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Oral Medicine > Vesiculobullous Disease 1 > Flashcards

Vesiculobullous Disease 1 Flashcards

1
Q

Immune mediated disease

A

Hypersensitivity
- type 1
- type 2
- type 3
- type 4
- type 5

Immunogenic
- cell mediated immunity
- antibody mediated immunity

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2
Q

2 Types of Immunological Oral Disease

A

Local disease
- Aphthous ulcers
- Lichen planus
- Orofacial granulomatosis

Systemic with local effects on oral mucosa
- Erythema multiforme
- Pemphigus
- Pemphigoid
- Lupus erythematosis
- Systemic sclerosis
- Sjogren syndrome

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3
Q

What type is Erythema multiforme?

A

Type 3 hypersensitivity
- antigen antibody complexes

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4
Q

What is in cell mediated immunity?

A
  • aphthous ulcers
  • lichen planus
  • orofacial granulomatosis
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5
Q

What is in antibody mediated immunity?

A
  • pemphigus
  • pemphigoid
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6
Q

Immunological skin disease

A
  • linked with immunological oral disease
  • share many common antigens and epitopes
  • embrologically oral mucosa develops from the same precursor tissue of skin
  • many blistering skin conditions can also affect mouth
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7
Q

Difference Epitopes vs Antigen

A
  • antigen are big immunogenic site within a protein
  • antibody will only bind to one small part, such as different epitopes in sequence of protein antigen
  • antibody may only bind to one particular site of antigen
  • important as antigen-antibody binding will affect shape or confirmation of protein antigen and change in shape which occurs will well detect seen clinically
  • Epidermolysis Bullosa, where different epitopes invovled will determine whether disease ranges from mild immunobullous condition to a more lethal form
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8
Q

What happens in Immunological skin disease?

A
  • auto-antibody attack on skin components -> cause loss of cell- cell adhesion
  • split forms in skin
    1. fills with inflammatory exudate
    2. forms vesicles/ blister
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9
Q

Vesicles vs Blisters

A
  • size of lesion involved
  • blisters are larger
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10
Q

Desmosome/ Hemidesmosome Attachment

A
  • involved them attach the epithelial cells to each toher and basement membrane and to protein desmoglein.
  • desmoglein are the target for many antibodies involved in immunobullous diseases
  • causes loss of adhesion between desmosomes allowing cell layers to split
  • test to biopsy sites and look of presence of antibodies within skin tissues
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11
Q

How does Direct immunofluorescence work?

A
  • if suspect there is an antibody bound to the tissue
  • pemphigoid in this case, antibody (blue) bind to tissue and causing disease
  • manufacturing another antibody, which has a fluorescein marker tag onto it
  • second antibody will bind to first antibody already attached to the tissue
  • when tissue is examined with fluorescence lighting, the fluorescein will show where the antibody is bind to the tissue
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12
Q

Types of Immunofluorescence?

A
  1. Direct Immunofluorescence
  2. Indirect Immunofluorescence- circulating antibodies not yet bound to tissues
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13
Q

About direct immunofluorescence?

A
  • gold standard
  • looks for antibody bounds to tissue
  • useful test when its is immunobullous condition
  • remember a sample biopsy for immunofluorescence, must not be put into a formaline containing transport medium
  • will cause binding sites to be lost
  • must be transport fresh and process quickly
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14
Q

About indirect immunofluorescence

A
  • looks for CIRCULATING antibody not yet bound to tissues
  • detected by immunofluorescence from a plasma sample
  • less reliable as a diagnostic aid
  • good for monitoring disease like disease activity, looking for levels of antibody in disease such as Pemphigus can give a good guide for tx need
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15
Q

Which test to do for a new pt?

A

DIF is always preferred than IIF

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16
Q

Examples of Vesiculobullous conditions

A
  1. Erythema Multiforme
  2. Pemphigus
  3. Pemphigoid
  4. Angina Bullosa haemorrhagica
  5. Bullous Lichen Planus (lichen pemphigoides)
17
Q

What is erythema multiforme?

A
  • ## spectrum disorder caused by immunogenic related skin and mucosa ulceration
18
Q

How is erythema multiforme formed?

A
  • in the body, an antigen presents, which is targeted by an antibody
  • there is usually an antigen which has been met before and therefore a prompt immune response results quickly generating antibodies from memory B cells
  • these antigens and antibodies combine within circulations and this large complex is unable to pass through capillaries
  • when complex gets to the tissues, it becomes wedges and activates compliment within blood vessels
  • causing a perivascular inflammatory response
  • pt will get blistering or ulceration of tissue
  • depends upon individual antigen-antibody complex
  • hence, some may get skin lesions and no genital lesions
  • spectrum disorder
  • most extreme form is known as Stevens Johnson Syndrome
19
Q

What do you call a severe multisystem involvement fr Erythema Multiforme?

A

Stevens- Johnson syndrome
- skin, conjunctivae, nose, pharynx, mouth genital

20
Q

About erythema multiforme

A
  • acute onset
  • M>F
  • skin as a target lesion
  • mucosa- ulcers
  • young males- recurrent within a short period of time (late teens, ulceration lasting 2-3 weeks)

Aetiology
- drugs
- herpes simplex-> leads to type 3 sensitivity
- mycoplasma

Lips and anterior part of mouth
- crops, heal in 2 weeks
- very painful- unable to eat/ drink (dehydration)

21
Q

Management of Erythema Multiforme

A

For oral lesions
1. Urgent medical therapy
- systemic steroids (up to 60mg/day)- Prednisolone
- systemic Aciclovir

  1. Encourage fluid intake
    - may need IV fluid if unable to drink
  2. Encourage analgesia
  3. If recurrent problems - consider prophylactic aciclovir daily (400mg/twice daily)
    - allergy test for environmental triggers
    - infective agent -> Mycoplasma- fungal infection
22
Q

Angina Bullosa Haemorrhagica

A
  • commonest oral blistering condition
  • blood filled blister in oral mucosa
  • usually painless
  • BM and soft palate are normally common sites
  • rapid onset-> appear in a few minutes, last about an hour then burst (mildly symptomatic for a day or so)
  • initiated by minor trauma, ie: eating
  • heal with no scarring within days
  • no aetiology
23
Q

Management of ABH

A
  1. non- specific ulceration
  2. DIF -ve
  3. IIF -ve
  4. no platelet/ coagulation defect
  5. may recur

Management for symptomatic
- chlorhexidine MW
- Difflam spray until lesion heals

  • normally no tx available
  • reassure pt that is benign
  • explain triggers and course of disease, ie: eating, use of steroid inhalers
  • avoid using inhalers
  • will not spread into systemic issues
24
Q

Resolving Angina Bullosa Haemorrhagica

A
  • left with a small ulcer
  • remember to ask pt if they start as blisters or ulcers
25
Q
A

Oral Medicine (24 decks)

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