Dermatology Flashcards
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
State the causes of erythema multiforme
HSV, mycoplasma, penicillin, sulfonamides, autoimmune diseases, and malignancies.
Skin rash with insulin resistance
Insulin resistance is associated with acanthosis nigricans which is characterized by epidermal hyperplasia with a darkened appearance in areas of the skin, typically in the axilla and groin. Another important association of acanthosis nigricans is malignancy, especially gastric carcinoma.
What is associated with acanthosis nigricans
Insulin resistance and malignancy, especially gastric carcinoma.
Compare epidermal cyst with a ganglion cyst
Epidermoid (sebaceous) cyst: usually benign swelling in the skin arising in the sebaceous gland, typically filled with yellowish sebum. These are usually easily seen as they lead to a swelling of the skin.
Ganglion cyst or synovial cyst: a non-neoplastic soft-tissue collection that may occur in any joint but most often develops in dorsum of wrist hand
https://www.medicinenet.com/cyst/article.html (GREAT LINK FOR CYSTS!)
Lump on the dorsum of the wrist that transilluminates. Reduced sensation on the lateral side of the hand
A ganglion cyst is a benign tumor which most often develops in the dorsum of the wrist and hand. It is a compressible, moveable cyst which transilluminates and can cause pain or paresthesia if it compresses the ulnar or median nerve. It can be left untreated or treated with surgery.
(in this case the ulnar nerve is affected!)
What kind of lumps usually develop in the following conditions:
- Osteoarthritis
- Tenosynovitis
Osteoarthritis:
Development of nodes in the PIP and DIP joints, called Bouchard’s and Heberden’s nodes respectively.
It is also characterized by pain and stiffness in the joints, and would be detected on an X-ray which would show osteophytes, joint space narrowing, subchondral cysts, and subchondral sclerosis.
Tenosynovitis:
Tenosynovitis is inflammation of a tendon and its sheath, and is a result of infection or inflammation caused by diabetes, overuse, or arthritis.
It usually causes swelling, pain, and a fever if infectious. The absence of swelling and any signs of infection in this woman make this diagnosis unlikely.
Are giant cell tumours of tendon sheath malignant or benign?
Benign
Patient has a lump near the DIP joint of the left infex finger. It is immobile and does not transilluminate.
Giant cell tumors of the tendon sheath are benign tumors which are typically painless. In most cases, these masses develop near the DIP joints of the index and long fingers. The lesions are firmly fixed to the underlying structures and do not transilluminate.
Actinic keratosis description?
Very common, non-malignant skin lesion that occurs due to sun damage.
It has a thick crust surface
What is keratoacanthoma.
T/F is spreads slowly and metastasises
A keratoacanthoma is a variant of SCC which grows rapidly but does
not metastasise.
Kaposi’s sarcoma caused by which agent
Kaposi’s sarcoma is a systemic disease caused by infection with human herpesvirus
8 (HHV-8),
T/F Kaposi’s sarcoma is a late complication in HIV
F
It is an AIDS-defining illness that is
often the first AIDS-related complication in HIV patients.
Explain the distribution of Kaposis sarcoma
Lesions appear mainly on
the extremities, but can occur on the trunk, back, face and mucous membranes.
Organ involvement is sometimes present in the gastrointestinal and respiratory tract
and can result in death.
What type of virus causes molluscum contagiosum
Pox virus
What are the mechanism of spread in children vs adults. Who does it more commonly occur in
virus. It mainly occurs in
children (90%!) and is spread via skin-to-skin contact.
In adults, it tends to be transmitted via
sexual contact and occurs on the lower abdomen and genital area.
Describe the lesion in molluscum contagiosum. How long does the lesion last
dome-shaped, firm and smooth with an umbilicated centre.
The lesions will last for around 8 months.
Define squamous cell carcinoma
Compare with marjolins ulcer
Malignancy of the epidermal keratinocytes of the skin.
Marjolin’s ulcer is a squamous cell carcinoma that arises in an area of chronically inflamed/scarred skin (it’s aggressive)
Explain the aetiology / risk factors of squamous cell carcinoma
Differentiate it from actinic keratosis and bowen’s disease
Risk factor:
- UV radiation from sunlight exposure (leading to actinic keratoses=precancerous lesions)
- Radiation
- Carcinogens (tar derivative, cigarette smoke, soot)
- Chronic skin disease (lupus)
- HPV
- Long term immunosupression (transplant recipients and HIV)
- DNA repair genetic defect (xeroderma pigmentosum)
Actinic keratosis (squamous cells begin to produce too much keratin, and are premalignant)–> bowen’s disease (squamous carcinoma in situ) –> squamous cell carcinoma
Bowen’s disease is intra-epidermal carcinoma in situ (proliferation of atypical keratinocytes JUST IN THE EPIDERMIS, BASEMENT MEMBRANE is intact) and may be seen as solitary or multiple red-brown scaly patches.
In squamous cell carcinoma the malignant keratinocytes invade locally into the dermis and even hypodermis and can then spread to local lymph nodes and distally metastasise e.g. lungs, liver. Staging is based on the TNM system.
Recognise the presenting symptoms of squamous cell carcinoma
Treatment mechanisms?
Surgery and reconstruction
and radiotherapy (the lesions are RADIOsensitive, NOT chemosensitive)
Recognise the signs of squamous cell carcinoma on physical examination
Variable appearance: ulcerated, hyperkeratotic, crusted or scaly, nonhealing lesion, often on sun-exposed areas. Palpate for local lymphadenopathy.
Actinic keratosis- “sand-paper like lesions”
Bowen’s disease- “small, well-circumscribed, red elevations with scaly plaques”
As the lesion turns cancerous and enlarges, the centre becomes necrotic and can turn into an ulcer
Identify appropriate investigations for squamous cell carcinoma and interpret the results
Skin biopsy:
Confirms malignancy and distinguishes it from other skin lesions. Form pearls in the most aggressive part, under microscopy (don’t confuse with BCC!’s pearly macroscopic appearance).
Deep biopsy including subcutaneous tissue is needed.
Squamous cell carcinoma cells on microscopy:
-pleomorphic
-hyperchromatic nuclei
-numerous mitoses
Actinic keratosis: partial thickness of the epidermis dysplasia
Bowen’s disease
Bowen’s disease: full thickness dysplasia of the epidermis (BM intact)
Fine-needle aspiration or lymph node biopsy: Only necessary if suspicion of metastasis.
Staging: CT and/or MRI, PET scanning
Define molluscum contagiosum
Skin infection caused by the molluscum contagiosum virus that often occurs on the trunk, face and genitalia
Explain the aetiology / risk factors of molluscum contagiosum
Modes of transmission? Type of virus?
Describe the skin lesions
Risk factors?
DNA poxvirus
Transmission:
- Direct skin contact (contact sports, STIs)
- Autoinoculation (scatching or touching lesion e.g. whilst shaving)
- Fomites (e.g. on bath sponges/towels)
Smooth, dome-shaped papules with central umbilication
RISK FACTORS:
Immunosuppression ,
Active atopic dermatitis (in children) ,
hot and humid climates,
Crowded living conditions
Summarise the epidemiology of molluscum contagiosum
Male more commonly than female
It is more common in childhood as well as early adolescence, particularly in males, and is usually transmitted at this age via skin contact and autoinoculation.
In adults, it is considered a sexually transmitted infection.
Prevalence
More common in warm and humid climates or areas with poor hygiene
Up to 18% of HIV-positive patients and up to 33% if CD4 cell count is < 100 cells/μL
Recognise the presenting symptoms of molluscum contagiosum
Location in children vs adults?
The healing?
Individual lesions may be painful/pruritic but usually non-tender
2-5mm, but in immunocompromised may go up to >15mm
In children: face , trunk , and extremities (e.g., axilla, antecubital and popliteal fossa)
In adults: lower abdomen, groin, genitalia, and proximal thighs
In healthy patients, molluscum contagiosum is generally self-limiting and heals spontaneously after several months.
However, in immunosuppressed individuals, lesions can be very large, widespread, and persistent.
Recognise the signs of molluscum contagiosum on physical examination
Non-tender, skin coloured, pearly, dome shaped papules with central umbilication
Papules contain a caseous plug (squeezing produces white cheesy fluid consisting of molluscum bodies)
Identify appropriate investigations for molluscum contagiosum and interpret the results
What does it show on histology
Clinical diagnosis
Seek out underlying aetiologies (HIV testing) if lesions are widespread
A biopsy is usually not necessary, but consider in cases of immunosuppression, as the diagnostic differential is wide
Histology:
- Localised to epidermis
- Acanthosis (thickened epidermis)
- Cup-shaped invagination (epidermis invaginated into the dermis)
- Molluscum bodies: keratinocytes with eosinophilic intracytoplasmic inclusion bodies containing viral particles
When is treatment indicated for molluscum contagiosum, and what would the first treatment option nbe
If treatment is indicated (e.g., for sexually transmitted molluscum contagiosum), cryotherapy with liquid nitrogen is usually the first treatment option.
Large, persistent, widespread dome-shaped papules with central umbilication?
Suspect molluscum contagiosum which is widespread DUE TO AIDS
Complication of molluscum contagiosum
Chronic follicular conjunctivitis may occur as molluscum contagiosum viral particles spread into the conjunctiva of the eye.
Secondary bacterial infections
What diameter of lesion is worrying for a melanoma
6mm