, AD
  • Get little dark spots around lips and big irregular pigmented lesions on the skin
  • Get GI polyps which can become malignant
  • More susceptible to carcinomas
93
Q

Melanocytic naevus

A

hamartoma/mole

regular well-defined borders that don’t grow or change but biopsy if looks suspicious

94
Q

Haemochromatosis

A
  • Autosomal recessive
  • Too much iron absorbed so excessive gets stored as haemosiderin and makes skin tinted, can cause liver cirrhosis, diabetes and more susceptible to infections.
  • Tx = regular partial blood draining (venesection)
95
Q

Types of hypersensitive reactions

A
  1. anaphylactic
  2. cytotoxic (cyTWOtoxic)
  3. immune complex
  4. delayed cell-mediated
96
Q

Type 1 hypersensitivity

A

IgE binds to free antigen and triggers Mast cells to release histamines (on 2nd exposure)
= vasodilation, vaso-permeability, bronchospasm, nose and eye secretions, rashes
- Fast reaction

Use flare and wheel skin test
Tx = adrenaline, anti-histamines, corticosteroids

97
Q

Type 2 hypersensitivity

A

Cytotoxicity

Antigen binds to and enters cells
IgG and IgM auto-antibodies bind to the cell and trigger an immune reaction which destroys the affected cells
- macrophages
- Complement system

E.g. pemphigus/pemphigoid

98
Q

Type 3 hypersensitivity

A

Immune complex formed

Soluble antigens and antibodies bind, accumulate and precipitate in joints, blood vessels and glomeruli
= activation of the complement system
= inflammation and tissue damage

E.g. systemic LE, erythema multiforme

99
Q

Type 4 hypersensitivity

A

Delayed cell-mediated

An antigen binds to a cell = releases cytotoxins
T-cell (CD4) responds
- Cytotoxic cells kill basal cells so no new epithelial cells so limited healing
- Apoptosis of affected cells w the antigen (via T-cells and natural killer cells)
- Perforin (pore-forming) released by T-cells
- macrophages

E.g. contact dermatitis, lichenoid, OLP

100
Q

Hypersensitivity vs allergy vs autoimmunity

A

Hypersensitivity = immune system reacting in an exaggerated/inappropriate way to an extrinsic non-self (allergy) or intrinsic self-antigen (autoimmunity)

101
Q

Causes of Ulcers (general)

A 
Manifestations of systemic (GI/haem/dermatological)
Idiopathic (RAS)
Developmental (epidermolysis bullosa)
Neoplastic
Iatrogenic (drugs, radiotherapy)
Infective
Trauma
102
Q

Drug induced oral mucosa pigmented lesions

A
  1. Stimulate melanocytes = more melanin
  2. Or damages blood vessels = more RBC broken down and haemosiderin released.
  3. Or have heavy metals in them

E.g. antimalaria, amiodarone

103
Q

Black hairy tongue

A

Overgrowth of filiform papillae which get stained by bacteria (e.g. acintomyces) or smoking

Can be caused by soft diet, PEG, smoking, antibiotics

104
Q

HIV opportunistic infections

A

Bacterial = TB, strep, s. pyogenes, salmonella
Viral = EBV, HSV, HHV8
Fungal = candida
Other e.g. toxoplasma

105
Q

HIV medications

A

Meds that stop DNA from being transcribed properly e.g. Fusion-inhibitors, integrase-inhibitors, protease-inhibitors (fat loss from legs, fat gain in belly) and reverse transcriptase inhibitors (SE = nausea, headache, anaemia, rash, lactic acid)

Anti-retroviral drugs ART = good at stopping the progression to AIDS and reducing opportunistic infections

Preventing and treating opportunistic infections

106
Q

How to diagnose HIV

A

Bloods - CD4 levels

ELISA test for HIV antigens

107
Q

HIV associated oral manifestations

A

Group 1 /v HIV = Kaposi sarcoma, Non-Hodgkin lymphoma, candidiasis (thrush, erythematous candidosis), hairy leukoplakia, periodontitis/ANUG

2 = ulcers, viral infections, low platelets

3 = other candida/fungal infections

108
Q

Normal histological structure of different types of oral mucosa [4]

A

Attached gingival mucosa = keratinised SSE, less submucosa, just attached straight onto the bone
Palate = Keratinised SSE, less submucosa, minor salivary glands
Normal mucosa = non-keratinised SSE, lamina propria, submucosa, muscle/fat
Specialised mucosa e.g. tongue = keratinised SSE + papilla - filiform (keratin extensions, abrasion), foliate/fungiform (taste), circumvalate

109
Q

Variations of normal mucosa [4]

A

White spongey naevus
Fordyce spots - ectopic sebaceous glands
Geographic tongue
Leukoedema

110
Q

Age-related changes to oral mucosa [3]

A

Less elastic
Thinner/atrophic
Smoother

111
Q

Mucosal changes with trauma

A 
Ulcer
Atrophic
- erosive OLP
Hyperplastic
- Increased CT/collagen = fibroepithelial polyp, papillary hyperplasia, 
Keratosis
Hyperkeratosis
- Stomatitis nicotina
- Frictional keratosis
112
Q

Factors that affect the healing of oral mucosa [8]

A 
Blood supply
Radiotherapy
Immunity/immunocompromised
Foreign body (neutrophils and lympcytes surround it and cause an abscess)
Primary or secondary healing intention
Nutritional deficiencies (e.g. VitC)
Infection
Malignancy
Age of patient, hormones, risk factors, smoking
113
Q

White sponge naevus

A

Inherited, AD
Keratinocyte mutation = Keratinised hyperplastic epithelium
Shows as thick white plaques that can’t be wiped off/don’t disappear on stretching, bilateral and symmetrical and usually on FOM, buccal mucosa
Don’t need to treat
Differentials = OLP, frictional keratosis, leukodaema

114
Q

Leukodaema

A

+/- smoking
Diffuse milky areas that disappear on stretching
Bilateral/symmetrical
Doesn’t need treatment
histology = larger clear epithelial cells
Differentials = OLP, leukoplakia, white sponge naevus, frictional keratosis

115
Q

Geographic tongue

A

Red areas with white halos on dorsum of tongue
Can be sore to food + have aggrevating factors
Lesions can move around tongue
Doesn’t need treatment or biopsy

116
Q

Frictional keratosis and how to diagnose

A

Needs to have a continuous traumatic cause that when removed, makes the lesion heal.
Normal healing response of the mucosa
I it doesn’t heal, may need to reconsider diagnosis e.g. leukoplakia, OLP

117
Q

Stomatitis nicotina

A

Hyperkeratosis of palate with red spots where minor salivary glands have been traumatised
Response to smoke/thermal trauma
Improves with smoking cessation
Not premalignant

118
Q

Papillary hyperplasia

A

Ill-fitting denture
Causes hyperplasia and nodules, erythema
Need to improve denture fit and hygiene (can get superimposed w candida)

119
Q

What is an ulcer - histology, different types

A

Loss of the full thickness of the epithelium, revealing the underlying CT
Fibrin/neutrophil slough covers it, with granulation tissue under to allow healing + inflammatory cells
- Primary
- Secondary - bulla/vesicle that bursts and becomes an ulcer

120
Q

Questions / examinations when a patient presents with an ulcer

A 
SH - smoking, alcohol, diet
MH - new drugs
FH
Ulcer pain history
How many do you have, where, for how long
Ulcer free period
Oral, genital, skin lesions
Any other symptoms
Aggravating/alleviating factors

E/O = lymph nodes (fixation = SCC?), skin and eye lesions

I/O

  • how many ulcers, where, describe them (shape, size, raised, rolled margins?
  • Tongue movement or fixation
  • Any dysesthesia/nerve issues
121
Q

Further investigations for non-healing ulcer

A

Biopsy
Blood tests - FBC, VitB, folate, iron,
Viral/fungal/bacteria

122
Q

Ulcer biopsies

A

Only to rule out malignancy or dysplasia
Otherwise, it will be a non-specific ulcer
Can test for candida?

123
Q

Differential diagnosis/causes for ulcers

A 
MMIDNIIT (MIDNIGHT)
Manifestations of systemic disease (haem, GI)
Manifestations of dermatological disease - OLP, pemphigus/pemphigoid
Infection
Developmental - epidermolysis bullosa
Neoplastic
Idiopathic - RAS
Iatrogenic - drugs, radiotherapy
Trauma
124
Q

Traumatic ulcers

A

Can be due to mechanical, physical, thermal, chemical or self-inflicted trauma
Remove the cause of trauma and see if the ulcer resolves
+ Symptomatic relief
If it doesn’t resolve, may need to reconsider the diagnosis

125
Q

Malignant ulcers

A

SCC
Salivary gland tumour
Lymphoma
- raised rolled margins on a suspicious site e.g. FOM, lateral borders of the tongue, posterior mouth. 3+ weeks
- Biopsy to diagnose + need more imaging e.g. chest x-ray, CT

126
Q

Ulcers caused by infection

A

Viral - herpes, coxsackie, HIV
Bacterial - TB, syphilis, gonorrhoea, ANUG bacteria
Fungal - candida
Erythema multiforme is triggered by bacteria and viruses too

127
Q

Drugs that cause ulcers

A

Methotrexate
Cytotoxins
Nicorandil
Radiotherapy

128
Q

RAS (diagnosis, risk factors, causes)

A

Recurrent aphthous stomatitis
Risk factors = familial, smoking, stress, hormones, poor OH.
Causes = low Vit B12, folate, iron levels, immunocompromised, GI tract disease, food intolerances
Blood tests and clinical form to diagnose (+/- biopsy to rule out cancer) - FBC, folate, iron levels, B12

129
Q

Minor RAS

A

1-5 ulcers, <10mm
Front of mouth, non-keratinised tissues
Heal after 7-10 days, without scarring
Young patients 10-30yrs

130
Q

Major RAS

A 
5+ ulcers, 1.5-2mm
All over mouth inc posterior and keratinised tissues
Heal w scarring
Take 3 weeks-months to heal
Older patients
131
Q

Herpetiform RAS + Tx

A

Lots of little pinprick ulcers, that can merge together
FOM, tongue, lips
7-10 days to heal
- Treat w doxycycline MW

132
Q

Management of RAS

A

Prevent

  • Correct any underlying conditions e.g. B12, iron
  • Improve OH
  • Reduce RF e.g. smoking

Symptoms

  • benzydamine mouthwash (Difflam)
  • Corsodyl/chlorhexadine
  • Covering gel

Suppress

  • Topical steroids e.g. hydrocortisone pellets, betamethasone MW, beclomethasone spray
  • Systemic steroids e.g. prednisolone,
133
Q

Behcet’s disease

A
  • Affects the whole body, high mortality
  • RAS and recurrent oro-genital ulcers
    GI, joints, skin lesions, neuropathy, retinal vasculitis = blindness
  • Diagnose using clinical signs
134
Q

Different types of mucocutaneous diseases

A 
Pemphigus
- Vulgaris
- Foliaceous
- Paraneoplastic
Pemphigoid
- Bullous
- Mucous membrane
Dermatitis herpetiform
Epidermolysis bullosa
Erythema multiforme
Lichen planus
Lichenoid reactions
135
Q 
Define:
Macule
Papule
Blister [2]
Erosion
Ulcer
A

Macule = flat, not palpable, circumscribed/well-defined
Papule = palpable, raised circumscribed/well-defined lesion
Blister - fluid-filled sub or intra-epithelial area
Erosion = partial-thickness loss of epithelium
Ulcer = Full-thickness loss of epithelium

136
Q

Pemphigus

A

Autoimmune, type 2 hypersensitivity
Autoantibodies attack desmosomes (releasing desmoglein) and cause intra-epithelial separation.

Blisters can burst but because it’s only a partial loss of epithelium, the body doesn’t heal. Loss of permeability membrane = loss of tissue fluid and infection gets in.

Variable sized, short-lived ulcers on the palate, gingiva, buccal and can get skin lesions

Pemphigus vulgaris = desmoglein 3
Pemphigus foliaceous = desmoglein 1
Pemphigus paraneoplastic

Histology = intraepithelial separation, Tsank cells (floating epithelial cells)

137
Q

How to diagnose pemphigus/pemphigoid

A

Para-lesional biopsy to see intra or subepithelial separation

Direct immunofluorescence of fresh sample = IgG w immunofluorescence, specific to human autoantibody added to sample. Binds to autoantibodies.

  • Pemphigus = fishnet appearance
  • Pemphigoid = thick line at the basement membrane
  • Dermatitis herpetiform = speckled granular line at the basement membrane.

Indirect immunofluorescence (patient’s blood sample used on tissue) = negative for pemphigoid

Blood tests = autoantibodies and free desmoglein (pemphigus)

Blunt probe on healthy mucosa - pemphigus will develop a blister

138
Q

Different types of pemphigus

A

Pemphigus vulgaris = desmoglein 3. Most common
Pemphigus foliaceous = desmoglein 1. Surface and skin lesions (less oral)
Pemphigus paraneoplastic = can lead to lymphoma and chronic lymphocytic leukaemia

139
Q

Bullous pemphigoid

A

Autoimmune Type 2 hypersensitivity
Against hemidesmosomes that connect epithelium to basement membrane = subepithelial separation
- Proteins BP180 and BP230 affected

Bullae are less fragile bc full thickness, and if they rupture they become an ulcer and get normal healing

Skin usually involved + oral mucosa - large, shallow ulcers

140
Q

Mucus membrane pemphigoid

A

Hemidesmosomes, subepithelial separation
- Hemidesmosome protein BP230, lamina and Alpha4Beta6 affected

Chronic disease of the elderly
Affects mucous membrane e.g. mouth, genital, anal, larynx, pharynx, nasal
Desquamative gingivitis
Get blisters and vesicles which rupture and cause scarring
In the eyes, this can lead to conjunctive scarring, eyes sticking to eyelids and inverted lashes/inverted eyelids
These patients need referrals.

141
Q

Dermatitis herpetiform

A

In kids
Like bullous pemphigoid but lots of small vesicles and ulcers on the palate and buccal mucosa which can merge
+ Desquamtive gingivitis
Can be linked with Coeliacs so patients need to be gluten-free

142
Q

Epidermolysis bullosa congenita

A

Inherited AS - not autoimmune, from birth
Problems with epithelium connecting to CT
- EB Simplex = intraepithelial separation
- EB junctional = above basement membrane
- EB dystrophic = basement membrane separated from CT
V bad :(

143
Q

Erythema multiforme

A

Type 3 or 4 hypersensitivity
Acute, young patients, resolves in 2-3 weeks
Single episode = drugs, radiotherapy
Recurrent episodes = HSV antigen (type 4 hypersensitivity) - give acyclovir

Bleeding, haemorrhage crusting on lips
Eye problems
Bullseye ulcer lesions on skin
Lots of irregular mucosal ulcers and bulla

144
Q

General management of muco-cutaneous diseases

A

Prevention

  • Diet
  • OH
  • Risk factors e.g. stress. smoking, trauma

Symptoms

  • Difflam
  • Corsodyl (alcohol-free?)

Steroids
- Topical or systemic

Immunosuppression
- Cyclosporin MW

145
Q

Lichen planus - mucosal presentations [6]

A 
Radicular interconnecting striations
Ulcers
Desquamative gingivitis
Erosive
Plaque-like
Bullous form
146
Q

Lichen planus - skin presentations

A

Purple itchy papules and striations, especially on wrists and shins.
Itch them = more papules

147
Q

Lichen planus vs lichenoid reactions

A

Lichenoid

  • Closely related to a cause
  • Type 4 hypersensitivity
  • Unilateral, asymmetrical
  • No skin lesions

Lichen planus

  • Idiopathic
  • Type 4 hypersensitivity
  • Skin and gingiva signs
  • Bilateral, symmetrical
148
Q

Cause of lichen planus

A 
Smoking
Stress
OH
Trauma
Infections

T-cell mediated - Basal cells destroyed by lymphocytes so epithelium can’t heal = erosive lesions
Or responds by overproduction of epithelial cells and keratin = plaque-like lesions

Rate of destruction: rate of new cells determines if it’s plaque-like or erosive

149
Q

Management of lichen planus

A

Prevention

  • Reduce risk factors
  • Avoid food triggers
  • OH improvement

Symptomatic relief

  • Topical steroids - beclomethasone spray, betamethasone MW, hydrocortisone pellets
  • Benzodyamine MW
  • Cyclosporin (MW)

Systemic immunosuppression
- Prednisolone

Warn patient that 1-3% become malignant

150
Q

Lichenoid reactions - causes

A

Metal from restorations, instruments
Diet
Medications
Graft vs host disease

151
Q

Histological signs of OLP

A

Loss of basal cells
Lots of blue lymphocytes under the basal layer
Can be erosive, ulcerated, bullous or hyperplastic depending on the presentation

152
Q

GORD

A

Gastric-oesophageal reflux disease
RF = obesity, smoking, alcohol

Symptoms = dyspepsia (indigestion e.g. heartburn, acid reflux, abdo pain, nausea, vomiting) and oral symptoms (tooth erosion, ulcers, halitosis)

Can lead to Barrett’s oesophagus (squamous cells metaplasia to cuboidal cells, premalignant)

Tx = reduce risk factors, PPI e.g. omeprazole
SE of PPI = interacts w warfarin, the pill and can cause erythema multiforme, taste disturbances, dry mouth.

153
Q

Coeliac’s

A

Type 4 hypersensitivity to a-gliadin peptides in gluten
Inflammatory bowel disease

Histology:

  • The surface layer of bowels
  • Crypt hyperplasia
  • Villous atrophy
Clinical signs - full body
- Abdo pain
- Fatty stool
- Diarrhoea
- Malabsorption - Iron, folate, Vit B12, D, C, calcium
- Tired
\+ Osteomalacia (less VitD/calcium)
\+ Peripheral neuropathy (less B12/folate)
Oral signs
- ulcers
- opportunistic infections e.g. candida
- angular cheilitis
- glossitis
\+ dermatitis herpetiform
\+ enamel hypoplasia (less calcium/VitD)

Treatment = No gluten, immunosuppression if needed/manage symptoms with topical stuff

Risk of bowel malignancy/lymphoma so monitor patient

154
Q

Crohn’s

A

Idiopathic inflammatory bowel disease
Affects the elderly more

Histology
- Affects full thickness and length of GI tract
- Granulomatous inflammation
\+ non-caseating granulomas
\+ Tags
Clinical signs (general)
- Abdo pain
- Diarrhoea
- Weight loss
- Tired
- Malabsorption
\+ Blood in poo
Oral signs
- Ulcers
- Glossitis
- Angular cheilitis
- Opportunistic infections 
\+ Cobblestone appearance
\+ Lip swelling and fissures
\+ Mucosal tags

Treatment
- Prevent
- Replacement therapy/food already broken down
- Symptomatic relief
- Topical and systemic steroids and immunosuppression
+ Anti-TNF

Need to rule out other granulomatous inflammation and other inflammatory bowel diseases

155
Q

OFG

A

Idiopathic but possibly linked to food allergies
Oral signs of Crohn’s - granulomatous inflammation

Oral signs

  • Ulcers
  • Angular cheilitis
  • Cobblestone appearance
  • Lip swelling and fissures

Treatment
= prevent (diet, exclude chocolate, cinnamon, benzos, etc), symptomatic relief, topical and systemic immunosuppression if needed

Need to rule out other granulomatous inflammation and Crohn’s (endoscopy, bowel signs/symptoms)

156
Q

Ulcerative colitits

A

Idiopathic inflammatory bowel disease
Affects younger people more (10-30yrs)

Histology

  • Surface mucosa/epithelium
  • Bleeding and ulceration
  • Large intestines and rectum affecting
Clinical signs (general)
- Abdo pain
- Diarrhoea
- Malabsorption
- Weight loss
- Tired
\+ Bleeding in poo
\+ ankylosing spondylitis (fused back)
\+ iritis (iris inflammation)

Oral signs
- Ulcers
- Furred tongue (not eating enough)
- Pyostomatitis vegetans (pus and inflamed gums)
+ Vit B12/folate/iron deficiencies from malabsorption

157
Q

Inflammatory bowel diseases

A

Crohn’s
Coeliac
Ulcerative Colitis

158
Q

Tests to diagnose inflammatory bowel diseases

A

Clinical
Blood tests - FBC, inflammatory markers (ESR, CRP), Vit/iron/folate levels, antibodies (for A-gliadin = Coeliac’s)
Endoscopy
Biopsy - non-caseating granulomatous inflammation = OFG/Crohn’s, histological signs of Coeliac’s, surface or full mucosa involved?)
Exclusion diet - does it work

159
Q

Granulomatous inflammation differentials and differentiating between them

A

Crohn’s - full thickness and length of GI + oral
OFG - only in mouth
TB - caseating granulomas (others are non-caseating) + lungs
Sarcoidosis - in lungs (take X-ray)

160
Q

Causes of lip swelling

A

Crohn’s
OFG
TB (rare)
Sarcoidosis

161
Q

Similarities/differences in presentation between Coeliac’s, OFG, UC, Crohn’s - how to spot each one

A

Coeliac’s
- Specific histology: crypt hyperplasia, villous atrophy
- Caused by antibodies to a-gliadin
- genetic so in kids
+ specific signs e.g. hypoplastic enamel, osteomalacia, fatty stool

Crohn’s

  • Blood in stool
  • granulomatous inflammation = tissue tags, cobblestone, lip swelling and fissure
  • Full-thickness and length of GI + oral
  • Only one that is treated w anti-TNF

OFG - only in mouth

Ulcerative Colitits
- Blood in stool
- Large intestines and rectum, surface of mucosa only
+ Specific signs e.g. iritis, ankylosing spondylitis
- No granulomatous inflammation

162
Q

Treatment for inflammatory bowel disease (+ Coeliacs)

A 
Prevention
Replacement therapy if malabsorption
Symptomatic relief
Steroids - topical and systemic
Immunosuppression
Monitor GI for malignancy (esp Coeliacs)
163
Q

Intestinal polyposis syndromes

A

Peutz Jehgers

  • Genetic
  • Small pigmented lesions in the mouth and around the lips
  • Risk of malignancy in ovaries, liver, pancreas

Gardner’s syndrome

  • Osteomas, odontomas, supernumerary teeth
  • GI polyps, cysts,
  • Risk of GI malignancy
164
Q

Different types of anaemia and causes

A

Normocytic

  • Leukaemia/not enough RBC made
  • Bleeding, period, need more

Microcytic

  • Low iron
  • Due to diet, malabsorption, increased demand e.g. pregnancy, period,

Macrocytic

  • Low B12/folate
  • Due to malabsorption, diet, hypothyroid, medications (azathioprine for Crohn’s), alcohol/liver disease
165
Q

Leukaemia

A

Bone marrow space obliterated with one type of malignant WBC = not enough space for the others.

  • ALL, AML, CLL, CML
  • Acute forms are more aggressive
  • ALL in kids

Malignant cells take over marrow space and can go into other organs =

  • Symptoms of anaemia
  • Reduced healing and immunity
  • Fewer platelets = bleeding and bruising
  • Bone pain
  • Lymphadenopathy, hepato/splenomegaly
  • General cancer signs e.g. weight loss, sweating, tired
166
Q

Multiple myeloma

A

Malignancy if plasma cells that obliterate bone marrow space = leukaemia symptoms
+ release lots of monoclonal antibodies which go all over body and aggregate in areas = bad
- Joints
- Osteoporosis
- Kidneys/nephrons damaged

167
Q

Oral symptoms of anaemia

A 
Palor
Ulcers
Depapillated tongue
Altered taste
Candida
Dysphagia (webbing in the oesophagus can be pre-malignant)
Burning mouth
168
Q

General signs/symptoms of anaemia

A 
Palor
Tired
Palpitations/fast heart rate
Slow healing
Mucosal atrophy
Skin and nail changes
Hair loss
Headrush/dizzy

Oral medicine (4 decks)

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