Dermatology Flashcards
cellulitis (4x key signs, what can usually be found, 4 signs of nec fasc, 3x ix + what else to do, what to do if suspect nec fasc, abx mx (empirical, MRSA, nec fasc, GAS) and bite (normal, pen allerg, mod/severe infection inc if pen allerg)
◦ Key signs found are dolor, calor, rubor and tumor (pain, heat, redness and swelling)
◦ Typically it is unilateral (rarely bilateral – consider other differentials e.g. venous/varicose eczema)
◦ Usually a break in the skin (the source of the infection) can be found (e.g. a pressure sore or a cut from gardening etc.)
◦ Look out for signs of necrotising fasciitis (caused by Group A Streptococcus (GAS)), which is an emergency = disproportionate pain/anaesthesia, bullae/gas in the tissue, necrotic areas, rapid spread
Swab, consider cultures and bloods
◦ The site of inflammation/redness should be demarcated with a skin marker, to check for signs of progression beyond this line or regression (e.g. with successful treatment)
◦ If Nec fasc is suspected = urgently call the plastic surgeon SpR on-call, as it is an emergency = debridement and Abx are required
◦ For CELLULITIS empirical treatment is with Flucloxacillin 500mg-1g PO QDS or IV if moderate-severe
◦ If Penicillin allergic or MRSA+ive = Doxycycline PO or Vancomycin IV is used instead
◦ For NEC FASC empirical treatment is with Tazocin 4.5g IV TDS + Clindamycin 1.2g IV (single dose), then 900mg IV TDS
◦ If Group A streptococcus is confirmed = Benzylpenicillin 2.4g IV QDS + Clindamycin 1.2g IV (single dose), then 900mg IV TDS
if pt has been bitten: ◦ Co-amoxiclav (prophylaxis) PO 5-7 days
◦ Doxycyline + Metronidazole PO (if penicillin allergic)
If moderate-severe infection:
◦ Co-amoxiclav IV 5-7 days
◦ PO Doxycycline and Ciprofloxacin and Metronidazole (if pen allergic)
◦ Or IV Vancomycin, Ciprofloxacin and Metronidazole
erysipelas and cellulitis - description, causes - 2 main bugs, 6 main risk factors, presentation (where most commonly, local and systemic signs, distinguishing the two conditions, management (x5), complications (x3)
● Spreading bacterial infection of the skin
● Cellulitis involves the deep subcutaneous tissue
● Erysipelas is an acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue
Causes
● Streptococcus pyogenes and Staphylococcus aureus
● Risk factors include immunosuppression, wounds, leg ulcers, toe web intertrigo, oedema/lymphoedema, DM
Presentation
● Most common in the lower limbs
● Local signs of inflammation – swelling (tumor), erythema (rubor), warmth (calor), pain (dolor); may be associated with lymphangitis
● Systemically unwell with fever, malaise or rigors, particularly with erysipelas
● Erysipelas is distinguished from cellulitis by a well-defined, red raised border; may have more blisters
Management
● Antibiotics (e.g. flucloxacillin or benzylpenicillin)
● Supportive care including rest, leg elevation, sterile dressings and analgesia
Complications
● Local necrosis, abscess and septicaemia
14 cellulitis mimics (5:6:3 then names of rest)
consider
erysipelas
Sharply demarcated erythema
Blistering
Oedema
Intense warmth from the affected area
Systemic symptoms, such as fever, malaise, and nausea.
nec fasc
Severe pain, seemingly disproportionate to the clinical findings
Oedema or tenderness extending beyond the erythematous border of the affected area
Cutaneous gangrene and blistering
Crepitus (due to subcutaneous gas produced by anaerobic organisms)
Fluctuance, indicating purulent material in the soft tissues
Rapid expansion despite antibiotic therapy.
Herpes zoster
A sudden onset of fever
Localised rash with pain, swelling, heat, redness.
dermatomal distribution and umbilicated vesicles
dependent rubor/venous insufficiency
venous eczema
thrombophlebitis/DVT
Lipodermatosclerosis
eczema
contact dermatitis
panniculitis
Lymphoedema
Vasculitis
Capillaritis
Erythromelalgia
managing intertrigo (what is it, 3 non-medical mx, first med mx inc why good choice and when to stop, 2 steps if treatment failure, 3 ddx and how to tell from intertrigo, 2 ix to send if infection suspected)
commonly seen red soreness in skin folds, especially in obese ppl
try to keep skin dry, keep folds separated and aired out if possible, wash regularly
generally responds to combined steroid/antifungal: daktacort is a good option (weak so not too likely to thin skin, generally give for a week or so -> can advise to stop 1-2 days after sx resolve)
in case of treatment failure consider abx for bacterial intertrigo, or oral antifungals -> guided by ix results where possible
consider also flexural psoriasis, eczema, tinea cruris; Flexural lesions in psoriasis are usually symmetrical, red, glistening, and well-demarcated, tinea lesions are often annular or polycyclic, and tend to have a leading erythematous scaly edge
If a secondary infection is suspected a swab should be taken for MC&S
If there is scale, skin scrapings should be sent for mycology to look for tinea
erythrasma
chronic superficial infection of the intertriginous areas of skin caused by Corynebacterium minutissimum. Involvement of the toe clefts is common, but clinically important infections present as slowly enlarging pink or brown patches on the inner thighs and groins, the axillae, and the intergluteal and submammary flexures
usually asymptomatic, occasionally it can be itchy
more common in warm climates, in diabetic pts, and in adults (but can affect all ages)
Slowly enlarging, irregular, well-demarcated patches
New lesions are smooth, and pink-red or brown
Older lesions are brown with a wrinkled, scaly appearance
ddx inc Tinea - which has a leading scaly edge
Psoriasis - which has a shiny, glazed appearance
Eczema
Intertrigo (non-infective, candidal, bacti)
self-limiting but can give topical fusidic acid or benzoyl peroxide, and if severe then systemic macrolide or tetracycline
quick summary of common paediatric rashes
rash on 1 or both cheeks plus a high temperature, runny nose, sore throat and headache may be parvovirus aka slapped cheek syndrome
Blisters on the hands and feet, with ulcers in the mouth, could be hand, foot and mouth disease
rash of small, raised bumps that feels rough, like sandpaper, could be scarlet fever
spotty rash that appears on the head or neck and spreads to the rest of the body could be measles
rash of small, raised spots that feels itchy or prickly could be heat rash (prickly heat)
Skin that’s itchy, dry and cracked may be atopic eczema
Raised, itchy patches or spots could be urticaria
itchy, dry, ring-shaped patch of skin may be ringworm aka tinea. The patch may look red, pink, silver, or darker than surrounding skin
Small, itchy spots that turn into blisters and scabs could be chickenpox
Sores or blisters that burst and leave crusty, golden-brown patches could be impetigo
Very itchy raised spots could be caused by scabies
Very small spots, called milia, often appear on a baby’s face when they’re a few days old. Milia may appear white or yellow
Raised red, yellow and white spots (erythema toxicum) can appear on babies when they’re born. They usually appear on the face, body, upper arms and thighs
Small, firm, raised spots could be molluscum contagiosum. The spots can be the same colour as surrounding skin, darker than surrounding skin, or pink.
baby with red/sore bottom could be nappy rash
Spots that appear on a baby’s cheeks, nose or forehead within a month after birth could be baby acne
Yellow or white, greasy, scaly patches on your baby’s scalp could be cradle cap
viral rashes usually appear as blotchy red spots commonly affecting most of the body. They sometimes appear quite quickly and usually last for only a few days. Treatment is supportive if required. If particularly pruritic, antihistamines or emollients can be used. Antipyretics may be useful if a child is uncomfortable with fever
high fever: lasting a few days, followed later by a maculopapular rash - classically 3 days fever then rash on the 4th, starting on trunk and limbs, may be roseola
6 functions of skin and structure of epidermis (4/5 layers, 4 types of cell)
functions: i) Protective barrier against environmental insults ii) Temperature regulation iii) Sensation iv) Vitamin D synthesis v) Immunosurveillance vi) Appearance/cosmesis
structure:
epidermis with 4 cell types
Keratinocytes Produce keratin as a protective barrier Langerhans’ cells Present antigens and activate T-lymphocytes for immune protection
Melanocytes Produce melanin, which gives pigment to the skin and protects the cell nuclei from ultraviolet (UV) radiation-induced DNA damage
Merkel cells Contain specialised nerve endings for sensation
Stratum basale
Actively dividing cells, deepest layer (Basal cell layer) Stratum spinosum Differentiating cells (Prickle cell layer)
Stratum granulosum So-called because cells lose their nuclei and contain (Granular cell layer) granules of keratohyaline. They secrete lipid into the intercellular spaces.
Stratum corneum Layer of keratin, most superficial layer
In areas of thick skin such as the sole, there is a fifth layer, stratum lucidum, beneath the stratum corneum. This consists of paler, compact keratin.
dermis structure (3 main contents, 5 other things it contains)
dermis is made up of collagen (mainly), elastin and glycosaminoglycans, which are synthesised by fibroblasts. Collectively, they provide the dermis with strength and elasticity.
The dermis also contains immune cells, nerves, skin appendages as well as lymphatic and blood vessels.
sweat glands types and 2 general path possibilities
Sweat glands regulate body temperature and are innervated by the sympathetic nervous system. * They are divided into two types: eccrine and apocrine sweat glands. * Eccrine sweat glands are universally distributed in the skin. * Apocrine sweat glands are found in the axillae, areolae, genitalia and anus, and modified glands are found in the external auditory canal. They only function from puberty onwards and action of bacteria on the sweat produces body odour. * Pathology of sweat glands may involve: a) inflammation/infection of apocrine glands e.g. hidradenitis suppurativa b) overactivity of eccrine glands e.g. hyperhidrosis
sebaceous glands function, stimulation + when become active
Sebaceous glands produce sebum via hair follicles (collectively called a pilosebaceous unit). They secrete sebum onto the skin surface which lubricates and waterproofs the skin.
- Sebaceous glands are stimulated by the conversion of androgens to dihydrotestosterone and therefore become active at puberty.
skin types
Fitpatrick scale has 6 from always burns never tans to always tans never burns, with increments; type 4 is olive skin (tans more often than burns)
pruritus (9) and purpura (8) causes
pruritus: chronic liver/kidney disease, fe def anaemia, polycythemia, lymphoma, hyper/hypothyroid, DM, rashes, allergies, scabies
purpura: meningococcal/DIC, ALL, thrombocytopenia (all causes), NAI, bleeding disorders; bone marrow failure, vit c def, certain drugs
topical steroids weak to strong (brand names x4) (and versions with antimicrobials 3 mild 1 potent) + which steroid has 2x strengths
hydrocortisone, clobetasone, beclomethasone, clobetasol (hydrocortisone, eumovate, betnovate, dermovate)
(mild antimics inc canestan HC (clotrimazole and hydrocort) and daktacort (hydrocort and miconazole) as well as fucidin H (HC and fusidic acid) then potent is fucibet (betamethasone and fusidic acid)
note also betnovate available in 2 strengths with 0.025% equiv to clobet 0.05 (eumovate) and betnovate 0.05% more potent but still less than clobetasol
corticosteroids (5 metabolic actions, 7 anti-inflam actions (+effect on healing), how signalling through glucocort receptor works, 3 other effects
many actions inc: decrease glucose uptake by muscle/fat, inc gluconeogensis, inc protein metabolism, dec protein anabolism, redistribution of fat
also antiinflam actions inc: dec activity/influx of leucocytes, dec activity of monocytes, dec clonal expansion of T/B cells, switch from Th1 to Th2, dec pro-inflam cytokine production, dec eicosanoid production, inc release of antiinflam factors; will get reduced healing
bind to glucocorticoid receptor in cytoplasm which is bound to hsp90 (and other proteins), ligand binding causes hsp90 to dissociate and r’s to form homodimers which translocate to nucleus to transactivate/repress up to 1% of genome, thus drugs very broad spectrum with side effects; either binds to positive glucocorticoid response element within promoter, bind to negative GRE to displace tfs etc
also rapid non-genomic effects that arent well understood eg hydrocortisone rapidly inhibs neutrophil degranulation and GR antags dont stop this, same for IgE mediated mast cell degranulation and IV betamethasone reduces nasal itching after pollen applied within 10 mins, too fast to be genomic effects
staph scalded skin syndrome description inc cause, time course, worse in what 4 areas, 4 skin features (inc time to resolve and how painful), 2x mx
● Commonly seen in infancy and early childhood
Cause
● Production of a circulating epidermolytic toxin coagulase positive staphylococci
Presentation
● Develops within a few hours to a few days, and may be worse over the face, neck, axillae or groins
● A scald-like skin appearance is followed by large flaccid bulla
● Perioral crusting is typical
● There is intraepidermal blistering in this condition
● Lesions are very painful
● Recovery is usually within 5-7 days
Management
● Antibiotics (e.g. a systemic penicillinase-resistant penicillin like fluclox, fusidic acid, erythromycin or appropriate cephalosporin)
● Analgesia
impetigo
two main types of impetigo: non-bullous and bullous.
Non-bullous impetigo (70% of cases) is caused by Staphylococcus aureus, Streptococcus pyogenes, or a combination of both.
Bullous impetigo is caused by S. aureus.
Non-bullous impetigo is characterized by thin-walled vesicles or pustules that rupture quickly, forming golden-brown crusts. The most commonly affected sites are the face (especially around the nose and mouth), limbs, and flexures (especially the axillae).
Bullous impetigo is characterized by large, fragile, flaccid bullae (fluid-filled lesions) that rupture and ooze yellow fluid, leaving a scaley rim (collarette). The most commonly affected sites are the flexures, face, trunk, and limbs.
Differential diagnoses, such as chicken pox, eczema, tinea corporis/capitis, HSV, contact dermatitis, and cellulitis, should be excluded.
Swabs for culture and sensitivities should be considered if impetigo is persistent, recurrent, or widespread, but otherwise is a clinical diagnosis.
pt should not attend a setting (such as school, other childcare facilities, or work) until all lesions (sores or blisters) are healed, dry, and crusted over or until 48 hours after commencing treatment
pt may need admitting if septic, immunocompromised + widespread infection
Wash affected areas with soap and water.
Avoid touching or scratching patches of impetigo.
Wash hands regularly, including after touching affected areas.
Cover affected areas where possible.
Not share towels, facecloths, and other personal care products.
Wash clothing and bedding in the hottest setting (at least 60 degrees). During the first few days of treatment, clothing and bedding should be washed and changed daily
non-bullous - hydrogen peroxide 1% cream (to be applied two to three times daily for 5 days).
If hydrogen peroxide 1% cream is unsuitable, offer topical fusidic acid 2% (to be applied three times daily for 5 days).
If fusidic acid resistance is suspected or confirmed, offer topical mupirocin 2% (to be applied three times daily for 5 days).
If widespread consider fluclox
bullous - oral fluclox for 5 days (7 if more severe), if worsening/resistant then swab, consider MRSA swabs (nose etc), and re-consider ddx
boils and carbuncles
A boil (or furuncle) is an infection of the hair follicle where there is purulent extension into the subcutaneous tissue, in which a small abscess forms.
A carbuncle occurs when several adjacent boils join beneath the skin
Normally caused by staph aureus, sometimes MRSA
GAS can also cause, and sometimes anaerobes in anogenital region
Boils initially appear as firm, tender, erythematous nodules, which after several days enlarge and become painful and fluctuant; they occur in hair bearing sites; may have a slight fever
Boils may rupture spontaneously, draining pus or necrotic material. They heal (over several days to several weeks) to leave a violaceous macule, and possibly a permanent scar
A carbuncle appears as a large, hard, red, dome-shaped, very painful lump that increases in size over a few days.
Pus may drain from many follicular orifices.
Carbuncles soon develop a yellow-grey irregular crater centrally, caused by necrosis of the intervening skin.
They heal slowly, often leaving a permanent scar.
ddx:
Cystic acne
epidermoid cyst
folliculitis - small inflammatory papules or pustules
Hidradenitis suppurativa — a chronic inflammatory suppurative disease of the apocrine sweat glands causing painful, inflamed nodules and sterile abscesses. Consider this if only the groin and the axillae are involved
Arrange for urgent same-day incision and drainage for:
All large and/or fluctuant boils
All carbuncles
Consider admission for intravenous antibiotics if the person:
Is systemically unwell.
Has cellulitis
Is immunocompromised
Swab if persistent or recurrent to exclude atypical mycobacteria or Panton-Valentine leukocidin Staphylococcus aureus (PVL-SA - esp likely if severe or recurrent, or in eg prison with an outbreak; if confirmed discuss with micro).
advise:
To apply moist heat three to four times a day to alleviate pain, localize the infection, and hasten the drainage of pus.
That a small boil may drain spontaneously — once this has occurred, the lesion should be covered with a sterile dressing
To seek urgent medical advice if they become systemically unwell, or if boil becomes fluctuant (needs drainage)
7 days fluclox if painful, fever, cellulitis, on face, diabetic or immunocomp
hiradenitis suppurativa
chronic autoinflammatory skin condition that affects apocrine gland-bearing skin in the axillae, groin, and under the breasts. It is characterised by persistent or recurrent boil-like nodules and abscesses that culminate in a purulent discharge, sinuses, and scarring
often starts at puberty, is most active between the ages of 20 and 40 years, and in women can resolve at menopause
associations: FH, obesity, smoking, PCOS, IBD, metabolic syndrome
characterised clinically by:
Open double-headed comedones
Painful firm papules and nodules
Pustules, fluctuant pseudocysts, and abscesses
Draining sinuses linking inflammatory lesions
Hypertrophic and atrophic scars.
diagnosis requires all three components of the triad to be met:
Characteristic lesions
Typical distribution
Presence and recurrence of lesions.
swabs typically negative, consider: Staphylococcal skin infections, including abscesses, carbuncles, and furuncles/boils;
Cysts, like Bartholin cyst or epidermoid cys
Weight loss
Smoking cessation
Loose fitting clothing
Absorbent dressings
Analgesics.
if flare consider infection, avoid steroid therapy and treat with flucloxacillin 1000 mg QDS for 10-14 days, if fluctuant areas refer for US and I&D
longer term mx:
prescribe antiseptic such as 4% chlorhexidine wash, to reduce the spread of bacteria on the skin
consider topical clindamycin BD, or oral doxycycline 200 mg OD (or lymecycline 408 mg caps, two caps once a day) both initially for 3 months. Aim for reduction in flares and improved disease control
If topical therapy is used and does not control symptoms then swap to doxycycline / lymecycline (do not prescribe oral tetracyclines if less than 12 years of age)
In pregnancy, consider topical clindamycin BD for 3 months and review
Review at 3 months and if symptoms improved, consider treatment break but restart treatment after two or more flares
In patients with PCOS and/or pre-menstrual flares, consider spironolactone (max. 100mg OD; off-license) and/or an oral contraceptive with a favourable progestogen profile (eg Yasmin, Eloine, Mercilon)
Metformin (500-1500 mg; off-license) may help patients with PCOS and metabolic syndrome
refer if:
Severe psychological impact
No improvement following adequate first-line treatment (mild-moderate disease; refer whilst instituting second-line treatment)
Severe disease (refer whilst instituting first-line treatment)
Diagnostic uncertainty
Pregnancy
secondary care can consider dapsone, methotrexate, isotretinoin, and biologics (adalimumab first)
superficial fungal infection of skin - 3 main groups; 6 tinea presentations, 2 yeasts px; 2x dx (if cant do clinically), mx (general x3 and what to avoid+why, capitis x2, pityriasis mx step 1, step 2 (2 parts))
● Three main groups: dermatophytes (tinea/ringworm), yeasts (e.g. candidiasis, malassezia), moulds (e.g. aspergillus)
Presentation
● Varies with the site of infection; usually unilateral and itchy
● Tinea corporis (tinea infection of the trunk and limbs) - Itchy, circular or annular lesions with a clearly defined, raised and scaly edge is typical
● Tinea cruris (tinea infection of the groin and natal cleft) – very itchy, similar to tinea corporis
● Tinea pedis (athlete’s foot) – moist scaling and fissuring in toewebs, spreading to the sole and dorsal aspect of the foot
● Tinea manuum (tinea infection of the hand) – scaling and dryness in the palmar creases
● Tinea capitis (scalp ringworm) – patches of broken hair, scaling and inflammation
● Tinea unguium (tinea infection of the nail) – yellow discolouration, thickened and crumbly nail
● Candidiasis (candidal skin infection) – white plaques on mucosal areas, erythema with satellite lesions in flexures
● Pityriasis/Tinea versicolor (infection with Malassezia furfur) – scaly pale brown patches on upper trunk that fail to tan on sun exposure, usually asymptomatic
Management
● Establish the correct diagnosis by skin scrapings, hair or nail clippings (for dermatophytes); skin swabs (for yeasts)
● General measures: treat known precipitating factors (e.g. underlying immunosuppressive condition, moist environment)
Topical antifungal agents (e.g. terbinafine cream in adults, clotrimazole in kids)
● Oral antifungal agents (e.g. itraconazole) for severe, widespread, or nail infections
● Avoid the use of topical steroids – can lead to tinea incognito
tinea capitis needs oral antifungal (griseofulvin first line, or terbinafine) + antifungal shampoo (ketoconazole) - oral needed as topical doesn’t penetrate the hair follicle
pityriasis versicolor use ketoconazole shampoo, failure to respond send scrapings to check dx and give oral itraconazole
kerion
A kerion is an abscess caused by fungal infection.
It most often occurs on the scalp (tinea capitis), but it may also arise on any site exposed to the fungus such as face (tinea faciei) and upper limbs (tinea corporis)
presents as a boggy pus-filled lump, often several centimetres in diameter. It is characterised by marked inflammation.
Hairs within the kerion are loose and fall out, often resulting in a bald area (localised alopecia).
To confirm the diagnosis, scrapings and hair samples may be taken from the affected area for microscopy and fungal culture
should be treated by oral antifungal agents. A course of 6-8 weeks of treatment is normally prescribed at minimum with griseofulvin or terbinafine
Antibiotics may be needed if there is bacterial co-infection
scabies caused by what, spread how, and typically affects who; pathology, what then causes the itchiness and when, 2 main features, where else affected in infants x2, 2 secondary features due to scratching, 2 mx steps, how long does itching persist, how to manage close contacts x2, x2 mx for crusted scabies)
caused by the mite Sarcoptes scabiei and is spread by prolonged skin contact. It typically affects children and young adults.
The scabies mite burrows into the skin, laying its eggs in the stratum corneum. The intense pruritus associated with scabies is due to a delayed-type IV hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection.
Features
widespread pruritus
linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist
in infants, the face and scalp may also be affected
secondary features are seen due to scratching: excoriation, infection
permethrin 5% is first-line
malathion 0.5% is second-line
pruritus persists for 4-6wks post erad
close contacts should be treated at same time even if asymp, and should launder clothes and bedding on day 1 to kill mites
isolation and ivermectin for crusted scabies
pubic lice
Pubic lice infestation commonly presents as genital itching, which is worse at night.
The diagnosis is confirmed if visible pubic lice and/or eggs are found on examination
if sexual contact then refer to GUM; consider possibility of sexual abuse, but note non-sexual transmission is possible too
consider scabies, seb derm, dermatophyte, blepharitis, folliculitis
For lice on body areas other than the eyelashes, treat with permethrin 5% cream or malathion 0.5% aqueous solution
For lice on eyelashes, treat with an inert occlusive ophthalmic ointment (such as simple eye ointment BP) or paraffin eye ointment, twice a day for 8–10 days. Alternatively, permethrin 1% lotion should be applied to the eyelashes, keeping the eyes closed during the application, and washed off after 10 minutes.
Re-examine the person 1 week after completion of treatment to ensure that all lice have been killed.
If live lice are seen at follow up, confirm whether the correct treatment technique has been used.
If the correct technique has not been used, repeat the previous treatment with the correct technique.
If the current technique has been used, treat with the alternative insecticide.
management of insect bites, tick bites, and bed bugs
Bee sting — the sting may still be visible in the skin (remove immediately).
Flea bites — bites from cat or dog fleas are typically found below the knees.
Bed bugs — pruritic maculopapular lesions with haemorrhagic punctums (the site of the bite) may appear on exposed skin about 10 days after a bite from a bed bug.
Other presentations include isolated pruritis, nodules, bullae or urticaria.
Large numbers of bites can lead to widespread erythema or urticaria.
Suspect bed bugs if similar symptoms develop in people sharing a bed or travelling together.
Tick bites — the tick itself may be visible in the skin (remove immediately unless known to be allergic to ticks).
Acute tick bites may appear as an erythematous macule, papule or nodule.
Bites from infected ticks may result in Lyme disease which can present with erythema migrans (sometimes called a bullseye rash). For more information, see the CKS topic on Lyme disease.
Horse flies and stable flies — painful bites which may bleed and often become secondarily infected.
Midge bites — typically multiple small papular lesions on exposed skin.
Spider bites — may leave 2 clearly visible puncture wounds.
Head, body and pubic lice — can lead to excoriation due to itching caused by louse salivary antigens.
Consider if tetanus prophylaxis is appropriate
If a stinger is visible in the skin - remove it as quickly as possible by scraping sideways with a fingernail, a piece of card or a credit card
If a tick is visible in the skin then remove as soon as possible by grasping it close to skin with a pair of forceps, tweezers or specialist tick remover and pulling gently but firmly perpendicular to the skin
Once removed, clean the skin with antiseptic
Do not routinely offer antimicrobial prophylaxis or carry out serological tests for Lyme disease, but advise that if a rash appears at the site of the bite (erythema migrans) or a fever develops, the person should promptly seek medical advice
Clean the area and advise the person that simple first aid measures such as the use of cold compresses may help reduce local pain and swelling.
Advise the person on:
Prevention of secondary infections with good hygiene and avoidance of itching.
When to seek medical help for example, if secondary infection (ongoing or worsening erythema, pain, or fever), a large local reaction or systemic reaction develops.
bites are thought to be due to infestation with:
Bedbugs — advise the person to contact pest control services. Pest control is necessary as bedbugs can be difficult to eradicate and insecticide resistance is common.
Fleas — advise the person that flea bites are often associated with contact with domestic pets (especially cats and dogs) and that animals should be examined and treated if necessary. If the person has recently moved house, flea infestations may remain from previous pet owners.
Lice and scabies can be treated as in above flashcards
Oral antihistamines (such as chlorphenamine [sedating]) or topical corticosteroids (such as hydrocortisone 1%) may help reduce itching associated with cutaneous reactions but use is generally off-label and good quality evidence in support of use is lacking. May also be used if large reaction occurs.
Treat any cellulitis that develops. Ensure they arent having an anaphylacic reaction.
Discuss with an allergy specialist (with urgency depending on clinical judgement) the need to refer people who:
Have had a large local reaction (area of oedema, erythema and pruritus more than 10 cm in diameter which peaks between 24 and 48 hours after the sting). or if a systemic reaction occured
basal cell carcinoma - how fast growing, which cell type, how common, 8 risk factors, 5 subtypes, 5 features of commonest type, where most commonly found, 2 mx
slow-growing, locally invasive malignant tumour of the epidermal keratinocytes normally in older individuals, only rarely metastasises ● Most common malignant skin tumour Causes ● Risk factors include UV exposure, history of frequent or severe sunburn in childhood, skin type I (always burns, never tans), increasing age, male sex, immunosuppression, previous history of skin cancer, and genetic predisposition
Presentation ● Various morphological types including nodular (most common), superficial (plaque-like), cystic, morphoeic (sclerosing), keratotic and pigmented ● Nodular basal cell carcinoma is a small, skin-coloured papule or nodule with surface telangiectasia, and a pearly rolled edge; the lesion may have a necrotic or ulcerated centre (rodent ulcer) ● Most common over the head and neck
Management ● Surgical excision - treatment of choice as it allows histological examination of the tumour and margins ● Mohs micrographic surgery (i.e. excision of the lesion and tissue borders are progressively excised until specimens are microscopically free of tumour) - for high risk, recurrent tumours ● Radiotherapy - when surgery is not appropriate
squamous cell carcinoma (skin) - cancer of what cell type, 5 risk factors, 3 appearance features, 2 mx, 2 features making prognosis worse
A locally invasive malignant tumour of the epidermal keratinocytes or its appendages, which has the potential to metastasise Causes ● Risk factors include excessive UV exposure, pre-malignant skin conditions (e.g. actinic keratoses/bowens disease), chronic inflammation (e.g. leg ulcers, wound scars), immunosuppression (eg HIV or post renal transplant) and genetic predisposition
Presentation ● Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate Management ● Surgical excision - treatment of choice ● Mohs micrographic surgery – may be necessary for ill-defined, large, recurrent tumours ● Radiotherapy - for large, non-resectable tumours
prognosis worse if immunosup’d, >20mm in diameter (this will need 6mm margins rather than 4)
malignant melanoma - tumour of what cell type, 4 risk factors, 6sx and common locations, subtypes (x4), 3mx, most important prognostic factor
invasive malignant tumour of the epidermal melanocytes, which has the potential to metastasise
Causes ● Risk factors include excessive UV exposure, skin type I (always burns, never tans), history of multiple moles or atypical moles, and family history or previous history of melanoma
Presentation ● The ‘ABCDE Symptoms’ rule (major suspicious features): Asymmetrical shape Border irregularity Colour irregularity* Diameter > 6mm Evolution of lesion (e.g. change in size and/or shape)* Symptoms (e.g. bleeding, itching) ● More common on the legs in women and trunk in men
Types ● Superficial spreading melanoma – 70% of all cases,common on the lower limbs, in young and middle-aged adults; related to intermittent high- intensity UV exposure ● Nodular melanoma - common on the trunk, in young and middle- aged adults; related to intermittent high-intensity UV exposure ● Lentigo maligna melanoma - common on the face, in elderly population; related to long-term cumulative UV exposure ● Acral lentiginous melanoma - common on the palms, soles and nail beds (subungual pigmentation), in elderly population; no clear relation with UV exposure Management ● Surgical excision - definitive treatment ● Radiotherapy may sometimes be useful ● Chemotherapy for metastatic disease
invasion depth is most important prognostic factor
actinic keratoses - what are they and what are they caused by, 5 features
Actinic, or solar, keratoses (AK) is a common premalignant skin lesion that develops as a consequence of chronic sun exposure
Features
small, crusty or scaly, lesions
may be pink, red, brown or the same colour as the skin
typically on sun-exposed areas e.g. temples of head
multiple lesions may be present
keratoacanthoma - what it is, more common when, how lesion starts and evolves, what often happens, mx (why)
benign epithelial tumour. They are more common with advancing age and rare in young people.
Features - said to look like a volcano or crater
initially a smooth dome-shaped papule
rapidly grows to become a crater centrally-filled with keratin
Spontaneous regression of keratoacanthoma within 3 months is common, often resulting in a scar. Such lesions should however be urgently excised as it is difficult clinically to exclude squamous cell carcinoma
What is a dermatofibroma, usually where and what is it made of, 3 egs of cause, 4 sx, can be sign of what, malignancy risk, 16 other skin lumps, what is epidermoid cyst, derived from what and filled with what, usual cause, 4 features
common benign fibrous nodule usually found on the skin of the lower legs, composed of proliferating fibroblasts, sometimes forms in response to injuries eg injections, thorn injury, insect bite etc
size varies from 0.5–1.5 cm diameter; tethered to skin surface and mobile over subcut tissue, dimples on pinching the skin around the lesion; if many erupt this can be sign of immunosuppression inc eg HIV; does not give rise to cancer
sebaceous/dermoid cyst, lipoma, BCC, warts, xanthomas, skin tags, SCC, melanoma, pyogenic granuloma, keratoacanthoma, rheumatoid nodule, gouty tophi, keloid scar, NF lesion, skin met, or infection (leprosy, leishmaniasis, syphilis)
epidermoid/sebaceous cyst: benign, derived from hair follicle, filled with keratin/lipid, generally due to occluded pilosebaceous unit, firm flesh coloured nodule fixed to skin but mobile over deeper layers, 1-3cm, with central punctum that may discharge, may become infected/inflamed
mycosis fungoides - what they look like x2 and how to tell from common ddx, what is it a form of
itchy red plaques, a little like psoriasis, but tend to vary in colour around the plaque and from lesion to lesion; or may be hypopigmented in kids but it is rare in kids, it’s a rare form of T cell lymphoma
seborrhoeic keratoses - what are they, 3 features, 2 mx
benign epidermal skin lesions seen in older people.
Features
large variation in colour from flesh to light-brown to black
have a ‘stuck-on’ appearance
keratotic plugs may be seen on the surface
Management
reassurance about the benign nature of the lesion is an option
options for removal include curettage, cryosurgery and shave biopsy
peutz jeghers syndrome - 3 sx, inheritance pattern, big risk, screening needed x5
perioral pigmentation/freckles, abdo pain +/- GI bleed due to hamartomatous polyps usually in small bowel
AD inheritance
inc’d risk of cancers of breast, colon (40%), panc, stomach (30%), ovaries, lung (15%), small intestine, cervix, uterus, testes
if have then upper endoscopy, colonoscopy beginning at age 8, repeat at 18 or every 2-3yrs if polyps seen; every 2-3yrs after 18yo
mammogram every 2-3yrs beginning at age 20; yearly testicular exam for boys; pancreas MRI or endu USS beginning at 30-35yo
atopic eczema - usual start and end age, how common, 2 risk/cause theories, general appearance x5, common where in infants vs everyone else, 3 features of acute lesion, 2 of chronic scratching, 2 nail features, 3 genera measures, 2 topical therapies (when), 3 oral therapies (when), 2 options for severe cases, 4 complications, how much steroid is right
- usually develops by early childhood and resolves during teenage years (but may recur)
Epidemiology ● 20% prevalence in <12 years old in the UK
Causes ● Not fully understood, but a positive family history of atopy (i.e. eczema, asthma, allergic rhinitis) is often present ● A primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin) appears to underlie atopic eczema
Presentation ● Commonly present as itchy, erythematous dry scaly patches ● More common on the face and extensor aspects of limbs in infants, and the flexor aspects in children and adults ● Acute lesions are erythematous, vesicular and weepy (exudative) ● Chronic scratching/rubbing can lead to excoriations and lichenification ● May show nail pitting and ridging of the nails
Management ● General measures - avoid known exacerbating agents, frequent emollients +/- bandages and bath oil/soap substitute ● Topical therapies – topical steroids for flare-ups; topical immunomodulators (e.g. tacrolimus, pimecrolimus) can be used as steroid-sparing agents ● Oral therapies - antihistamines for symptomatic relief, antibiotics (e.g. flucloxacillin) for secondary bacterial infections, and antivirals (e.g. aciclovir) for secondary herpes infection ● Phototherapy and immunosuppressants (e.g. oral prednisolone, azathioprine, ciclosporin) for severe non- responsive cases
Complications ● Secondary bacterial infection (crusted weepy lesions) ● Secondary viral infection - molluscum contagiosum (pearly papules with central umbilication), viral warts and eczema herpeticum
1 fingertip unit of steroid cream good to cover one hand rubbed in
pompholyx (aka, 2 precipitants, 4 features, 3 mx)
also known as dyshidrotic eczema.
Pompholyx eczema may be precipitated by humidity (e.g. sweating) and high temperatures.
Features
small blisters on the palms and soles
often intensely itchy
sometimes burning sensation
once blisters burst skin may become dry and crack
Management
cool compresses
emollients
topical steroids
periorificial dermatitis (typical pt, 2 things liked to development, general appearance and spared area, 2 mx
condition typically seen in women aged 20-45 years old. Topical corticosteroids, and to a lesser extent, inhaled corticosteroids are often implicated in the development of the condition.
Features
clustered erythematous papules, papulovesicles and papulopustules
most commonly in the perioral region but also the perinasal and periocular region
skin immediately adjacent to the vermilion border of the lip is typically spared
Management
steroids may worsen symptoms
should be treated with topical or oral antibiotics
contact dermatitis (2 types triggered by what and look how, mx), which form can cement cause, 2 features making this more likely than atopic
irritant contact dermatitis: common - non-allergic reaction due to weak acids or alkalis (e.g. detergents). Often seen on the hands. Erythema is typical, crusting and vesicles are rare
allergic contact dermatitis: type IV hypersensitivity reaction. Uncommon - often seen on the head following hair dyes. Presents as an acute weeping eczema which predominately affects the margins of the hairline rather than the hairy scalp itself. Topical treatment with a potent steroid is indicated
Cement is a frequent cause of contact dermatitis. The alkaline nature of cement may cause an irritant contact dermatitis
if site of exposure rather than flexural, and in adult rather than young child (esp <5yo) then contact derm more likely than atopic eczema
eczema herpeticum - complication of what, caused by what, 2 features, 2 mx, 4 complications
● Widespread eruption - serious complication of atopic eczema or less commonly other skin conditions
Cause ● Herpes simplex virus
Presentation ● Extensive crusted papules, blisters and erosions ● Systemically unwell with fever and malaise
Management ● Antivirals (e.g. aciclovir) ● Antibiotics for bacterial secondary infection
Complications ● Herpes hepatitis, encephalitis, disseminated intravascular coagulation (DIC) and rarely, death
acne vulgaris what it is, how common, 5 contributing factors, 2 features dep on severity and commonly affects where, 3 topical therapies and 3 oral; and choice and 3 reasons to avoid, pregnancy contraindication to what + option in pregnancy, 3 complications
An inflammatory disease of the pilosebaceous follicle
Epidemiology ● Over 80% of teenagers aged 13- 18 years
Causes ● Hormonal (androgen) ● Contributing factors include increased sebum production, abnormal follicular keratinization, bacterial colonization (Propionibacterium acnes) and inflammation
Presentation ● Non-inflammatory lesions (mild acne) - open and closed comedones (blackheads and whiteheads) ● Inflammatory lesions (moderate and severe acne) - papules, pustules, nodules, and cysts ● Commonly affects the face, chest and upper back
Management ● General measures - no specific food has been identified to cause acne, treatment needs to be continued for at least 6 weeks to produce effect ● Topical therapies (for mild acne) - benzoyl peroxide and topical antibiotics (antimicrobial properties), and topical retinoids (comedolytic and anti-inflammatory properties) ● Oral therapies (for moderate to severe acne) - oral antibiotics, and anti-androgens ie COCP as alt to oral antibiotics (in females) ● Oral retinoids (for severe acne); oral abx of choice are tetracyclines like doxy or lemy but shold be avoided if preg, breastfeeding, <12yo; erythromycin can be used in pregnancy; alongside oral abx topical retinoid should be used unless contra’d; pregnancy is contra to oral and topical retinoids
Complications ● Post-inflammatory hyperpigmentation, scarring, psychological and social effects
acne treatment flowchart
Topical Treatments
- Most suitable for facial acne.
- Use at night to affected areas to prevent new spots from developing.
- Tell patients that it will take 4 to 6 weeks to start to work and they should have a 3-month trial.
Topical retinoids (contraindicated in pregnancy): have anticomedonal properties
- Counsel women of childbearing age to use effective contraceptive
- Warn regarding irritancy, photosensitivity (wash off before direct sunlight) peeling / dryness and need to moisturise.
Benzoyl peroxide: has keratolytic and antimicrobial properties (can be purchased from community pharmacy)
- Start at 5% and increase to 10% if necessary.
- Warn patients that it can bleach bedding and clothing and advise using a white towel
Single topical treatment
- Topical retinoid (if comedomal element) OR benzoyl peroxide (can be
purchased from a community pharmacy)
Combination topical treatments for example:
- Duac® gel (benzoyl peroxide + clindamycin), once daily
when not responding to above or widely distributed involving neck/back/chest use tetracycline or macrolide (note stop any topical abx before starting oral)
If inadequate response after 3-4 months with oral antibiotic OR if there are other reasons to take COCP such as contraception and menstrual control, then consider adding COCP to treatment.
Refer to dermatology:
- All patients with severe acne (nodulocystic acne or systemically unwell, please refer urgently).
- Inadequate response to above treatment.
- Acne causing significant scarring.
- Severe psychological distress regardless of physical sign.
Please ensure women who are sexually active are on a reliable form of contraception (COCP or LARC) in addition to a barrier method before referral for consideration of oral isotretinoin treatment.
Oral isotretinoin (contraindicated in pregnancy)
To be initiated & prescribed by consultant dermatologist due to serious side effects including teratogenic & possible psychiatric
effects
psoriasis - due to what, 6 types, how common, 5 triggers for attack, 6 meds that trigger/worsen, what can trigger guttate form
chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration
Types ● Chronic plaque psoriasis is the most common type ● Other types include guttate (raindrop lesions), seborrhoeic (naso-labial and retro-auricular), flexural (body folds), pustular (palmar-plantar), and erythrodermic (total body redness)
Epidemiology ● Affects about 2% of the population in the UK
Causes ● Complex interaction between genetic, immunological and environmental factors ● Precipitating factors include trauma (which may produce a Köebner phenomenon), infection (e.g. tonsillitis), drugs, stress, and alcohol
drug exacerbaters inc: beta blockers, lithium, antimalarials, ACEi, NSAIDs, inflixmab; strep infection can trigger guttate
Psoriasis appearance and 3 sx, common where, auspitz sign of what, how common to have nail changes and 2 egs, how common to have psoriatic arthropathy and 6 ways it presents, 7 mx, areas vulnerable to steroid atrophy x3 and so how long to use max, how much BSA for systemic side effects, how long to break before another steroid course, max length for potent steroids and very potent, how vit D analogues work and when they should be avoided
Well-demarcated erythematous scaly plaques ● Lesions can sometimes be itchy, burning or painful ● Common on the extensor surfaces of the body and over scalp ● Auspitz sign (scratch and gentle removal of scales cause capillary bleeding) ● 50% have associated nail changes (e.g. pitting, onycholysis)
5-8% suffer from associated psoriatic arthropathy - symmetrical polyarthritis, asymmetrical oligomonoarthritis, lone distal interphalangeal disease, psoriatic spondylosis, and arthritis mutilans - also dactylitis (ie swollen or sore, red finger)
NICE recommend a step-wise approach for chronic plaque psoriasis
regular emollients may help to reduce scale loss and reduce pruritus
first-line: NICE recommend:
a potent corticosteroid applied once daily plus vitamin D analogue applied once daily
should be applied separately, one in the morning and the other in the evening)
for up to 4 weeks as initial treatment
second-line: if no improvement after 8 weeks then offer:
a vitamin D analogue twice daily
third-line: if no improvement after 8-12 weeks then offer either:
a potent corticosteroid applied twice daily for up to 4 weeks, or
a coal tar preparation applied once or twice daily
Phototherapy (for extensive disease) - phototherapy i.e. UVB and photochemotherapy i.e. psoralen+UVA ● Oral therapies (for extensive and severe psoriasis, or psoriasis with systemic involvement) - methotrexate, retinoids, ciclosporin, mycophenolate, infliximab
scalp, face and flexures are particularly prone to steroid atrophy so topical steroids should not be used for more than 1-2 weeks/month
systemic side-effects may be seen when potent corticosteroids are used on large areas e.g. > 10% of the body surface area
NICE recommend that we aim for a 4-week break before starting another course of topical corticosteroids
they also recommend using potent corticosteroids for no longer than 8 weeks at a time and very potent corticosteroids for no longer than 4 weeks at a time
vit d analogues work by dec epidermal prolif, should be avoided in pregnancy
bullous pemphigoid - is what, cause and what layers split, 3 sx and where usually affects, 3 mx, main ix, mucosa?
blistering skin disorder which usually affects the elderly
Cause ● Autoantibodies against antigens between the epidermis and dermis causing a sub-epidermal split in the skin; blister is subepidermal and contains fibrin and large numbers of inflammatory cells including eosinophils; Direct immunofluorescence shows linear deposition of IgG (most often IgG4 subtype) and C3 along the basement membrane
Presentation ● Tense, fluid-filled blisters on an erythematous base ● Lesions are often itchy ● May be preceded by a non-specific itchy rash ● Usually affects the trunk and limbs (mucosal involvement less common)
Management ● General measures – wound dressings where required, monitor for signs of infection ● Topical therapies for localised disease - topical steroids ● Oral therapies for widespread disease and generally mainstay of tx after biopsy to confirm diagnosis – oral steroids, combination of oral tetracycline and nicotinamide, immunosuppressive agents
there is usually no mucosal involvement
pemphigus vulgaris - usually affects who, cause including layer affected, 3 features, 2 mx
blistering skin disorder which usually affects the middle-aged Cause ● Autoantibodies against antigens within the epidermis causing an intra-epidermal split in the skin;Early lesions of pemphigus vulgaris show suprabasal epidermal acantholysis, clefting and blister formation. The blister cavity may contain inflammatory cells including eosinophils; Direct immunofluorescence may be positive in perilesional skin with intercellular deposits of IgG and/or C3 in the epidermis
Presentation ● Flaccid, easily ruptured blisters forming erosions and crusts ● Lesions are often painful ● Usually affects the mucosal areas (can precede skin involvement)
Management ● General measures – wound dressings where required, monitor for signs of infection, good oral care (if oral mucosa is involved) ● Oral therapies – high-dose oral steroids, immunosuppressive agents (e.g. methotrexate, azathioprine, cyclophosphamide, mycophenolate)
epidermolysis bullosa - what it is, AD form inc what it is and where it is, AR version is what layer, dystrophic form what layer, 2 forms and features of the latter x4
v rare skin condition; simplex is AD, no scarring, in first year, esp over contact areas when crawling starts (knees/palms), generalised blistering in basal cell layer
junctional is AR at birth w generalsied bullae/blisters at junction of derm and epiderm
dystrophic form has AD form w less scarring, at onset of crawling; and AR form oft v severe w mucous membrane involvement, nail loss, syndactylyl, oesophageal strictures; in both blistering is in upper dermis
bullous reactions in kids - ddx 10:4:3:4 (what kind of hypersens is last kind, and 3 features), 4 mx, 5 things to get in history, 3 things in exam, 6 features of the blisters, ix needed for diagnosis usually, 7 other ix
bullae uncommon in kids but can be caused by various reasons
differential diagnosis for bullous skin lesions include infectious causes such as bullous impetigo, bullous tinea, eczema herpeticum, bullous scabies, mycoplasma pneumoniae, GAS, staph aureus/TSS, kawasaki disease, chickenpox, and herpes simplex infection; infection- and drug-associated causes such as erythema multiforme, DRESS, SJS and TEN; hereditary conditions such as epidermolysis bullosa, Kindler syndrome, and incontinenti pigmenti; and autoimmune conditions such as linear IgA bullous dermatitis, bullous pemphigoid, pemphigoid vulgaris, and fixed drug eruptions (type IV hypersens, mostly to abx or NSAIDs, always in same place in body, plaque or blister)
treat cause and depending on severity +/- response escalate from oral pred to IV eg methylpred to IVIg
approach
1. History
Timeline of disease
Prodromal symptoms ie symptoms that occurred before the rash started such as fever, difficulty eating, sore joints,
New medications, including over-the-counter and natural products
Previous reactions to drugs
Family history of reactions to medications
- General examination
Is the patient well or sick?
Check temperature, heart rate, blood pressure, respiratory rate
Feel for enlargement of lymph nodes, liver or spleen - Blisters
Localised or widespread?
Appearance — tense or flaccid, clear or containing pus or blood
Distribution on the skin
Evolution — are new ones still developing and old ones resolving, or are all the blisters at the same stage of development?
Involvement of mucous membranes (eg, inside mouth, eyes, vagina, etc.)
Nikolsky sign — pressure applied to skin pulling sideways — positive if the skin detaches - Histopathology
Often required to make the correct diagnosis
Other ix inc mycoplasma IgM serology, + test for EBV, HHV6, HSV, CMV, Hep ABC, ASOT
