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CD 16 Flashcards

1
Q

Inflammatory skin conditon are they infaction?

A

No. Not an infection.

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2
Q

In general what is Inflammatory skin diseases

A

superficial inflammation of the skin
not caused by infectious agents are an immune dysfunction to innocuous substances (allergens) or self proteins (autoimmunity)

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3
Q

Inflammatory skin diseases involves response from ?

A

immediate responses from GRANULOCYTE – mast cells, eosinophils, neutrophils, basophils
delayed/acquired response – T CELLS (Th cells), many differen types with diff roles

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4
Q

What is Acne (Acne vulgaris)?

A

Very common skin disease, chronic inflammation of sebaceous gland
common at puberty, also present in adults

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5
Q

What is the pathogenesis of Acne?

A

Hyperseborrhoea (ecssisive sebum production) & abnormal follicular keratinization

Bacterial proliferation & inflammation

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6
Q

Step 1 what is the pathogenesis of Hyperseborrhoea production occur for acne production?

A

Androgen Stimulte sebaceous glands and sebum production

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7
Q

Step 3 how bacterial prolifiration & inflammation occur in Acne production?

A

P.acne & P.granulosum bacteria secret toxins and initiate inflammation through interection with keratinocytes.

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8
Q

Step 2 How pathogenesis of follicular keratinization occur in acne production?

A

spontaneous changes in keratinocytes – increased turnover

altered pattern of kertinisation

keratinous material becomes denser,

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9
Q

What are the common bacteria responsible for acne ?

A

P. acne, P. granulosum, P. parvum

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10
Q

What are the factors cause acne ?

A

Genetics: polygenic(means lots of genes)
—Twin study – 82% concordance in monozygotic twins, 40% in di-zygotic.

Environment:

  • no link between‘cleanliness’ and acne
  • diet??
  • stress??
  • smoking??
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11
Q

Treatment for Acne ?

A

Usually heals spontaneously, main treatment aim is to reduce scarring and prevent new lesions

To pop or not to pop?

CAM use is widespread – no good evidence to support use but gives a feeling of control & being more natural. Can have adverse effects

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12
Q

Types of Dermatitis

A

-Atopic dermatitis (atopic/allergic eczema)

  • Contact dermatitis (contact eczema) – can occur in ‘normal’ and allergic/atopic individuals, some evidence for increased rates of ACD in atopic individuals
    - irritant contact dermatitis (ICD)
    - allergic contact dermatitis (ACD)
    - protein contact dermatitis (PCD)
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13
Q

What is Atopic dermatitis/eczema?

A
  • Chronic
  • allergic mediated immune dysfunction disease

-immune mediated (Th2) to allergens

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14
Q

What are the symptoms of Atopic dermatitis/eczema ?

A

Dry, red, cracked,
weeping, itching skin

Sometimes associated with other inflammatory condition like asthma, arthritis, IBD

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15
Q

Who is commonly diagnosed in Atopic dermatitis?

A

childhood

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16
Q

Pathogenesis of Acute

Atopic Dermatitis ?

A

allergens enter via damaged skin & stimulate mast cells etc to degranulate

17
Q

Pathogenesis of chronic Atopic Dermatitis?

A
  • driven by cytokines released by T cells

- keratinocyte (KC) dysfunction

18
Q

Contact dermatitis is 3 types?

A

Irritant Contact Dermatitis (ICD)
Allergic Contact Dermatitis (ACD)
Protein Contact Dermatitis (PCD)

19
Q

Who is responsible of causing Irritant Contact Dermatitis (ICD)

A

physical (UV, heat, cold, damp) or chemical (detergents, solvents, bleaches) agents causing direct injury
Can be acute (minutes to hours) or chronic/cumulative, mild or severe, recurrent

20
Q

Who is responsible of Allergic Contact Dermatitis (ACD)

A

Immune response to small organic & inorganic allergens that can penetrate skin eg nickel
Sensitizing phase (asymptomatic) of weeks to months then an inflammatory phase.
Type 4 response – cellular Th1 cells

21
Q

Who is responsible for Protein Contact Dermatitis (PCD)

A

Immune response to large protein allergens
Can not penetrate intact skin
Sensitizing phase (asymptomatic) of weeks to months then an inflammatory phase.
IgE & cellular response – similar to allergic dermatitis

22
Q

What is Nappy rash (ammoniacal dermatitis)

A

ICD caused by irritants (ammonia in urine, proteolytic enzymes in faeces), friction, damp

Symptoms of Nappy rash:
redness, swelling, initially scaly, progresses to erosions, can be acute or chronic
complication is yeast infection (pustules) or bacterial (crusty) secondary infection

treatment:
Regular nappy changes, careful cleaning,
barrier creams
If gets complicated: treat infections

23
Q

What is Urticaria

A 
Common
Itchy, red (hives),localized oedema of the
 upper dermis, or can occur in deeper 
dermal layers (angioedema)
Can be acute or chronic – self resolving
24
Q

Urticaria Pathophysiology

A

mediated by mast cell

de-granulation

25
Q

What causes Urticaria

A

pressure (scratching), heat, cold, chemical contact, allergies,diet

26
Q

What is the Treatment

A

avoid triggers

see workshop

27
Q

What is Psoriasis vulgaris?

A

-chronic T cell mediated
inflammatory disease that can
develop into psoriatic arthritis
(within 10 years)

28
Q

What are the causes of Psoriasis vulgaris?

A

Genetics

Environment: alcohol, smoking, drugs

29
Q

What is the pathogenesis ofPsoriasis of vulgaris ?

A

-Initiation:
damaged KC release ‘danger’ molecules that activate DC, go to lymph node & activate T cells
Antigen - self?????

-Inflammation:
Th cells release cytokines – activate KC, neutrophils, mast cells, macrophages
dermal hyperplasia, impaired KC differentiation –plaque formation

30
Q

Psoriasis - CAM

A

CAM use 42-69%
Usually used along with instead of replacing traditional therapies
consistent evidence for fish oils supplements, some (weak) evidence for vitamin D (?), vitamin B12, and selenium supplementation
concerns over quality of preparations & presence of contaminants, drug interactions
disclose and discuss with clinicians

31
Q

What is the AD vs psoriasis ?

A

-Both immune mediated & can be treated with cytokine antagonists & immune suppression
- different
but
similar
Issues are following
-Cost
-Systemic immunesuppression

CD (23 decks)

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