Dermatology SC024: I Have An Itchy Rash (Eczema, Urticaria, Tinea Infection And Psoriasis) Flashcards

1
Q

History taking in Acne

A
  1. Onset
  2. Duration
  3. Symptom (itch, pain)
  4. Provocative / Alleviating factors
  5. Location
  6. History of Atopy (asthma, allergic rhinitis)
  7. Family history of acne scarring (scarring can be genetically related)
  8. Psychosocial impact
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2
Q

Acne

A
  • Common in teenage (80%)
  • M>F
  • Family history +ve (esp. for scarring)
  • Often neglected: asymptomatic, not life threatening
  • Some patients / parents consider acne to be normal for puberty
  • Main problem with Acne: ***Scarring (e.g. Keloid)

Etiology:
1. Sex hormone
- ***Testosterone: a definite role
- ↑ Sebum production
- M>F
- Female: flare up occur with menstrual period (when estrogen ↓ —> testosterone ↑), irregular period more resistant to treatment

  1. Sebum production
    - Hormone
    - ?Genetic
    - ?Food (carbohydrates —> insulin —> growth factor effect —> enhance keratinocyte proliferation)
    - Together with dead cells block hair follicle —> comedome (blackhead)
  2. **Bacteria proliferation
    - **
    Propionibacterium: P. acnes, P. avidum, P. granulosum (can be antibiotic-resistant —> antibiotic use limited to 3 months + Keratolytic agent / Retinol to prevent resistance)
    - Blockage of hair follicle —> Serum attract bacteria —> Bacteria proliferation causing inflammation —> Inflammed hair follicle —> Red papule
  3. Host response
    - Defence mechanism against bacteria proliferation —> WBC infiltration —> Secretion of enzyme that lead to non-specific destruction of bacteria + dermal tissue —> Pustules, scarring, cyst formation

Pathogenesis:
- Sebum from sebaceous gland + Dead keratinocyte
—> Block hair follicles (Blackhead) to prevent sebum excretion
—> Sebum collection cause bacterial overgrowth
—> Inflammed hair follicle
—> WBC collection in follicle
—> Pustules

Clinical features:
- Comedome (blackhead)
- Papule (red)
- Pustule
- Scarring
- Cyst

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3
Q

Treatment for Acne

A
  1. Topical
    - **Benzoyl peroxide
    - **
    Antibiotic
    - **Retinoid (e.g. Tretinoin)
    - **
    Azelaic acid
    - Sulphur

Normal use: Antibiotic cream —> step up to Benzyol peroxide / Azelaic acid —> Retinoid therapy 1 month later (can lead to acne flare when initiating ∴ need to use other agents first to control acne) (step up strength of Retinoid every 4-6 weeks then maintanence)

  1. Systemic
    - Antibiotic
    - Hormonal therapy
    - ***Isotretinoin

Previous indication of systemic therapy:
- Moderate to severe acne
- Depressed
- Significant post-inflammatory hyperpigmentation
- Acne-excoriee
- Acne keloidalis
- Gram -ve folliculitis (resistant to Tetracycline —> need skin swab)

Recent trend:
- Start early treatment to prevent scarring
- Oral contraceptive (reduce effect of testosterone) + antibiotic for 3-4 months —> gradual step up to cream —> cream only for long term

  1. Ablative resurfacing (aka Laser) (gold standard)
    - Fractional photothermolysis
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4
Q

Benzoyl peroxide

A
  • Conc: 2.5-10%

MOA:
- ***Keratolytic agent —> unblock hair follicle
- Reduce comedomes
- Suppress skin surface free acid
- Reduce skin surface bacteria
- Use in combination with other topical therapy esp. Antibiotic to prevent antibiotic resistance

SE:
- Irritation
- Dryness

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5
Q

Azelaic acid

A

MOA:
- ***Keratolytic
- Reduce free fatty acid + bacteria load
(- Lightening effect: less post-inflammatory hyperpigmentation)
- As effective as Benzyol peroxide, Retinoid, Tetracycline

SE:
- Mild irritation

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6
Q

Antibiotics

A

Topical: Erythromycin, Tetracycline, Clindamycin
- use in combination with other topical therapy e.g. Benzyol peroxide / Retinoid
- MOA: ***Anti-microbial effects: reduce P. acnes

Systemic:
1. Tetracycline / related
2. Erythromycin / related

MOA:
- Anti-microbial
- ***Anti-inflammatory (take 3 weeks to work, 1 course ~3-4 months —> step up topical medications meanwhile)

SE:
- GI (take probiotic)
- Rarely for Tetracycline group: Phototoxic, Liver damage, SLE-like
- Relapse if discontinued

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7
Q

Retinoid

A

Topical:
- Tretinoin, Isotretinoin

Systemic:
- Isotretinoin

MOA:
- ***Vit A analogue —> regulate epithelial cell growth
- Reduce comedogenesis
- Reduce inflamed + non-inflammed lesions
(- Reduce sebum production)

SE:
- Irritation
- Dryness

CI:
- Avoid in pregnancy (Teratogenic): Stop contraception ***1 month after completion of isotretinoin

Examples:
1. Adapalene gel
- new generation of topical retinoid
- as effective as tretinoin 0.025% but less SE (scaling, irritation, erythema)
- gel / cream preparation

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8
Q

Isotretinoin

A
  • Only effective mean to long term cure
  • Significant SE
  • Only dermatologist can use the treatment

MOA:
- ***Reduce sabaceous gland volume —> reduce sebum production
- Alter cutaneous immunological function

SE (significant):
- **Teratogenicity (cleft palates, neurological problems affecting 4-7% of baby) —> need to have contraceptive method: Stop contraception **1 month after completion of isotretinoin
- Chelitis
- Conjunctivitis
- Myositis
- Arthralgia
- Hair loss
- **Liver impairment —> check LFT (baseline + 4 weeks)
- **
Raised TG —> check TG + lipid (baseline + 4 weeks)
- Raised benign ICP
- Headache
- ***Mood changes —> relative CI in previous depression

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9
Q

Hormonal therapy

A
  • Oral contraceptive / Anti-androgen (Cyproterone)
  • For female that have hormonal disturbance / contraceptive needs
  • Takes 4-6 weeks to improve

SE:
- Relapse if discontinued

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10
Q

Ablative resurfacing (aka Laser)

A

Gold standard

Several problems:
- “Unforgiving” system
- Pain, oozing, prolonged erythema
- Risk of infection + scarring
- Can leave unnatural skin sheen
- Avoid certain skin surfaces —> scar
- Pigmentary problems

Example:
- Fractional photothermolysis

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11
Q

History of Eczema

A
  • Itchiness
  • Area: Flexural area of limb
  • Family history of atopy (asthma, allergic rhinitis, eczema —> lungs, nose, skin are organs most exposed to external environment)

Atopic march: Difference in prevalences of allergic diseases
- ?Allergen load
- ?Tolerance
- ?Differ in immunological response

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12
Q

Approach to Dermatitis

A
  1. History
    - Onset
    - Duration
    - Site
    - Occupation
    - Atopic tendency
    - Family history
  2. P/E
    - Type
    - Distribution
    - Arrangement
    - Secondary changes
    - Nail, Scalp, Back of ear, Genitalia
  3. Investigation
    - Patch test (allergic test)
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13
Q

Classification of Dermatitis

A
  1. Endogenous
    - Atopic dermatitis
  2. Exogenous
    - Primary irritant
    - Allergic contact

ALL 3 can ***overlap

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14
Q

Patch test

A

Indications:
- Dermatitis for hands, feet, face, legs that persist despite avoiding irritant
- Chronic medicament use
- Atypical / Persistent discoid eczema

Screening series:
- Metals
- Rubber chemical
- Medicaments
- Cosmetics
- Balsams
- Others (e.g. Preservatives, Metal impurities)

NOT the same as Skin prick test:
Patch test:
- Detect allergic contact dermatitis (**Type 4 hypersensitivity reaction)
- Allergy to hair dye, shoes, active ingredients, preservative and fragrances in sunscreens, cosmetics and medicaments
- Allergic reactions usually appear **
2 to 4 days after applying the allergen on the skin but it can take up to a week to react

Skin prick test:
- Test **Type 1 allergy causing hay fever, asthma and contact urticaria (hives)
- Involves needle pricking
- Results read **
20 minutes after skin pricking

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15
Q

Atopic eczema (Atopic dermatitis / AD)

A
  • Associated with asthma, allergic rhinitis (***Atopic march)
  • Early onset <2
  • Genetic predisposition (one parent: 30%, both: 80%)
  • Due to immunological imbalance (in skin, tendency to mount reaction against harmless substance e.g. food, pollutants but diminished reaction against harmful substance e.g. bacteria)
  • Common in HK: 5-28%

4 problems:
1. Weakened immunological system against pathogens
2. Reduced ability to preserve water —> Transepidermal water loss
3. Infection / Scratching make thing worse (scratching —> skin cell protein (e.g. keratin) can mimic allergens —> simply avoiding allergen does not help)

Clinical features:
- ***Itchy rash
- Ill-defined Erythema (vs Psoriasis: more defined), Papules, sometimes Maculo-papular eruptions —> scratching —> may cause Lichenification (secondary changes)
- Infants: Face + Extensor surface
- Children: Flexural surface
- Chronic + Relapsing in nature
- Dry skin

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16
Q

Management of Dermatitis

A

1st line:
1. Avoid irritant / allergen
2. Emollient
3. Topical steroid
4. Antihistamine
5. Potassium permanganate
6. Treat secondary infection

17
Q

Seborrhoeic dermatitis

A
  • Occurs in ***extreme of age (Infants / Elderly) —> ∵ Poor immunological system
  • Etiology thought to be associated with ***yeast overgrowth
  • Can be difficult to differentiate from AD
  • Resolve ***within 6-12 weeks of life (when immunological system mature)

Treatment:
- Olive oil for scalp
- **Emollient
- **
Mild potency steroid
- ***Antifungal cream

18
Q

***Atopic dermatitis (AD) vs Seborrhoeic dermatitis (SD)

A

AD:
- start at 3 months (later)
- **chronic
- **
itchy
- **+ve family history for atopic disease
- **
face, flexural surface
- ***raised IgE (although usually clinical diagnosis —> no need to take blood)

SD:
- start at 6 weeks (earlier)
- **resolve by 3 months
- **
non-itchy
- **-ve family history
- **
scalp, face, axilla, napkin
- IgE normal

19
Q

Irritant contact dermatitis (Primary irritant dermatits)

A
  • ***Non-immunological (everyone can develop)
  • Direct chemical / physical damage to the skin
  • If exposure to the irritant is sufficient (i.e. concentration, duration) —> direct cumulative response —> everyone will develop irritant dermatitis

Types:
1. Acute toxic
- e.g. caustic injury
- Single insult is over threshold for clinical apparent disease —> impairment of skin (transepidermal water loss) immediately

  1. Chronic cumulative
    - e.g. soaps, detergents
    - Recurrent insult to skin —> impairment of skin (transepidermal water loss) later

Risk factors:
- Age (very young, elderly)
- Skin site (face, back of hands, scrotum (i.e. jog itch))
- Underlying skin disease
- Occupational (building and construction, catering, cleaning, dairy farming, engineering, gardening, hairdressing, housework, motor mechanics, nursing)

20
Q

Allergic contact dermatitis

A
  • ***Delayed type 4 hypersensitivity (several weeks / months)
  • Host immunological response to allergen
  • Occurs in ***susceptible individuals that become sensitised

Pathogenesis:
- Allergens come into contact with Langerhans cells (APC)
—> present to CD4 T cells
—> sensitisation
—> re-exposure
—> cytokine released by CD4 T cells
—> inflammatory infiltration + local oedema + erythema

21
Q

Dermatitis from Traditional Chinese Medicine (TCM)

A

Can be both Irritant contact dermatitis / Allergic contact dermatitis

Use of TCM in dermatology:
1. Aches, pain
- headache, abdominal pain
- contain camphor, methanol, essential oil
- cross reactivity can occur with fragrances / balsam of Peru

  1. Orthopedic injury
    - promote healing after physical injury
    - used to set bone “bonesetter”
    - contain >10 herbs
    - Allergic contact dermatitis to mastic, myrrh
  2. Skin disease
    - Eczema
    - Psoriasis
    - Tinea
    - contain contaminants including steroid, NSAIDs, keratolytic agents (e.g. salicylate)
    - Irritant + Allergic contact dermatitis reported