Dermatology SC025: Skin Rash - Doctor: I Have A Rash (History, Examination And Basic Investigations) Flashcards
***Describing skin lesions
- Primary vs Secondary lesions
- Primary: macule vs patch, papule vs nodule, plaque, vesicles vs bulla
- Secondary: scales, crust, fissures, scar, excoriation marks, erosion vs ulcer - Colour
- Border (well demarcated?)
- Distribution
- Arrangement
DDx of Penile ulcer
Infective (**Considered first):
1. **Syphilis
2. ***Herpes
3. Chancroid
4. Lymphogranuloma venereum
Non-infective (Dx of exclusion usually):
1. Malignancy
2. Trauma
3. Fixed drug eruption
4. Behçet’s disease (systemic vascular inflammatory disorder)
5. Erythema multiforme
Diagnosis of Genital sores
Recurrent vesicles
—> Swab + HSV culture + Ag detection
—> ***Herpes
No vesicles (Ulcers)
—> DGE -ve
—> Multiple sore / Solitary / Painful / Painless
—> Specific test —> **LGV
—> Swab + Culture: H. Ducreyi —> **Chancroid
—> All tests -ve —> Non-infective
No vesicles (Ulcers)
—> DGE x3, VDRL, FTA, TPHA
—> ***Syphilis
Herpes (疱疹)
- Commonest cause of genital ulcer in HK
- HSV1 (10%), HSV2 (90%)
- Incubation period: 2-5 days
S/S:
- Recurrent painful ulcers in genitalia preceded by vesicles
- Primary attack particularly painful with tender inguinal LN
- Primary attack can last ~3 weeks
Complications:
- HSV encephalitis (rare but significant)
- **Cutaneous dissemination (Eczema herpeticum (self notes)) (esp. immunocompromised, history of eczema, DDx: chicken pox)
- Sacral radiculomyelopathy (in primary infections)
- Urinary retention (in primary infections)
- Bacterial superinfection
- **Erythema multiforme (body immunological system react to viral infections —> concentric colour changes with central blister (targetoid patches) often in hands)
- Neonatal herpes (give antiviral prophylaxis to mother just before delivery)
Recurrent herpes infection:
- HSV remain as latent infection in sensory + autonomic ganglion
—> Reactivation by Trauma, Menstruation, Stress
—> Recurrent local infection
—> Local, Less symptomatic, Shorter
Investigations of Herpes infection
- Viral Ag detection
- Viral culture
Tend not to do:
3. Immunoassay (detect viral Ab)
4. EM
5. PCR
6. Serology (inaccurate)
Management of Herpes infection
- Symptomatic control
- ***Antiviral agents (Oral: topical does not work well, use as soon as feel discomfort)
- Topical antibiotics to reduce superimposed infection
- Contact tracing
- Screen for other STD
Syphilis (梅毒)
- Now less common
- ***Treponema pallidum
- Incubation period: 9-90 days
- Congenital / Acquired
- Primary / Secondary / Tertiary
- Early / Latent
- ***Painless ulcer with LN
Primary Syphilis
- Solitary, **Painless ulcer (i.e. **Chancre) with ***Indurated base
- At site of trauma during sexual intercourse (e.g. anywhere where skin breaks e.g. breast, mouth, not necessarily only genitalia)
- Inguinal lymphadenopathy: **non-tender, **discrete, ***rubbery
Management:
- Antibiotics
Secondary and Tertiary Syphilis
Secondary Syphilis:
- Several ***weeks after Primary Syphilis
- Erythematous macules affect whole body including palm
Tertiary Syphilis:
- Neurological + CVS system involvement
Leg ulcers
DDx:
1. Venous
2. Arterial
3. Neuropathic
4. Pressure
5. Pyoderma gangrenosum
6. Dysglobulinaemia
7. Sickle cell, Thalassaemia
8. BCC (usually not in legs)
9. SCC (usually not in legs)
10. Panniculitis (inflammatory reactions of SC fat)
11. Vasculitis
Varicose eczema + Venous ulceration
Pathophysiology:
Venous hypertension causing distension + elongation of capillary loops
—> Fibrinogen leaks into tissue
—> Form cuffs in capillary
—> Prevent diffusion of O2 + nutrients to skin (esp. more superficial layer)
—> Local ischaemia
—> Ulceration
From JC002:
Venous reflux
—> Venous hypertension
—> **Capillary hypertension
—> Diffusion process + Leukocyte-damaging process
—> Lymphatics overloaded + ↓ Reabsorption of tissue fluid at Venous end
—> **Fluid accumulation
—> Edema
During diffusion process:
1. RBC
—> goes out and die in interstitium (but cannot reabsorbed by veins)
—> Iron-containing Hb stays as **Haemosiderin
—> **Brown pigmentation of legs
- Plasma proteins + Fibrin
—> chronic inflammatory reaction in tissues
—> deposit of fibrin / fibrinogen around capillary (form cuffs)
—> prevent active effusion of nutrients to supply skin
—> **Thickening of skin (unhealthy skin)
—> **Dark, Itchy skin
—> Breakdown of skin
—> ***Ulcer
Clinical features of Venous ulcers
- Eczema
- impairment of skin to preserve water —> dry + crack —> inflammation - Varicosities
- Edema
- Pigmentation
- esp. common in skin of colours
- ∵ pigment cells produce more pigment after inflammatory reaction —> Post-inflammatory hyperpigmentation
- ∵ Fe deposition (Haemosiderin) - Ulceration (i.e. involving dermis)
- After minor injury
- **Painless often
- Well-defined border
- **Shallow ulcer with **yellowish base
- **Medial + Lateral malleoli - Atrophie blanche
- healed ulcer —> scar which appear white (∵ increased collagen production in the scar which reflect light) - Venous flare
Management of Venous ulcers
Aim: Reduce edema
- Rest + Leg elevation
- Compression dressing
- Exercise
- Diet to reduce weight
- Treatment of Eczema (moisturiser, topical steroids)
- Antibiotic if superimposed infection
- Cleansing agent
- Surgical (skin graft)
(9. UV light - Growth factors, Special dressing to promote healing)
Arterial ulcers
Arterial insufficiency
—> Skin ulceration
Risk factors:
- Smoking
- DM
- HT
Clinical features:
1. Painful worse at night
2. Deep, punched-out lesions
3. Dry + Scaly skin (∵ poor nutrition to skin)
4. Hair sparse / absent (∵ poor nutrition to skin)
5. Toenail thickened (∵ poor nutrition to skin / primary infection)
6. Absent pulse
7. Gangrene
8. Symptoms of arterial insufficiency
- Intermittent claudication
- Coldness
- Numbness
Management of Arterial ulcers
- Doppler USG
- Arteriographic assessment
- Control of risk factors
- Surgical assessment
- ***Elastic stocking absolute CI
***Arterial vs Venous ulcer
Arterial:
- Painful
- Toes, heels, shins
- Pulse weak / absent
- Dry, scaly, atrophic, shiny skin
- Hair absent
- Nail dystrophic
- Pallor, cyanosis
Venous:
- Painless
- Malleoli
- Pulse normal
- Eczema
- Pigmentation
- Hair normal
- Normal nail
- No pallor, cyanosis (No signs of arterial insufficiency)
Pyoderma gangrenosum (PG)
- **Painful nodule / pustule —> break down to form progressive enlarge **ulcer
- Single / Multiple
- Irregular, purplish brown (Overhanging purple edge)
- Known association with systemic diseases
Investigation:
- Exclude infection by skin swab and tissue culture
- Skin biopsy
- ***Pathergy test: inject normal saline intradermally —> pustule formation (Diagnostic)
- Investigate for associated conditions once diagnosis confirmed
Management:
- **Injury / Inducing damage —> even get worse (e.g. skin graft, incision and drainage can make it worse)
- Treat underlying disease
- **Systemic immunosuppressive
Association with systemic disease:
- **IBD
- **CTD
- Arthritis
- Gammopathy
- ***Haematological malignancy
- Other (Bechet’s disease: apthous ulcers, genitalia ulcers, PG, erythema nodosum, eye problems)
Scabies
- Infestation with a mite (Sarcoptes scabiei) that burrow into the stratum corneum
- Transmitted by physical contact
- Itchiness due to immune response to the mite (∴ not develop immediately —> always several weeks later)
- Develop itchiness several weeks after being infestated and will **persist for weeks / months **after treatment
Clinical features:
- Itchy rash that ***spare the face in adult but could affect face in infant
- Burrows esp. in finger + toe web
- Scabies nodules / bumps in genitalia + breast
- Excoriation marks without much inflammation (cutaneous inflammatory reactions)
DDx:
- Eczema (tend to have more inflammation)
- Generalised pruritics of systemic disease (can affect face)
- Urticaria (short-lasting, can be induced by dermographism)
Treatment:
—> ***Treat the whole family —> asymptomatic until several weeks later
—> 2x application
1. Benzyl benzoate
2. Gamma benzene hexachloride
3. Permethrin
4. Malathion
5. Monosulfiram
Scabies pruritis after treatment:
- Eurax (Crotamiton)
- Topical steroid
—> Scabies nodule can be very resistant and need potent topical steroid
***Norwegian scabies (Crusted scabies):
- Severe form of scabies
- Patients with neuropathy (e.g. DM, HIV, lymphoma, stroke) cannot scratch skin —> cannot reduce volume of mite —> severely infestated
- may need oral Ivermectin
Generalised pruritis of systemic disease
- Generalised itchiness affecting the whole body without inflammatory dermatoses
- Cutaneous manifestation of ***systemic disease
- Difficult to manage
DDx of generalised pruritus:
- Scabies (face-sparing)
- Mild asteatotic eczema (esp. in elderly during winter months)
- Dermatographism
Causes:
1. Thyroid disease
2. Parathyroid diseases
3. Hepatic disease (esp. Obstructive jaundice)
4. Lymphoma
5. Uraemia
6. Fe deficiency
7. Myeloproliferative diseases
8. DM (only localised itchiness unless uraemic)
Investigations:
- CBP
- LRFT
- Ca
- TSH
- ESR
Urticaria
Urticaria:
- ***Last <24 hours, comes and goes
Vs Urticarial vasculitis:
- >24 hours, painful, associated with bruises
Acute vs Chronic:
- Acute: food and drug allergy, viral infection
Causes:
- Idiopathic
- **Infection (hepatitis, fungal infection, H. pylori, parasitic infestation)
- **Systemic disease (SLE, autoimmune)
- ***Immunological (food, drug allergy, insect bite)
- Physical
- Genetic
Chronic idiopathic / spontaneous urticaria (CSU):
- 40% resolve within 1 year
- associated with deep pressure urticaria (e.g. carry heavy bags)
- **need to exclude causes e.g. chronic infections (hepatitis, onychomycosis), autoimmunity diseases
- ~50% patients have **Ab against IgE / IgE receptor
- some associated with organ-specific autoimmunity (e.g. Thyroid disease)
- can associate with angioedema / anaphylactic shock
Physical urticaria:
- Cholinergic (develop urticaria whenever start to sweat e.g. exercise, ∵ congenital: nerve innervating mast cells also innervate sweat gland)
- Deep pressure
- Dermographism
- Cold (need to exclude cryoglobulinaemia, cold-agglutinin disease)
- Heat
- Aquagenic
- Vibratory
Approach to Urticaria:
- Very often clinical diagnosis (do not rely on investigations)
- History + P/E
—> Duration (<24 hours)
—> Trigger
—> Associated angioedema / anaphylactic shock
Investigations:
- Physical challenge (run up and down in Cholinergic urticaria)
- CBC, LRFT, ESR, ANA, C3, C4, C1EI, Stool for ova
- Prick test (not very accurate), RAST (Radioallergosorbent test)
- Skin biopsy (if suspect vasculitis)
- Oral challenge test
Psoriasis
- Chronic inflammatory, hyperproliferative, immune-mediated skin condition
- affecting 2-3% of population (western), 0.2-0.3% (asian)
- 2 peak of onset: young + late middle age
- earlier onset —> tends to be associated with worse prognosis
- can have other comorbidities e.g. ***joint involvement, chronic inflammation (childhood obesity syndrome)
Pathogenesis:
- Genetic predisposition
—> Trigger / Initiating events (e.g. infection, stress, obesity)
—> Cytokines + Chemokines (e.g. IL12, IL23, IL17)
—> Dendritic cell + T cell activation
—> **Keratinocyte activation + **hyperproliferation
—> ***Plaque formation
—> Cytokines + Chemokines
—> Leukocyte recruitment, Angiogenesis
—> Dendritic cell + T cell activation
—> Vicious cycle
Histology:
1. Epidermal hyperplasia
2. Dilated, prominent blood vessels in dermis
3. Infiltrate of leukocytes in dermis
4. Accumulation of neutrophils
Causes / Triggers:
1. **Genetic (different genetics can lead to same phenotype)
2. **Drugs (e.g. abrupt withdrawal of steroids)
3. **Infection (strept)
4. **Stress
5. Trauma (Koebner phenomenon)
Types and Clinical features of Psoriasis
**Types of psoriasis:
1. **Chronic plaque psoriasis
2. **Guttate psoriasis
3. **Pustular psoriasis
4. ***Erythrodermic psoriasis
Clinical features:
- Chronic large plaque / Guttate / Pustular / Erythroderma
- Nail: Pitting, Onycholysis (separation of nail from nail bed)
- Scalp
- **Psoriatic arthropathy (examine extensor surfaces when hands presenting with ulnar deviation)
- **Auspitz’s sign (punctate bleeding spots when scales scraped off **vs Eczema)
- **Koebner phenomenon (skin lesions on lines of trauma)
Comorbidities in psoriasis patients
Psoriasis have increased risk for:
- Obesity
- Smoking
- DM
- HT (∵ chronic inflammation accelerate atherosclerosis)
- Heart failure
- MI
- CVS mortality
- Depression
- Mortality
DDx of Pustular psoriasis
- Pustular psoriasis
- Drug-induced acute pustular eruption (**AGEP: Acute generalised exanthematous pustulosis) —> **have to exclude drug esp. 1st appearance
- ***Staphylococcal scalded skin syndrome (usually in younger age group / immunocompromised, staphylococcus produce protein that split skin, usually adult immunological system can neutralise them unless immunocompromised)
- ***Subcorneal pustular dermatosis
- Dermatitis herpetiformis
- Pemphigus foliaceous
Generalised pustular psoriasis
- Sudden onset of ***sterile pustules (negative with swab, culture) with fever
- ***Erythema surrounds pustules
- Become **extensive + **confluent
- Nail involvement common
- Unusual to see other forms of psoriasis at the same time
- Often provoked by infection, **drug (steroid withdrawal, lithium, **oral contraceptive)
Treatment:
1. Bed rest
2. Treat / Withdraw provoking factor
3. Avoid irritant: Tar, Dithranol, Phototherapy
4. Methotrexate, Iso-Acitretin (Retinoid), Cyclosporin
Investigations of Psoriasis
- Drug history
- Skin swab + blood culture
- CBC for WBC
- LRFT
- Ca
- CXR
- Skin biopsy
Management of Psoriasis
General treatment:
- General counselling
- Avoid aggravating factor
- Eradicate infection
Chronic plaque psoriasis:
- Topical agents
1. **Diprosalic ointment (Betamethasone + Salicylate, in the morning)
2. **Daivonex ointment (Calcipotriol (Vit D analogue), at night)
3. Polytar shampoo
4. **Topical steroid (*NEVER give systemic steroid)
Pustular psoriasis:
1. Bed rest
2. **Clarithromycin
3. Emulsifying ointment as soap
4. Aqueous cream
5. **IV fluid
6. Careful fluid balance
