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BDS4 > Oral Medicine > Flashcards

Oral Medicine Flashcards

1
Q

What is Lichen Planus?

What are the 6 main oral types?

A

Lichen Planus = Chronic, mucocutaneous + premalignant disease that can be oral, cutaneous or genital and appear with a wide spectrum of presentation.

(Purple People Break And Enter Raves)

  1. Papular (small white spots)
  2. Plaque-like (white patch)
  3. Bullous (RARE - blood-filled blisters)
  4. Atrophic (Erythematous)
  5. Erosive (Ulcerative)
  6. Reticular
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2
Q

What is the aetiology and epidemiology (3) of Lichen Planus?

A

Aetiology:
Unknown (may be AI)

Epidemiology:

  • Age (4th-8th decade)
  • Gender (60% female)
  • Europeans and Indians
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3
Q

What are the 4 histological signs seen from biopsy sample to diagnose Lichen Planus?

A
  1. +/- Hyperkeratosis
  2. “Saw tooth” rete ridges in epidermis
  3. (T) Lymphocyte cells dominant sub-epithelial band
  4. Basal cell degeneration and liquifaction
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4
Q

Clinical features of Oral Lichen Planus?

(THINK: Sites, Symptoms & Types)

A
  • Symmetrical/Bilateral - Often posterior buccal mucosa, labial mucosa, tongue or ginigva
  • Gingival involvement may = Desquamative gingivitis (differentials = LP, PV or MMP)*
  • Koebner Phenomenon - Often present in sites of increased friction (e.g. ill-fitting denture)
  • Asymptomatic or discomfort on heating spicy/acidic foo

6 Oral Presentations:

  1. Papular
  2. Plaque like
  3. Bullous (rare)
  4. Atrophic (Erythematous)
  5. Erosive (Ulcerative)
  6. Retricular
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5
Q

Clinical features of Cutaneous Lichen Planus?

A
  • Symmetrical/Bilateral
  • Koebner’s Phenomenon (e.g. knees/shins)
  • Purple Polygonal Pruretic (itchy!) Papules (flat-topped and few mm diameter)
  • Wickham’s Striae (surface network of fine white striations)
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6
Q

Other than Oral and Cutaneous, what are 3 other sites Lichen Planus may present?

(And how does it present?)

A

1) GENITAL

  • More common in females
  • Vulvo-Vaginal Gingival Syndrome → Scarring

2) NAILS

  • Dystrophic (poorly formed and discoloured)
  • Longitudinal grooving and pitting
  • Possible loss of nail

3) HAIR

  • Scarring alopecia
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7
Q

What is the difference in oral and cutaneous lichen planus in terms of longevity and quantity of patients who have both?

A

Oral (MORE COMMON)

  • Chronic (4-25 years)
  • 10-30% have cutaneous lesions

Cutaneous

  • Transitional (last average 18 months)
  • 70-77% have oral lesions
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8
Q

What are 3 differentials for Desquamative Gingivitis?

Which is most common?

A
  1. Lichen Planus (most common)
  2. Pemphigus Vulgaris
  3. Mucous Membrane Pemphigoid
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9
Q

What is the malignant transformation % of Lichen Planus?

What advice should be given to patients? (3)

A

~0.5-2%

(“Transformation = independent of smoking and alcohol”)

Patients should be warned of malignant potential and adviced:

  • Regular reviews
  • Smoking cessation
  • Good OH
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10
Q

What are 9 differentials for a white patch lesion in the mouth?

A
  1. Candidal Infection
  2. Epithelial Dysplasia
  3. Hyper-keratosis
  4. Lichen Planus
  5. Lichenoid Reaction
  6. Discoid Lupus Erythematous (DLE)
  7. Graft vs. Host Disease
  8. Leukoplakia
  9. Squamous Cell Carcinoma
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11
Q

How would you manage a patient with symptomatic oral Lichen Planus?

A
  • Educate pt: No cure, will manage symptoms but low risk of malignant change (so regular reviews and reduce risk factors e.g. smoking)
  • Eliminate provoking factors (e.g. sharp cusps or ill-fitting denture causing trauma)
  • Avoid chemical irritation (e.g. use Sensodyne SLS-free toothpaste and avoid spicy foods)

Treatment options:

1st line = Topical Corticosteroids (e.g. Hydrocortisone/Betamethasone0

2nd line = Topical Immunosuppressants (Calcineurin Inhibitors)

Severe = Systemic Corticosteroids or Immunosuppressants

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12
Q

Lichen Planus has no cure. Other than elimination of provoking factors and advice to reduce malignant risk factors, what 3 pharmaceutical interventions can be used?

A
  1. Topical Corticosteroids (1st Line)
    * E.g. Hydrocortisone, Betamethasone or Benzydamine (Difflam)*
  2. Topical Immunusuppressants (Calcineurin Inhibitors) (2nd line)
    * E.g. Ciclosporin, Tacrolimus or Pimecrolimus*
  3. SEVERE = Systemic Corticosteroids or Immunosuppressants
    * (E.g. above, Azathioprine, Dapsone, Mycophenolate mofetil or Thalidomide)*
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13
Q

What are 4 issues concerning long-term corticosteroid use?

A
  1. Adrenal gland suppression → Adrenal Insufficiency (ME)
  2. Skin thinning, easy bruising and slowed wound healing
  3. Increased risk of infection
  4. Hypertension
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14
Q

Topical Calcineurin Inhibitors are 2nd line treatment for Lichen Planus, how do they work, how long to they take to work and what are 3 examples?

A

Calcineurin = Protein involved in T-lymphocyte activation

Inhibition = Immunosuppression
(Use causes initial “burning sensation” followed by lesion resolution within 8-12 weeks)

  1. Ciclosporin
  2. Tacrolimus
  3. Pimecrolimus
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15
Q

What are 10 drugs that can cause drug-induced Lichenoid Reaction?

(HINT: Harry Potter is A BAD MAN G)

A
  1. Hypoglycaemics (oral)
  2. Penicillamine (RA)
  3. ACE inhibitors (“prils”)
  4. Beta blockers (e.g. Furosemide, Indapamine or Mannitol)
  5. Allopurinol (Gout)
  6. Diuretics
  7. Methyl-dopa (Hypertension)
  8. Anti-malarials
  9. NSAIDs
  10. Gold salts (RA)
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16
Q

How is the:

  1. Aetiology
  2. Presentation
  3. Histology
  4. Management

of Lichenoid Reaction different to Lichen Planus?

A

1) Aetiology
LP = Unknown (may be AI)
LR = Drug-induced or Dental-material related (resins or metals, e.g. amalgam)

2) Presentation
Similar, but LR:

  • Mostly erosive (ulcerative) type→ Soreness
  • Can affect palate
  • May be unilateral (e.g. if DM related)

3) Histology
Similar, but LR:

  • Deeper and less defined infiltrate
  • Lots of plasma and eosinophils

4) Management

  • Patch test to see if local (DM) cause - remove
  • If possible, withdraw drug and monitor
  • No pre-malignant risk
  • Otherwise, manage as with LP
17
Q

What is Graft vs. Host Disease?

What is the aetiology and risk factors (2)?

A

Immune reaction of graft lymphocytes against host cells

Aetiology: Following allogenic bone transplant (within first 6-24 months)

Risk Factors:

  • Poorly-matched graft
  • Old age doner or recipient

N.B. GvHD = Increased risk of OSCC

18
Q

What are 3 oral clinical features of Graft vs. Host Disease?

A
  1. Asymptomatic or Burning sesation (Erosive/Ulcerative or Reticular)
  2. Oral dryness → Superficial palatal and labial mucoceles
  3. Sclerotic GvHD → Trismus (reduced opening)
19
Q

How is Graft vs.Host Disease managed? (4)

A
  1. Topical analgesia (e.g. LA)
  2. Topical Corticosteroids (e.g. Betamethasone M/W)
  3. Topical Immunsuppressants (e.g. Tacrolimus ointment)
  4. Regular review (as GvHD = Increased OSCC risk)
20
Q

What is Lupus Erythematous?

What is the aetiology?

What are the 2 main types?

Are they more common in males or females?

A

Lupus Erythematous = Chronic, indolent (little/no pain) oral and cutaneous disease

Aetiology = AI (may be precipitated by drugs, virus’ or environment)

  1. Systemic LE (Multi-systemic + affects vascular and CT)
  2. Discoid LE

Both = More common in females (esp. child bearing age)

21
Q

In Discoid Lupus Erythematous, what are the clinical features of:

  1. Oral lesions? (seen in 20-50%)
  2. Cutaneous lesions?
A

1. ORAL LESIONS

  • Similar site to LP - Bilateral buccal/labial mucosa
    BUT also: Palate + Vermillion border
  • Less-well demarcated erythematous areas, surrounded by border of fine white striae
  • May ulcerate - Sign of active lesion or progression to SLE

2. CUTANEOUS LESIONS

  • Scaley, atrophic plaques on sun-exposed skin
  • Oval keratin-plug plaques (may appear on skin, hair, genitals or orally)
  • Increased blood vessel formation (telangiectasia)
  • Scarring alopecia or scalp pigmentation
22
Q

Main method of DLE diagnosis is biopsy (through in 25% cases autoantibodies are visible). What 6 histological features of DLE would you observe?

A
  1. Para or Ortho-keratosis
  2. Chronic inflammatory cell infiltrate in sub-epithelial CT
  3. Hyalinisation of sub-epithelial CT
  4. Basal cell liquefaction and degeneration
  5. Irregular pattern of acanthosis
  6. MAY SEE: Keratin plugs and Civatte bodies
23
Q

How are the following lesions treated/managed in Discoid Lupus Erythematous:

  1. Oral lesions? (hint: same as LP)
  2. Cutaneous lesions?
A

1. Oral Lesions

  • 1st line = Topical Corticosteroids
  • E.g. Hydrocortisone, Betamethasone or Benzydamine (Difflam)*
  • 2nd line = Topical Immunsuppressants (Calcineurin inhibitors)
  • Ciclosporin, Tacrolimus or Pimecrolimus*
  • Severe = Systemic Corticosteroids or Immunosuppressants

2. Cutaneous Lesions

  • Suncream (SPF 50)
  • Chloroquine (anti-malarial)
  • Potent steroids
24
Q

What are 10 causes of LOCALISED oral pigmentation changes?

A
  1. Diet/Beverages
  2. Ecchymosis (Bruising)
  3. Varices
  4. Black Hairy Tongue
  5. Amalgam Tattoo (Focal Agyrosis)
  6. Graphite Tattoo
  7. Ethnobotanical Tattoo
  8. Metal Salt deposits
  9. Oral Melanotic Macules
  10. Oral (Malignant) Melanoma
25
Q

What oral pigmentary changes may occur due to:

  1. Black Hairy Tongue?
  2. Amalgam Tattoo?
  3. Graphite Tattoo?
  4. Ethnobotanical Tattoo?
  5. Metal Salt Deposits?
A

1. Black Hairy Tongue
Brown and white lesions on dorsum of tongue

2. Amalgam Tattoo
Slate grey/ blue-black macules on mandibular gingivae or alveolar mucosa - with no elevation

3. Graphite Tattoo
Grey/black lesion often on anterior palate of young children

4. Ethnobotanical Tattoo
Grey/Black mucosal tattoo in African Sahel population

5. Metal Salt Deposits
Linear grey/black lines (“Burtons” or “Lead” lines) along gingival margin

26
Q

What oral pigmentary changes may occur in:

  1. Oral Melanotic Macule?
  2. Oral Malignant Melanoma?
  3. Ecchymosis?
  4. Varices?
A

1. Oral Melanotic Macule
Uniform, flat brown-black macule (less than 0.5cm diameter) with well-defined, distinct border - often on lip

2. Oral Malignant Melanoma
Dark brown-black (varied appearance as may appear red) with irregular borders and thickening in later “nodular” phase - often on palate, lip or gingiva.
Follow history of recent change in naevus (birthmark/freckle)

3. Ecchymosis
(Bruising) Red-blue-purple appearance.
Related to trauma or spontaneous (may suggest bleeding disorder)

4. Varices
Blue, lobulated lesions - often in lip or sublingual.
Painless + blanch with pressure (caused by abnormal venous dilation)

27
Q

What is the cause of Black Hairy Tongue?

What are 4 risk factors?

How do we treat/manage it? (4)

A

Elongation of filliform papillae (Hyperkeratosis) → Extrinsic staining and easier bacteria/fungi accumulation

Risk Factors:

  1. Poor OH
  2. Smokers
  3. Antiseptic mouthwashes
  4. Antibiotics (esp. tetracycline family - micocycline or doxycycline)

Management:

  1. Reassure pt
  2. Remove risk factors
  3. Encourage tongue brushing (not too hard)
  4. Oxidising mouthwashes (e.g. Peroxyl)
28
Q

Focal Agyrosis/ Amalgam Tattoo:

  1. What do you see? Does this change over time?
  2. What are 2 risk factors?
  3. What may you see histologically? (2)
  4. How would you manage it?
A

1.

  • Slate-grey/blue-black pigment
  • No elevation
  • Gingiva or alveolar mucosa (mandible)
  • NO change in size BUT may BLUR over time

2. ​ Recent amalgam removal or XLA of amalgam-filled tooth

3. Black/brown pigments seen in:

  • Lamina Propria (encase elastic fibres and capillary basement membrane)
  • Histiocye cytoplasm

4.

  • Reassure pt (no health concern) and observe
  • If aesthetic concern (e.g. lip) remove with laser
  • If doubt - Excise and biopsy
29
Q

Graphite Tattoo:

  1. What pigmentary changes would you observe?
  2. Do you need to investigate further?
  3. What would you see on histology? (5)
  4. How do you manage it?
A

1. Grey-black pigment on anterior palate (often young children, from chewing graphite pencils)

2. YES!

  • Manditory biopsy to rule out malignancy
  • Radiographs - may see r/o from graphite

3.

  • Chronic inflammatory cells
  • Granulation tissue
  • Multi-nucleated giant cells
  • Solid black granules (consistent with graphite)
  • Labial cortical bone destruction

4. Same as Amalgam tattoo

  • Reassure pt + observe
  • If aesthetic concern (e.g. lip) - laser
30
Q

How do oral melanotic macules and oral malignant melanoma differ in terms of:

  1. Pigmentary changes (appearance)?
  2. Risk factors?
  3. Management?
A
31
Q

Is the prognosis of oral malignant melanoma poor or good?

Where does it often metastasis to?

A

POOR - 5-20% 5 year survival (less than skin melanoma)

Often metastasises (due to rich blood and lymphatic supply) to the 3 L’s”

  1. Lymph Nodes
  2. Liver
  3. Lungs
32
Q

What are 3 causes of developmental generalised pigmentation?

A
  1. Racial pigmentation
  2. Peutz-Jeghers (“multiple peri-oral and vermillion freckles”)
  3. Pigmented naevi
33
Q

What is a naevi?

A

Pigmented moles, freckles or birthmarks caused by clustering of melanocytes (which produce melanin)

34
Q

What are 2 habits that can cause generalised oral pigmentation?

(HINT: Think Socal History)

A
  1. Paan/Betel chewing
    → Orange/Brown deposits on mucosa AND teeth
  2. Smoking
35
Q

How can a post-inflammatory response (healing) cause generalised oral pigmentary changes?

A

Melanin “drop out” during healing phase

Common site = Buccal mucosa in Chronic LP

36
Q

What is Addison’s Disease?

What pigmentary changes would you observe:

  1. In the mouth?
  2. On the skin?

What systemic features may be observed?
(HINT: Lost in the desert)

A

Underproduction of Aldosterone + Cortisol

(Pigmentary changes occur as reduced Cortisol stimulates increased ACTH → Stimulation of MSH, melanin-producing hormone)

  1. Mouth = “Water-Spaniel” Blue-black streaks or patches
  2. Skin = Bronzed

Systemic:

Weightloss, weakness, hypotension, hypoglycaemia, nausea and stomach pain

37
Q

What medications can cause:

  • Blue-grey (3)
  • Brown (5)

oral pigmentation?

A

Blue-Grey:

  • Minocycline
  • Chloroquine (anti-malarial)
  • Fluoxetine (SSRI)

Brown:

  • Minocycline
  • Doxycycline
  • Propranolol
  • AZT (HIV Anti-viral)
  • Bleomycin + Cyclophosphamide (cancer medication)
38
Q

What are 6 oral changes associated with Paan/betel chewing?

A
  1. Staining (orange-brown of mucosa and teeth)
  2. TSL (Attrition)
  3. Submucus Fibrosis! (Pre-malignant)
  4. Lichenoid Reaction
  5. Epithelial Dysplasia
  6. OSCC
39
Q

What are 5 broad catagories for causes of generalised oral pigmentary changes?

  1. Developmental
  2. ?
  3. ?
  4. ?
  5. ?
A
  1. Developmental (Racial, Peutz-Jeghers or Pigmented naevi)
  2. Habits (Paan or Smoking)
  3. Post-Inflammatory
  4. Medications
  5. Systemic Diseases (e.g. Addisons - water spaniel)

BDS4 (5 decks)

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