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
