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CFB > WCS09 Dermatology 2 > Flashcards

WCS09 Dermatology 2 Flashcards

1
Q

Dermatologic emergencies

A
  1. Eczema herpeticum
  2. Generalised Exofoliative Dermatitis (GED) / Erythroderma
  3. Bullous pemphigoid
  4. Pemphigus vulgaris
  5. Pustular psoriasis
  6. Acute Generalised Exanthematous Pustulosis (AGEP)
  7. Drug Rash with Eosinophilia and Systemic Symptoms (DRESS)
  8. Stevens-Johnson syndrome (SJS) / Toxic Epidermal Necrolysis (TEN)
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2
Q
  1. Eczema herpeticum
A

Caused by ***Herpes virus

  • starts with clusters of ***itchy / painful blisters (記: 好多細紅點)
  • Face + Neck
  • in normal skin / sites affected by Atopic dermatitis / other skin disease
  • ***unwell, fever, swollen local LN

Complications:
1. Secondary bacterial infection
- Staphylococcus / Streptococcus—> Impetigo / Cellulitis

  1. Affect multiple organs
    - eyes, brain, lung, liver
    - rarely fatal

Management:
- IV ***Aciclovir 15 mg/kg/day for >= 5 days

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3
Q
  1. Generalised Exofoliative Dermatitis (GED) / Erythroderma
A
  • Any ***inflammatory skin disease affecting >90% of body surface (記: 係咁甩皮 + 好紅)
  • Not a defined entity, but a clinical presentation of a variety of diseases

Epidemiology:
- True incidence unknown: 0.9 per 100,000
- 50-60 years of age
- Male : Female = 2-4 : 1

Challenge:
- Identify cause

**Underlying causes:
1. **Pre-existing dermatoses (53%)
- **Atopic dermatitis
- **Psoriasis (Pustular flare)
- Contact dermatitis: Airborne / Phytophotocontact dermatitis

  1. **Drug eruptions (5%)
    - Antiepileptics
    - Antihypertensive (Captopril, Furosemide)
    - **    Antibiotic (Penicillin, Sulphonamide)
    - ***Allopurinol
  2. **Malignancy (16%)
    - **    Cutaneous T Cell Lymphoma CTCL (including Sezary syndrome) (most common)
    - Hodgkin’s disease (2nd most common)
  3. Miscellaneous (rare)
  4. Idiopathic (26%)
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4
Q

Investigations for GED

A

Basic investigations:
- Full blood count, ESR
- Peripheral blood film
- **Buffy coat for Sezary cells (for CTCL)
- Urea, creatinine, electrolytes
- LFT
- CXR
- **Skin biopsy for history (>=2 sites): Direct Immunofluorescence (DIF) if immunobullous disease suspected
- Age appropriate ***malignancy work-up

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5
Q

Management of GED

A

Monitor + Correct:
- **Protein / Electrolyte imbalance
- **Circulatory status (e.g. BP, pulse rate)
- **Body temperature
- **Secondary sepsis

Control:
- Environmental temperature (avoid over-cooling / heating)
- Adequate fluid intake
- Diuretics / Plasma infusion if edema. Treat cardiac failure
- Consider drug cause - stop non-essential drugs
- Treat secondary infections
- ***Intensive topicals

Treatment:
- Severe / Persistent / Idiopathic / Drug causes: Prednisolone 0.5-1 mg/kg/day
—> Beware pustulation if have concurrent **psoriasis (*Pustular flare during withdrawal)

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6
Q

Intensive topicals

A

Scalp:
- Cetrimide / Coal tar shampoo
- Betamethasone valerate 0.1% scalp lotion BD

Trunk:
- Betamethasone valerate 0.1% BD (cream if oozy, ointment if dry)

Face and Flexures:
- Betamethasone valerate 0.025% (∵ thin skin) cream BD

Skincare:
- Chlorhexadine / Potassium permanganate wash (if oozy / infected)
- Emulsifying ointment (if dry)
- White soft paraffin: Liquid paraffin TDS to body
- Aqueous cream BD to face

Double pajamas (Wet wrap)

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7
Q
  1. Bullous pemphigoid
A

More common:
- Men
- >60

Etiology:
1. **Drugs (younger average age than idiopathic group)
2. Local irritation / damage
3. **UV light + PUVA
4. ***Immunisation in children

Pathogenesis (Autoimmune mediated):
- IgG AutoAb bind to **Hemidesmosomal proteins (BP230, BP180)
- Bind to **Dermal-epidermal junction of skin
- Binding of IgG to BP180 + BP230
—> ***Complement activation
—> Inflammatory cascade
—> Inflammatory cells release Lysosomal enzymes + Proteases
—> cleaves target antigens + disrupt hemidesmosomes
—> Blistering

Clinical features (記: 好多Bulla):
1. Prodromal phase (may not have)
- ***itch, non-specific rash (Urticaria like)

  1. Acute phase
    - acute generalised eruption of **blisters
    - **    Leukocytosis + ***Eosinophilia
  2. Healing phase
    - fluid in blisters reabsorbed
    - Milia may be profuse

Mucosal lesions less frequent + less severe
Infants: Acral
Older children: Genital involvement in > 50%

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8
Q

Treatment of Bullous pemphigoid

A
  • Suppress disease activity with minimum dose of drugs necessary
  • Aim for presence of a blister once every few weeks
  1. ***Topical steroids (potent topicals)
  2. ***Systemic steroids
  3. Other systemic therapies
    - Tetracyclines (e.g. Doxycycline + Nicotinamide)
    - ***Dapsone (1st choice)
    - Methotrexate (2nd choice)
    - Azathioprine + Mycophenolate mofetil (3rd choice)
    - IVIg / Rituximab

Immunosuppressant: beware TB, pneumonia, hepatitis
Steroid: monitor HbA1c

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9
Q
  1. Pemphigus vulgaris
A

Etiology:
- ***Drug-induced pemphigus: Pencillamine, Captopril
- Paraneoplastic pemphigus: associated with malignancy

Clinical presentation (記: 飛滋 + Bulla + 爛皮):
1. **Oral mucosal erosions
2. **Flaccid bullae
3. ***Cutaneous erosions

Serious bullous **autoimmune disease
- skin + mucous membrane
- start in mouth —> skin / generalised acute eruption of both
- **fatal unless treated with steroids + immunosuppressive aggressively
- painful mouth erosions (may affect food intake)

Age: 40-60

Pathophysiology:
- Autoimmune: AutoAb bind to **Desmoglein 3 + 1 (DSG 3, DSG 1) in **Epidermis intercellular layer

Variants:
- Pemphigus vegetans: **intertriginous areas (two skin areas touch or rub together) with vegetating lesions
- Pemphigus foliaceous: erythematous patches / erosions covered with **crustations
- Pemphigus erythematosus: erythematous crusted erosive lesions in ***butterfly area of face, forehead + chest, ANA +ve (related to SLE)

Management:
1. Correction of fluid + electrolyte loss
2. Antibiotics to treat infection
3. Systemic steroids
4. Immunosuppressive therapy (given with steroids)
- Azathioprine
- Methotrexate
- Cyclophosphamide
- Rituximab
- IVIg

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10
Q
  1. Pustular psoriasis
A
  • Erythematous plaques studded with pustules
  • 10% generalised pustular psoriasis have preceding psoriasis

Potential triggers:
1. **Sudden withdrawal of corticosteroids —> Pustular flare
2. **Drugs (Lithium, Aspirin, Indomethacin, Beta-blockers)
3. ***Infection

Laboratory findings:
- ***Neutrophilia
- Low albumin
- Low calcium

Management:
1. ***Withdraw culprit drugs

  1. ***Hospitalisation
    - monitor BP, temp, Ca, FBC, U/E/Cr
    - swabs for pyogenic culture
  2. ***Anti-staphylococcal antibiotics e.g. Cloxacillin
  3. Specific therapy
    - Methotrexate
    - Acitretin (retinoid)
    - Cyclosporin
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11
Q
  1. Acute Generalised Exanthematous Pustulosis (AGEP) —> DDx of Pustular psoriasis
A

Acute Generalised Exanthematous Pustulosis (AGEP)
- Absence of other features of psoriasis e.g. psoriatic nails
- Widespread nonfollicular pustules on edematous erythema with accentuation of skin folds
- Facial edema
- **Acute: < 10 days (*Spontaneous resolution < 15 days)

Etiology:
- Drugs (Aminopenicillin, ***Sulphonamide, Terbinafine, Diltiazem)

Clinical features:
- Acute pustular eruption
- Fever >38oC
- **Neutrophilia +/- Eosinophilia
- **Subcorneal / Intraepidermal pustules on biopsy
- ***Spontaneous resolution < 15 days

Prognosis:
- Mortality 5%

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12
Q
  1. Drug Rash with Eosinophilia and Systemic Symptoms (DRESS)
A

aka ***Drug Hypersensitivity Syndrome

Clinical presentation:
- Fever
- Facial edema
- Infiltrated papules
- Generalised papulopustular / exanthematous rash
- Purpura
- Scaling
- **Lymphadenopathy (Lymphoid hyperplasia)
- **Hypereosinophilia (90% of cases)
- Atypical lymphocytes / Mononucleosis (40% of cases)

***Organ involvement:
- Hepatitis
- Nephritis
- Myocarditis
- Hypothyroidism

Causative agents (SpC Medicine):
- **Allopurinol
- **Anticonvulsants (Carbamazepine, Phenytoin, Lamotrigine)
- ***Sulfonamides

Onset:
- 2-6 weeks after starting treatment (longer than AGEP)

Grading:
- ***RegiSCAR score

Pathophysiology (poorly understood):
- **Defective detoxification of reactive oxidative metabolites
- Genetic predisposition
- Slow acetylator
- **Reactivation of Human Herpes Virus 6 (HHV6)

Prognosis:
- 10% mortality

Management:
- ***Oral Steroids
- Supportive

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13
Q
  1. Stevens-Johnson syndrome (SJS) / Toxic Epidermal Necrolysis (TEN)
A

Start as **Target lesion —> **Diffuse erythema —> ***Skin necrosis + detachment

SJS: **<10% epidermal detachment + >=2 mucosal sites
TEN: **>30% epidermal detachment

Etiology:
- **Drug (exposure to onset: 1-3 weeks)
(SpC Medicine)
1. **Allopurinol
2. **Carbamazepine, **Phenytoin, Lamotrigine

Prodrome:
- Fever / flu-like
- Odynophagia
- Stinging pain in eyes
- Skin pain, burning + tenderness

Symptoms:
1. ***Mucous membrane
- painful + tender mouth lesions
- genital erosions
- ocular symptoms, conjunctival injection

  1. ***Nikolsky’s sign
    - detachment of intact superficial epidermis by shearing force (一掂就甩)
    - measured in Body Surface Area (BSA): palm: 1%

Sequelae:
- Integumentary system: Dyspigmentation, Onycholysis
- Ocular: Sjogren syndrome, Corneal scarring
- Pulmonary: Chronic bronchitis
- Oral cavity: Sjogren syndrome, Reduced salivary flow
- Genitourinary system: Dyspareunia
- GI system: Esophageal stricture

Prognosis:
- **High mortality rate (23-34%): **Sepsis leading multi organ failure
- Additional morbidity from GI bleeding, Pulmonary embolism, MI, Pulmonary edema

Prevention:
- Avoid potential offending agents + any cross reacting medications:
—> Antiepileptic
—> Sulfonamide
—> Beta-lactam

Genotype testing:
- HLA-B1502 before **Carbamazepine + **Phenytoin
- HLA-B5701 before Abacavir
- HLA-B5801 before **Allopurinol

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14
Q

Management of SJS/TEN

A

Assessment:
- **Haemodynamically stable
- **BSA involvement / SCORTEN scale

Investigations:
- **Blood culture
- **Wound swab of broken skin for Aerobic culture
- FBC, U/E/Cr, LFT, CXR, ECG +/- investigations for viral etiology if clinically indicated

Management (self-limiting, mainly **supportive, need early intervention):
1. **Stop causative drug

  1. ***IV hydration
    —> first 24 hour: 4ml x weight x BSA%
    —> 1st 50% in first 8 hours, 2nd 50% in subsequent 16 hours
  2. **Foley catheter, monitor **urine output
  3. ***Non-adhesive dressing
  4. Refer to ***Dermatology / Burns unit for wound care + management
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15
Q

***AGEP vs DRESS vs SJS/TEN

A
  1. Onset
    AGEP: 48 hours
    DRESS: 2-6 weeks
    SJS/TEN: 1-3 weeks
  2. Duration
    AGEP: <1 week
    DRESS: several weeks
    SJS/TEN: 1-3 weeks
  3. Mucocutaneous features
    AGEP: Facial edema, pustules, tense bullae, mucosal involvement, target lesions
    DRESS: Facial edema, morbilliform eruption, pustules, exfoliative dermatitis, tense bullae
    SJS/TEN: Bullae, atypical target lesions, ***mucocutaneous erosions

***4. Histological pattern of skin
AGEP: Subcorneal pustules
DRESS: Perivascular lymphocytic infiltrate
SJS/TEN: Epidermal necrosis

***5. Lymphadenopathy
AGEP: +
DRESS: +++ (lymphoid hyperplasia)
SJS/TEN: -

  1. Other organ involvement
    AGEP: possible
    DRESS: interstitial nephritis, pneumonitis, myocarditis, thyroiditis
    SJS/TEN: tubular nephritis, tracheobronchial necrosis

***7. Neutrophils
AGEP: ↑↑↑
DRESS: ↑
SJS/TEN: ↓

***8. Eosinophils
AGEP: ↑
DRESS: ↑↑↑
SJS/TEN: -

  1. Atypical lymphocytes
    AGEP: -
    DRESS: +
    SJS/TEN: -
  2. Mortality
    AGEP: 5%
    DRESS: 10%
    SJS/TEN: 5-35%
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