CD 16 Flashcards
Inflammatory skin conditon are they infaction?
No. Not an infection.
In general what is Inflammatory skin diseases
superficial inflammation of the skin
not caused by infectious agents are an immune dysfunction to innocuous substances (allergens) or self proteins (autoimmunity)
Inflammatory skin diseases involves response from ?
immediate responses from GRANULOCYTE – mast cells, eosinophils, neutrophils, basophils
delayed/acquired response – T CELLS (Th cells), many differen types with diff roles
What is Acne (Acne vulgaris)?
Very common skin disease, chronic inflammation of sebaceous gland
common at puberty, also present in adults
What is the pathogenesis of Acne?
Hyperseborrhoea (ecssisive sebum production) & abnormal follicular keratinization
Bacterial proliferation & inflammation
Step 1 what is the pathogenesis of Hyperseborrhoea production occur for acne production?
Androgen Stimulte sebaceous glands and sebum production
Step 3 how bacterial prolifiration & inflammation occur in Acne production?
P.acne & P.granulosum bacteria secret toxins and initiate inflammation through interection with keratinocytes.
Step 2 How pathogenesis of follicular keratinization occur in acne production?
spontaneous changes in keratinocytes – increased turnover
altered pattern of kertinisation
keratinous material becomes denser,
What are the common bacteria responsible for acne ?
P. acne, P. granulosum, P. parvum
What are the factors cause acne ?
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??
Treatment for Acne ?
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
Types of Dermatitis
-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)
What is Atopic dermatitis/eczema?
- Chronic
- allergic mediated immune dysfunction disease
-immune mediated (Th2) to allergens
What are the symptoms of Atopic dermatitis/eczema ?
Dry, red, cracked,
weeping, itching skin
Sometimes associated with other inflammatory condition like asthma, arthritis, IBD
Who is commonly diagnosed in Atopic dermatitis?
childhood
Pathogenesis of Acute
Atopic Dermatitis ?
allergens enter via damaged skin & stimulate mast cells etc to degranulate
Pathogenesis of chronic Atopic Dermatitis?
- driven by cytokines released by T cells
- keratinocyte (KC) dysfunction
Contact dermatitis is 3 types?
Irritant Contact Dermatitis (ICD)
Allergic Contact Dermatitis (ACD)
Protein Contact Dermatitis (PCD)
Who is responsible of causing Irritant Contact Dermatitis (ICD)
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
Who is responsible of Allergic Contact Dermatitis (ACD)
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
Who is responsible for Protein Contact Dermatitis (PCD)
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
What is Nappy rash (ammoniacal dermatitis)
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
What is Urticaria
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
Urticaria Pathophysiology
mediated by mast cell
de-granulation
What causes Urticaria
pressure (scratching), heat, cold, chemical contact, allergies,diet
What is the Treatment
avoid triggers
see workshop
What is Psoriasis vulgaris?
-chronic T cell mediated
inflammatory disease that can
develop into psoriatic arthritis
(within 10 years)
What are the causes of Psoriasis vulgaris?
Genetics
Environment: alcohol, smoking, drugs
What is the pathogenesis ofPsoriasis of vulgaris ?
-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
Psoriasis - CAM
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
What is the AD vs psoriasis ?
-Both immune mediated & can be treated with cytokine antagonists & immune suppression
- different
but
similar
Issues are following
-Cost
-Systemic immunesuppression
