Dermatology Flashcards
(138 cards)
Define urticaria (acute, chronic)
Urticaria is characterised by appearance of intensely pruritic erythematous plaques.
Pruritic, pale, blanching swellings of the superficial dermis lasting up to 24hrs.
Explain the aetiology / risk factors of urticaria (acute, chronic)
Urticaria and angiooedema involve mediator release by mast cells and basophils in the epidermis (urticaria) and deeper dermis (angio-oedema).
Many mediators released but mostly histamine, leading to:
- swelling
- pruritus
- vasodilation
ACUTE urticaria/angiooedema:
- Allergy. Mostly IgE-mediated type I hypersensitivity. Many agents activate mast cells (through IgE and also directly) e.g. foods, medication (Abx e.g. penicillin), stinging insects (e.g. Hymenoptera family incl. bees, wasps, hornets, and bed bugs), latex (particularly in patients chronically exposed e.g. spina bifida)
- Direct mast cell activation (non-immunological) e.g. foods (young kids have urticarial reaction to fruit and veg e.g. tomatos and strawbs, can also cause IgE in some patients), medications (opioids, NSAIDS), radiocontrast media
- Infection e.g. viral/bacterial infections responsible for urticaria/angiooedema in the majority of children with acute urticaria.
Viral: Viruses causing URTI and gastroenterirtis RSV, rhinovirus, rotavirus AND urticaria can precedeactive disease caused by chronic and indolent viral entities, such as hepatitis, cytomegalovirus (CMV), and Epstein-Barr virus (EBV).
Bacterial: those causing resp infections and gastroenteritis e.g. streptococcal agents and H. Pylori.
ParasiticL e.g. strongyloides, Toxocara and Fasciola (travel hisotry) - Systemic disease. Rarely, urticaria/angio-oedema precedes development of systemic diseases e.g. autoimmune diseases, malignancies , endocrinopatihies, autoinflammatory syndromes
- Physical causes:
Water, increase in core body temp with exercise or emotion (=cholinergic) , cold, heat, pressure, sunlight.
Other:
- Serum sickness (immune complex formation can activate mast cells and basophils)
- Progesterone associated urticaria (women on HRT/some patients in menstrual cycle)
- Mastocytosis (high numbers of mast cells in skin and other organs)
CHRONIC urticaria/angio-oedema (=persistance for more than 6 WEEKS):
- Acute urticaria lasting more than 6 weeks.
- Infection (most bacterial and viral infections resolve in 6 weeks, but hepatitis, EBV and CMV may be ass. w chronic urticaria).
- Foods (if food antigens hidden in processed foods and patients unknowingly continue to ingest them)
- Medications
- Latex
- Systemic (may be indolent and subclinical for long time)
- Progesterone associated: urticaria may be chronic but symptoms will often wax and wane with hormone fluctuations.
BUT
In health people and with absence of identifiable triggers:
In more than 90% of cases this is chronic idiopathic urticaria (CIU). Half of these may have an anti-IgE receptor antibody resulting in chronic release of mast cell mediators.
Summarise the epidemiology of urticaria (acute, chronic)
CIU can be associated with family or personal history of autoimmunity (e.g., autoimmune thyroiditis, vitiligo, pernicious anaemia, rheumatoid arthritis, insulin-dependent diabetes, alopecia areata), but can also occur in its absence.
Recognise the presenting symptoms of urticaria (acute, chronic)
Pruritic, pale, blanching swellings of the superficial dermis
Recognise the symptoms of urticaria (acute, chronic) on physical examination
Sites of angiooedema
pruritic, pale, blanching swellings of the superficial dermis that generally last well under 24 hours
NO overlying flaking or scaling
Angiooedema: colorless, non-pitting induration of the extremities, lips, and genitals.
Chronic MORE THAN 6 WEEKS
Identify appropriate investigations for urticaria (acute, chronic) and interpret the results
Acute:
Usually diagnostic testing not recommended, careful history enough.
But skin test/IgE may be useful for allergy, streptococcal antigen testing for urticaria w pharyngitis, ANA, ESR, dsDNA in systemic disease
Chronic: Complete blood count with differential Serum chemistry, including liver function testing ESR Urinalysis Thyroid studies.
Define basal cell carcinoma
Commonest form of skin malignancy aka “rodent ulcer”
Explain the aetiology / risk factors of basal cell carcinoma
Ass. with pathched/hedgehog signalling cascade, as seen in Gorlin syndrome (naevoid basal cell carcinoma syndrome)
Risk factors: Prolonged sun exposure/UV radiation Photosensitizing pitch Tar Arsenic
Pathophsyiology:
Small, dark blue staining basal cells growing in well-defined aggregates. Apopotic and mitotic bodies seen
Invades dermis and potential to invade and destroy local tissues.
DOES NOT METASTASIZE
No pre-cursor lesion for BCC
Summarise the epidemiology of basal cell carcinoma
Common in those with fair skin and areas of high sunlight exposure, common in the elderly, rare before the age of 40 years. Lifetime risk in Caucasians is 1:3.
Recognise the presenting symptoms of basal cell carcinoma
A chronic slowly progressive skin lesion usually on the face but also on the scalp, ears or trunk.
Recognise the signs of basal cell carcinoma on physical examination
(3 types- which is more aggressive?)
- Nodulo-ulcerative: Small glistening translucent skin over a coloured papule that slowly enlarges (early) or a central ulcer (rodent ulcer) with raised pearly edges.
Fine telangiectatic vessels often run over the tumour surface. Cystic change may be seen in larger more protuberant lesions.
- Morpheic: Expanding, yellow/white waxy plaque with an ill-defined edge (more aggressive).
- Superificial: Most often on trunk, multiple pink/brown scaly plaques with a fine whipcord edge expanding slowly; can grow to more than 10 cm in diameter.
Pigmented: Specks of brown or black pigment may be present in any type of basal cell carcinoma
Identify appropriate investigations for basal cell carcinoma and interpret the results
In which places is a BCC more likely to lead to complications
Biopsy rarely necessary- diagnosis on clinical suspicion
The central face and behind the ears are danger areas. BCC at embryological fusion lines may invade deeply making the risk of recurrence higher. Excision of tumour with clear margins is necessary in these areas.
Which is the commonest form of skin cancer
BCC
Define erythema nodosum
Panniculitis (inflammation of the subcutaneous fat tissue) presenting as red or violet subcutaneous nodules.
Explain the aetiology / risk factors of erythema nodosum
Delayed hypersensitivity reaction to antigens associated with various infectious agents, drugs, and other diseases.
Infection:
- Bacterial (Streptococcus, TB, Yersinia , rickettsia, Chlamydia , leprosy),
- viral (EBV),
- fungal (histoplasmosis, blastomycosis, coccidioidomycosis),
- protozoal (toxoplasmosis).
Systemic disease: Sarcoidosis, IBD, Behcets disease.
Malignancy: Leukaemia, Hodgkin’s disease.
Drugs: Sulphonamides, penicillin, oral contraceptive pills.
Pregnancy. 25 % of cases have no underlying cause identified.
Summarise the epidemiology of erythema nodosum
Female to male 3:1. Usually young adults
Recognise the presenting symptoms of erythema nodosum
Tender red or violet nodules develop bilaterally on the shins and occasionally on the thighs and forearms.
Fatigue, fever, anorexia, weight loss and arthralgia are often also present.
Symptoms of the underlying aetiology.
Recognise the signs of erythema nodosum on physical examination
Crops of red or violet dome-shaped nodules usually present on both shins (occasionally involving thighs or forearms) which are tender to palpation.
Low-grade pyrexia.
Joints may be tender and painful on movement.
Signs of the underlying aetiology.
The majority of cases resolve over 3– 6 weeks leaving bruise marks.
Identify appropriate investigations for erythema nodosum and interpret the results
Anti-strepsolysin-O titre 2-4 weeks later to assess for antecedent streptococcal infection. FBC, U&Es, CRP, ESR, LEFTs, serum ACE
Throat swab and culture
Mantoux/heaf skin testing for TB
CXR: To look for hilar adenopathy or other evidence of pulmonary sarcoidosis, TB and fungal infection
Why would you want to test form serum ACE in erythema nodosum
Sarcoidosis increases the level of this
Causes of pemphigus vulgaris, and where would antibodies be seen
Compare the blisters with bullous pemphigoid
IgG antibodies against desmosomes located on the surface of keratinocytes (desmoglein 1 and 3)
The following triggers of PV have been reported: thermal burns, infections, emotional stress, and drugs including penicillamine, captopril, cephalosporins, and NSAIDs
PV results in intra-epidermal blisters that are fragile and easily broken, manifesting as painful, flacid bullae and erosions on exam. This is in comparison with the tense bullae of bullous pemphigoid. As in this patient, the bullae demonstrate Nikolsky’s sign, in which gentle pressure to the bulla causes the epidermis to separate off.
What type of rash is associated with coeliac disease
Dermatitis herpetigormis, which are highly pruritic papules, vesicles and plaques located primarily on the extensor surfaces
Skin manifestations related to HIV infection
Skin manifestations of acute HIV are in the form of a generalized, pruritic papular eruption
Skin rash associated with HSV?
Erythema multiforme is a type IV hypersensitivity reaction with strong association with HSV. Targetoid rash beginning on extremities