Dermatology 🧖🏽♀️ Flashcards
MLA conditions and preperation
Erythema multiforme
Hypersensitivity reaction that is most commonly triggered by infections.
It may be divided into minor and major forms.
Typically appears like target lesions on the skin.
Features of Erythema multiforme
-target lesions
-initially seen on the back of the hands / feet before spreading to the torso
-upper limbs are more commonly affected than the lower limbs
-pruritus is occasionally seen and is usually mild
Causes of erythema multiforme
-viruses: herpes simplex virus (the most common cause), Orf (Parapox virus)
-idiopathic
-bacteria: Mycoplasma, Streptococcus
-drugs: penicillin, sulphonamides, -carbamazepine, allopurinol, NSAIDs, oral -contraceptive pill, nevirapine
-connective tissue disease e.g. Systemic lupus -erythematosus
-sarcoidosis
-malignancy
Erythema multiforme major
The more severe form, erythema multiforme major is associated with mucosal involvement.
Who gets erythema multiforme commonly
most common in young adults (aged 20–40 years) with a modest predominance in males. There is no association with race.
HLA-DQB1*0301 allele associated with herpes
Medications which may trigger erythema multiforme (4)
Antibiotics (including erythromycin, nitrofurantoin, penicillins, sulfonamides, and tetracyclines)
Anti-epileptics
Non-steroidal anti-inflammatory drugs
Vaccinations (most common cause in infants).
Conditions associated with erythema multiforme
Inflammatory bowel disease
Hepatitis C
Leukaemia
Lymphoma
Solid organ cancer malignancy.
Clinical features of ertythema multiforme
fatigue,
malaise,
myalgia,
or fever.
These likely represent the course of precipitating illness rather than true prodrome.
Serious complications of erythema multiforme
Keratitis
Conjunctival scarring
Uveitis
Permanent visual impairment.
What tests should be carried out if erythema multiforme is suspected
Complete blood examination
Liver functions tests
ESR
Serological testing for infectious causes
Chest x-ray.
Skin biopsy with histopathology and direct immunofluorescence
Treatment of erythema multiforme
- self limiting condition
- cease medication which causes
- prednisone for mucosal disease
- antiviral therapy aciclovir
Erythema nodosum
inflammatory disorder affecting subcutaneous fat. It most commonly presents as bilateral tender red nodules on the anterior shins
Who gets erythema nodosum
Erythema nodosum can occur in all ethnicities, sexes, and ages, but is most common in women between the ages of 25 and 40
It is 3–6 times more common in women than in men except before puberty when the incidence is the same in both sexes
Infective causes of erythema nodosum? (6)
- hypersensitivity reaction of unknown cause in 55%
-usually associated with drugs, infection or malignancy
Throat infections (streptococcal disease or viral infection)
Primary tuberculosis (TB), a rare cause in New Zealand
Yersinia infection; this causes diarrhoea and abdominal pain
Chlamydia infection
Fungal infection: histoplasmosis, coccidioidomycosis
Parasitic infection: amoebiasis, giardiasis
Viral and bacteria diseases which are associated with erythema nodosum
-HSV
- viral hepatitis
-HIV
- campylobacter infection
- Salmonella infection
Drugs which cause erythema nodosum (8) SHTEN
Sulfonamide
Hormonal
Tetracycline
ACE inhibitors
NSAIDs
Oral contraceptive
Non-steroidal anti-inflammatory drugs
Bromide
Salicylate
Iodide
Gold salt
Inflammatory diseases which cause erythema nodosum
Inflammatory bowel disease (ulcerative colitis or Crohn disease)
Sarcoidosis (11–-25%); X-ray shows bilateral hilar adenopathy in Löfgren syndrome
Malignancy
Lymphoma
Leukaemia
Behçet disease
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Pregnancy
Investigations for erythema nodosum
Complete blood count with differential, C-reactive protein levels (infectious and inflammatory causes)
Chest X-ray (tuberculosis and sarcoidosis)
Throat swab and anti-streptolysin O and streptodornase serology (streptococcal infection)
Viral serology (preferably two samples at four-week intervals)
Stool culture and evaluation for ova and parasites in patients with gastrointestinal symptoms
Mantoux test or QuantiFERON gold (tests for TB).
Deep incisional or excisional skin biopsy.
Septal Panniculitis
Various forms of scleroderma
Medium vessel vasculitis, for example, due to polyarteritis nodosa in which there are tender subcutaneous nodules associated with ulceration, necrosis, livedo racemosa, fever, joint pain, myalgia, and peripheral neuropathy
Necrobiosis lipoidica
Eosinophilic panniculitis
Rheumatoid nodule.
Guttate psoriasis
Distinct variant of psoriasis that is classically triggered by streptococcal infection (pharyngitis or perianal)
More common in Childern and adolescents
Features of guttate psoriasis
Tear drop papules on the trunk and limbs
gutta is Latin for drop
pink, scaly patches or plques of psoriasis
tends to be acute onset over days
Typically triggered by Streptococcal infection
What is the managment of guttate psoriasis
most cases resolve spontaneously within 2-3 months
there is no firm evidence to support the use of antibiotics to eradicate streptococcal infection
topical agents as per psoriasis
UVB phototherapy
tonsillectomy may be necessary with recurrent episodes
Prodome (guttate vs Pityriasis rosea)
Many patients report recent respiratory tract infections but this is not common in questions
Appearance (Guttate vs Pityriasis rosea)
‘Tear drop’, scaly papules on the trunk and limbs
Herald patch followed 1-2 weeks later by multiple erythematous, slightly raised oval lesions with a fine scale confined to the outer aspects of the lesions.
May follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance
Treatment (Guttate vs Pityriasis rosea)
Most cases resolve spontaneously within 2-3 months
Topical agents as per psoriasis
UVB phototherapy
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Self-limiting, resolves after around 6 weeks
Pityriasis rosea
Pityriasis rosea describes an acute, self-limiting rash which tends to affect young adults
characterised by a large circular or oval “herald patch”, usually found on the chest, abdomen, or back
Herald patch is followed some time later, typically two weeks or so, by the development of smaller scaly oval red patches, resembling a Christmas tree, distributed mainly on the chest and back.
What are the features of pityriasis rosea
In the majority of patients there is no prodrome, but a minority may give a history of a recent viral infection
herald patch (usually on trunk)
followed by erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance
Managment of pitiyriasis rosea
self-limiting - usually disappears after 6-12 weeks
Common microbe in animal bites
polymicrobial
most common isolated organism is Pasteurella multocida.
Managment of animal bites
cleanse wound.
Puncture wounds should not be sutured closed unless cosmesis is at risk
current BNF recommendation is co-amoxiclav
if penicillin-allergic then doxycycline + metronidazole is recommended
Microbes which are found in human bites (5)
Streptococci spp.
Staphylococcus aureus
Eikenella
Fusobacterium
Prevotella
Reccomended Tx for human and animal bites
Co-amoxiclav
other investigations/ tx after exposure to animal or human bites
HIV (6 weeks before sero-conversion, cosider pep)
Hepatitis C
Bed bugs
Cimex hemipteru.
Cimex lectulatius
Clinical features of bed bug bites
A small punctum (hole) may be seen at the site of the bite.
Some people develop cutaneous reactions with pruritus (itching) and (most commonly) 2–5 mm red bumps.
Purpura, petechiae, vesicles, urticaria, pustules, localised infection, and (rarely) anaphylaxis may also develop.
Hypersensitivity reactions may develop in some who become sensitised to bed bug saliva.
If bites are seen, they are often reported to be in a linear formation in groups of three, sometimes termed the ‘breakfast, lunch, and dinner’ pattern.
Bed bugs feed on exposed skin, therefore the limbs are a more common site for bites.
complications of bed bug bites
Localised infections including cellulitis, folliculitis, and infected eczema
Anaemia (a few reports of this secondary to chronic bed bug infestation)
Anaphylaxis
Psychological distress.
prophylaxis/ prevent future cases of bed bugs
Bed bug numbers may be controlled by hot-washing bed linen and using mattress covers.
managment of bed bug bites
A cool, damp cloth over areas of irritation can improve symptoms
Itchy lesions can be treated with topical steroids and/or oral antihistamines (hydrocortisone and ceterazie)
Secondary infection should be treated with antibiotics (Cephalexin, Doxycycline
Trimethoprim-sulfamethoxazole (co-trimoxazole)
Clindamycin)
Rare systemic anaphylactic reactions to bed bug bites may require intramuscular adrenaline.
Lyme disease microorganism
Borrelia burgdorferi
Early features of lyme disease in the first 30 days
erythema migrans
‘bulls-eye’ rash is typically at the site of the tick bite
typically develops 1-4 weeks after the initial bite but may present sooner
usually painless, more than 5 cm in diameter and slowlly increases in size
present in around 80% of patients.
Systemic features of lyme disease
headache
lethargy
fever
arthralgia
Later features of lyme disease
cardiovascular
heart block
peri/myocarditis
neurological
facial nerve palsy
radicular pain
meningitis
Investigations of Lyme disease
NICE recommend that Lyme disease can be diagnosed clinically if erythema migrans is present
erythema migrans is therefore an indication to start antibiotics
enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test
if negative and Lyme disease is still suspected in people tested within 4 weeks from symptom onset, repeat the ELISA 4-6 weeks after the first ELISA test. If still suspected in people who have had symptoms for 12 weeks or more then an immunoblot test should be done
if positive or equivocal then an immunoblot test for Lyme disease should be done
Erythema Migrans
typically a circular red area that sometimes clears in the middle, forming a bull’s-eye pattern.
Managment of tick bites
tick bites can be a relatively common presentation to GP practices, and can cause significant anxiety
if the tick is still present, the best way to remove it is using fine-tipped tweezers, grasping the tick as close to the skin as possible and pulling upwards firmly. The area should be washed following.
NICE guidance does not recommend routine antibiotic treatment to patients who’ve suffered a tick bite
fIrst aid response to
burns
airway, breathing, circulation
burns caused by heat: remove the person from the source. Within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes. Cover the burn using cling film, layered, rather than wrapped around a limb
electrical burns: switch off power supply, remove the person from the source
chemical burns: brush any powder off then irrigate with water. Attempts to neutralise the chemical are not recommended
Wallace Rule
Wallace’s Rule of Nines: head + neck = 9%, each arm = 9%, each anterior part of leg = 9%, each posterior part of leg = 9%, anterior chest = 9%, posterior chest = 9%, anterior abdomen = 9%, posterior abdomen = 9%
the palmar surface is roughly equivalent to 1% of total body surface area (TBSA). Not accurate for burns > 15% TBSA
Lund and Browder chart: the most accurate method
Superficial epidermal
-first degree
-Red and painful, dry, no blisters
Partial thickness (superficial dermal)
- second degree burn
-Pale pink, painful, blistered. Slow capillary refill
Partial thickness (deep dermal)
- second degree burn
Typically white but may have patches of non-blanching erythema. Reduced sensation, painful to deep pressure
Full thickness burn
- third degree burn
-White (‘waxy’)/brown (‘leathery’)/black in colour, no blisters, no pain
when referral to secondary care needed for burns?
-all deep dermal and full-thickness burns.
superficial dermal burns of more than 3% TBSA in adults, or more than 2% TBSA in children
superficial dermal burns involving the face, hands, feet, perineum, genitalia, or any flexure, or circumferential burns of the limbs, torso, or neck
any inhalation injury (even small injury next to the nose)
any electrical or chemical burn injury
suspicion of non-accidental injury
1st management of burn
initial first aid
review referral criteria to ensure can be managed in primary care
superficial epidermal: symptomatic relief - analgesia, emollients etc
-superficial dermal: cleanse wound, leave blister intact, non-adherent dressing, avoid topical creams, review in 24 hours
Burns which impact the airways
-smoke inhalation can result in airway oedema
-early intubation should be considered e.g. if deep burns to the face or neck, blisters or oedema of the oropharynx, stridor etc
IV fluids - when required in burns
- children with burns greater than 10% of total body surface area.
-Adults with burns greater than 15% of total body surface area
Parkland formula
volume of fluid= total body surface area of the burn % x weight (Kg) x4.
half fluid needs to be given in the first 8 hours
also insert urinary catheter
Managment of complex burns
Complex burns, burns involving the hand perineum and face and burns >10% in adults and >5% in children should be transferred to a burns unit.
Circumferential burns
Circumferential burns affecting a limb or severe torso burns impeding respiration may require escharotomy to divide the burnt tissue.
Escharotomies
Careful division of the encasing band of burn tissue will potentially improve ventilation (if the burn involves the torso),
relieve compartment syndrome and oedema (where a limb is involved)
Some causes of pruritis
hyper- and hypothyroidism
diabetes
pregnancy
‘senile’ pruritus
urticaria
skin disorders: eczema, scabies, psoriasis, pityriasis rose
Pruritis and liver- other symptoms
History of alcohol excess
Stigmata of chronic liver disease: spider naevi, bruising, palmar erythema, gynaecomastia etc
Evidence of decompensation: ascites, jaundice, encephalopathy
Pruritis and iron deficiency
Pallor
Other signs: koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis
Prutitis and Polycythemia
Pruritus particularly after warm bath
‘Ruddy complexion’
Gout
Peptic ulcer disease
Chronic kidney disease and pruritis
Lethargy & pallor
Oedema & weight gain
Hypertension
Lymphoma and pruritis
Night sweats
Lymphadenopathy
Splenomegaly, hepatomegaly
Fatigue
Signs of pruritis
excoriations
Persistent scratching over a period of time may lead to:
Lichenification (thickened skin, lichen simplex)
Prurigo papules and nodules.
epidemiology of pruritis
Affects all people
The incidence of chronic pruritus increases with age, it is more common in women, and in those of Asian background.
localised rashes (scalp, back, hands, genitals, legs and feet)
Scalp: seborrhoeic dermatitis, head lice
Back: Grover disease
Hands: pompholyx, irritant and/or allergic contact dermatitis
Genitals: vulvovaginal Candida albicans infection, lichen sclerosus
Legs: venous eczema
Feet: tinea pedis
Neuropathic localised pain (face, hands, arm, back, geniral, dermatomal)
Face: trigeminal trophic syndrome
Hand: cheiralgia paraesthetica
Arm: brachioradial pruritus
Back: notalgia paraesthetica
Genital: pruritus vulvae, pruritus ani
Dermatomal: herpes zoster (shingles) during the recovery phase
Managment of pruritis
Wet dressings or tepid shower to cool the skin
Calamine lotion (contains phenol, which cools the skin): avoid on dry skin and limit use to a few days
Menthol/camphor lotion: gives a chilling sensation
Local anaesthetics, such as pramoxine (also called pramocaine), applied to small itchy spots such as insect bites
Regular use of emollients, especially if skin is dry
Mild topical corticosteroids for short periods
Topical calcineurin inhibitors are also used to reduce itch associated with inflammatory skin conditions
Topical doxepin, a tricyclic antidepressant and antihistamine, is an antipruritic used in eczema.
antidepressants and antipruritic action
Doxepin and amitriptyline are tricyclic antidepressants have antipruritic action and act on the central and peripheral nervous systems.
Tetracyclic antidepressants such as mirtazepine and selective serotonin reuptake inhibitors (paroxetine, sertraline, fluoxetine) may also help some patients with severe itch including when it is caused by cholestasis, T-cell lymphoma, malignancy or a neuropathic cutaneous dysaesthesia.
Anti-epileptic drugs such as sodium valproate, gabapentin and prega
Asprin and pruritis
Aspirin is sometimes effective if pruritus is mediated by kinins or prostaglandins and is noted to be effective in patients with pruritus due to polycythaemia vera. Note: aspirin may cause or aggravate itch in some patients.
Phototherapy
Ultraviolet B (UVB) phototherapy alone, or in conjunction with UVA, has been shown to be helpful for pruritus associated with chronic kidney disease, psoriasis, atopic eczema and cutaneous T-cell lymphoma.
Pre-disposing factors of Keloid scars
ethnicity: more common in people with dark skin
occur more commonly in young adults, rare in the elderly
common sites (in order of decreasing frequency): sternum, shoulder, neck, face, extensor surface of limbs, trunk
erythema migrans
- Rash associated with Lyme disease
- centre dark, one round outside is clear
Uticaria
Urticaria describes a local or generalised superficial swelling of the skin. The most common cause of urticaria is allergy although non-allergic causes are seen.
-pale, pink raised skin. Variously described as ‘hives’, ‘wheals’, ‘nettle rash’
pruritic
what are the classifcations of uticaria
-Acute urticaria (< 6 weeks duration, and often gone within hours to days)
-Chronic urticaria (> 6 weeks duration, with daily or episodic weals)
acute causes of uticaria
Acute viral infection — upper respiratory infection, viral hepatitis, infectious mononucleosis, mycoplasma
Acute bacterial infection — dental abscess, sinusitis
Food allergy (IgE mediated)—usually milk, egg, peanut, shellfish
Drug allergy (IgE mediated drug-induced urticaria) — often an antibiotic
Drug-induced urticaria due to pseudoallergy — aspirin, nonselective nonsteroidal anti-inflammatory drugs, opiates, radiocontrast media; these cause urticaria without immune activation
Vaccination
Bee or wasp stings
Widespread reaction following localised contact urticaria — for example, latex
chronic uticaria causes ``
Chronic underlying infection, such as Helicobacter pylori (bowel parasites)
Chronic autoimmune diseases, such as systemic lupus erythematosus, thyroid disease, coeliac disease, vitiligo, and others.
Heat
Viral infection
Tight clothing
Drug pseudoallergy—aspirin, nonsteroidal anti-inflammatory drugs, opiates
Food pseudoallergy—salicylates, azo dye food colouring agents such as tartrazine (102), benzoate preservatives (210-220), and other food additives.
Inducible urticaria
Aquagenic urticaria
Hot or cold water
Fresh, salt, or chlorinated water
Vibratory urticaria
Jack hammer
Heat uricaria
Hot water bottle
Hot drink
Solar Uticaria
Sun exposure to non-habituated body sites
Often spare face, neck, hands
May involve long wavelength UV or visible light
Delayed pressure urticaria
Pressure on affected skin several hours earlier
Carrying heavy bag
Pressure from a seat belt
Standing on a ladder rung
Sitting on a horse
Contact urticaria
Eliciting substance absorbed through the skin or mucous membrane
Allergens (IgE-mediated): white flour, cosmetics, textiles, latex, saliva, meat, fish, vegetables
Pseudoallergens or irritants: stinging nettle, hairy caterpillar, medicines
Cholinergic urticaria
Sweat induced by exercise
Sweat induced by emotional upset
Hot shower
Cold urticaria
Cold air on exposed skin
Cold water
Ice block
Cryotherapy
Dermographism
Stroking or scratching the skin
Tight clothing
Towel drying after a hot shower
Managment of Utricaria
oral second-generation H1-antihistamine such as cetirizine or loratidine.
Onychomycosis
Fungal nail infection (onychomycosis) may involve any part of the nail, or the entire nail unit. Toenails are significantly more likely to become infected than fingernails
Severe Urticaria
A short course of an oral corticosteroid may required in addition to a non-sedating antihistamine
Toxic epidermal necrolysis
rare but important side effect of which to be aware of penicillins
life-threatening skin disorder that is most commonly seen secondary to a drug reaction
systemically unwell e.g. pyrexia, tachycardic
positive Nikolsky’s sign: the epidermis separates with mild lateral pressure
Drugs which induce TEN (6) SATAN
Sulfa drugs (sulfoamines)
Allopurinol
Tetracyclines
Anticonvulsant
NSAIDs (pircoxicam)
Managment of TENs
stop precipitating factor
supportive care
often in an intensive care unit
volume loss and electrolyte derangement are potential complications
intravenous immunoglobulin has been shown to be effective and is now commonly used first-line
other treatment options include: immunosuppressive agents (ciclosporin and cyclophosphamide), plasmapheresis
Chlorphenamine- sedating or non-sedating?
sedating
Loratadine- sedating or non-sedating?
non-sedating
ceterazine- sedating or non-sedating
non-sedating
What is this?
Erythema multiforme
What is this?
Erythema multiforme
What is this?
Erythema multiforme
What is this?
Erythema nodosum
What is this?
Erythema nodosum
What is this?
Erythema nodosum
what is this?
Guttate psoriasis
What is this?
Guttate psoriasis
What is this?
Pityriasis rosea
Acanthosis nigricans
Symmetrical, brown, velvety plaques
can be found
* neck
* axilla
* groin
Causes of Acanthosis nigricans
type 2 diabetes mellitus
gastrointestinal cancer
obesity
polycystic ovarian syndrome
acromegaly
Cushing’s disease
hypothyroidism
familial
Prader-Willi syndrome
drugs
combined oral contraceptive pill
nicotinic acid
Pathophysiology of acanthosis nigricans
insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)
What is this?
Acanthosis nigricans
What is this?
Acanthosis nigricans
Features of Lichen Planus
* itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
* rash often polygonal in shape,
* ‘white-lines’ pattern on the surface (Wickham’s striae)
* Koebner phenomenon may be seen (new skin lesions appearing at the site of trauma)
* oral involvement in around 50% of patients: typically a white-lace pattern on the buccal mucosa
* nails: thinning of nail plate, longitudinal ridging
Drugs which cause Lichen planus (3)
- gold
- quinine
- thiazides
What is this?
Lichen Planus
What is this?
Lichen Planus- buccal mucosa
Managment of Lichen Planus
- potent topical steroids are the mainstay of treatment
- benzydamine mouthwash or spray (oral)
- extensive lichen planus may require oral steroids or immunosuppression
What are the features of Rosacea?
- typically affects nose, cheeks and forehead
- flushing is often first symptom
- telangiectasia
- later develops into persistent erythema with papules and pustules
- rhinophyma
- ocular involvement: blepharitis
- sunlight may exacerbate symptoms
What is this?
Rosacea
What is this?
Rosacea
What is this?
Rosacea
simple managment of Rosacea
- high factor sunscreen
- camoflague creams
-
topical brimonidine gel may be considered for patients with predominant flushing but limited telangiectasia
*
Managment of mild-moderate papules or pustles
topical ivermectin is first-line
alternatives include: topical metronidazole or topical azelaic acid
Moderate- to-severe papules or pustles Rosacea
combination of topical ivermectin + oral doxycycline
When referral for rosacea needed
- symptoms have not improved with optimal management in primary care
- laser therapy may be appropriate for patients with prominent telangiectasia
- patients with a rhinophyma
Seborrhoeic dermatitis
flammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur
Organism causes Seborrhoeic dermatitis?
Malassezia furfur
formerly known as Pityrosporum ovale
What is this?
Seborrhoeic dermatitis
What is this?
Seborrhoeic dermatitis
conditions assoicated with Seborrhoeic dermatitis
- HIV
- Parkinson’s disease
Managment of Seborrhoeic scalp disease
- the first-line treatment is ketoconazole 2% shampoo
- over the counter preparations containing zinc pyrithione (‘Head & Shoulders’) and **tar **(‘Neutrogena T/Gel’) may be used if ketoconazole is not appropriate or acceptable to the person
- selenium sulphide and **topical corticosteroid **may also be useful
Face and body managment of seborrhoeic dematitis
- opical antifungals: e.g. ketoconazole
- topical steroids: best used for short periods
- difficult to treat - recurrences are common
Seborrhoeic dermatitis in children managment
- reassurance that it doesn’t affect the baby and usually resolves within a few weeks
- massage a topical emollient onto the scalp to loosen scales, brush gently with a soft brush and wash off with shampoo.
- if severe/persistent a topical imidazole cream may be tried
Cradle cap
- may develop in the first few weeks of life
- erythematous rash with coarse yellow scales.
- spontaneously may ressolve at 8 months
What is this?
Fungal nail change
Features of fungal nail changes
- ‘unsightly’ nails are a common reason for presentation
- thickened,
- rough, opaque nails are the most common finding
Risk factors for fungal nail infections
increasing age
diabetes mellitus
psoriasis
repeated nail trauma
what are the causative agents for fungal nail infections?
- dermatophytes (90% cases)
- mainly Trichophyton rubrum
yeasts (5-10% cases) - e.g. Candida
- non-dermatophyte moulds
ddx for fungal nail infections?
- psoriasis
- repeated trauma
- lichen planus
- yellow nail syndrome
Investigations for fungal nail infections?
- nail clippings +/- scrapings of the affected nail
- microscopy and culture
- should be done for all patients if antifungal treatment is being considered
- the false-negative rate for cultures are around 30%, so repeat samples may need to be sent if the clinical suspicion is high
Managment of fungal nail infections?
- asymptomatic- no treatment needed
- dermatophyte or Candida- amorolfine 5% nail lacquer; 6 months for fingernails and 9 - 12 months for toenails
- more extensive dermaphyte- oral terbinafine
- extensive candida- oral itraconazole is recommended first-line; ‘pulsed’ weekly therapy is recommended
Nail pitting
psoriasis
alopecia areata
Blue nails
Wilson’s disease
Leuconychia
hypoalbuminaemia
less common: fungal disease, lymphoma
Yellow nail syndrome
associated with congenital lymphoedema, pleural effusions, bronchiectasis and chronic sinus infections
What is this?
Yellow nail syndrome **
What is this?
Blue nail- wilsons disease
What is this?
Nail pitting psoriasis
Mild nail psoriasis
Onycholysis
separation of the nail plate from the nail bed
Causes on Onycholysis
- idiopathic
- trauma e.g. Excessive manicuring
- infection: especially fungal
- skin disease: psoriasis, dermatitis
- impaired peripheral circulation e.g. Raynaud’s
- systemic disease: hyper- and hypothyroidism
What nail changes are seen in psoriasis?
- pitting
- onycholysis (separation of the nail from the nail bed)
- subungual hyperkeratosis
- loss of the nail
Iron deficiency anaemia- features
- Pallor
- Other signs: koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis
Liver disease- features
- History of alcohol excess
- Stigmata of chronic liver disease: spider naevi, bruising, palmar erythema, gynaecomastia etc
- Evidence of decompensation: ascites, jaundice, encephalopathy
Polycythaemia
- Pruritus particularly after warm bath
- ‘Ruddy complexion’
- Gout
- Peptic ulcer disease
Chronic kidney disease- features
Lethargy & pallor
Oedema & weight gain
Hypertension
Lymphoma- features
Night sweats
Lymphadenopathy
Splenomegaly, hepatomegaly
Fatigue
other potential causes of pruritis?
- hyper- and hypothyroidism
- diabetes
- pregnancy
- ‘senile’ pruritus
- urticaria
- skin disorders: eczema, scabies, psoriasis, pityriasis rosea
Keloid scars
tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound
Pre-disposing factors for keloid scars?
- ethnicity: more common in people with dark skin
- occur more commonly in young adults, rare in the elderly
Sites where keloid scars are found?
- Sternum
- shoulder
- neck
- face
- extensor surface of limbs
- trunk
Managment of Keloid scars?
- early keloids-> intra-lesional steroids e.g.** triamcinolone**
- excision (careful consideration needs to given to the potential to create further keloid scarring)
Actinic keratoses
- premalignant skin lesion that develops as a consequence of chronic sun exposure
- AKA Actinic, or solar, keratoses (AK)
Features of AK
- 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
What is this?
Actinic keratoses
Managment of Actinic Keratoses
- Sun care (cover up, SPF)
- fluorouracil cream- 2-3 weeks
- milk AKs- topical diclofena
- topical imiquimod: trials have shown good efficacy
- cryotherapy
- curettage and cautery
Fluorouracil can cause inflammation of the skin, may need to prescribe steroids with it
Impetigo
- skin infection caused by Staphylcoccus aureus or Streptococcus pyogenes
- can be complication of eczema, scabies or insect bites
- common in children, warm weather
Where do Impetigo lesions normall occur?
face, flexures and limbs not covered by clothing.
How does impetigo spread?
- direct contact with discharges from the scabs of an infected person.
- incubation 4-10 days
Feaures of impetigo
- honey-coloured scab
- very contagious
What is this?
Impetigo
Managment of impetigo
- well or high risk of complications- **hydrogen peroxide 1% cream **
- topical antibiotic creams:
- topical fusidic acid
- topical mupirocin should be used if fusidic acid resistance is suspected
- MRSA suspected- retapamulin
Extensive disease (impetigo) managment
oral flucloxacillin
oral erythromycin if penicillin-allergic
Impetigo and school exclusion
- lesions must be crusted over and healed
or - 48hr after AB tx
Lipoma
common, benign tumour of adipocytes.
Pathophysiology of Lipoma
- they are generally found in subcutaneous tissues
- rarely, they may also occur in deeper adipose tissues
- malignant transformation to liposarcoma is very rare
epidemiology of lipoma
- lipomas are common, with an annual incidence of around 1 in 1,000
- most commonly seen in middle-aged adults
Features of Lipoma
- smooth
- mobile
- painless
Managment of lipoma
- observe lump
- remove if diagnosis not sure
Liposarcoma
- Size >5cm
- Increasing size
- Pain
- Deep anatomical location
Venous leg ulcers
Ulcers form due to capillary fibrin cuff or leucocyte sequestration
Features of venous insufficiency
- oedema
- brown pigmentation
- lipodermatosclerosis
- eczema
Managment of venous leg ulcers
- 4 layer compression banding after exclusion of arterial disease or surgery
- fail to heal after 12weeks or >10cm2- skin graft may be needed
What is this?
venous leg ulcer
Marjolin’s ulcer
Squamous cell carcinoma
Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-20 years
Mainly occur on the lower limb
What is this?
Marjolin’s ulcer
What is this?
Marjolin’s ulcer
Arterial ulcer
- Occur on the toes and heel
- Typically have a ‘deep, punched-out’ appearance
- Painful
- There may be areas of gangrene
- Cold with no palpable pulses
- Low ABPI measurements
Managment of Marjolin’s ulcers
Mohs surgery, wide local excision with 1 to 2 cm margins, and amputation proximal to the lesion.
Arterial ulcer managment
- Angioplasty
- Endarterectomy
What is this?
Arterial ulcer
Neuropathic ulcers
- Commonly over plantar surface of metatarsal head and plantar surface of hallux
- The plantar neuropathic ulcer—> amputation in diabetic patients
- Due to pressure
Managment of Neuropathic ulcers
cushioned shoes to reduce callous formation
What is this?
Neuropathic ulcer
Pyoderma Gangrenosum
- Associated with inflammatory bowel disease/RA
- Can occur at stoma sites
- Erythematous nodules or pustules which ulcerate
what is this?
Pyoderma gangernosum
5ps of Pyoderma gangerosum
Painful, Progressive, Purple, Pretibial, Pathergy
Managment of Pyoderma gangerosum
- cyclosporine.
- Other options include mycophenolate (Cellcept), immunoglobulins, dapsone, infliximab (Remicade) and tacrolimus (Protopic
Predisposition to leg ulcers (4)
- malnourishment
- incontinence: urinary and faecal
- lack of mobility
- pain (leads to a reduction in mobility)
scale used for pressure sores
waterlow score
Grade 1 of pressure ulcers
Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin
Grade 2 pressure ulcers
Partial thickness skin loss involving epidermis or dermis, or both. The
ulcer is superficial and presents clinically as an abrasion or blister
Grade 3 pressure ulcers
Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
Grade 4 pressure ulcers
Extensive destruction, tissue necrosis, or damage to muscle, bone or
supporting structures with or without full thickness skin loss
Managment of pressure ulcers
- Hydrocolloid dressings and hydrogel
- discourage soap use
- swab wounds
- consider referral to tissue viability nurse
- surgical debidement
Venous ulcer location
typically above the medial malleolus
Investigations for venous ulceration
- ankle-brachial pressure index (ABPI)
- normal- 0.9-1.2
- below or above could be arterial disease
Managment of venous ulceration
- compression bandages (4 layers)
- oral pentoifylline (peripheral vasodilator)
Atrophic vaginitis
- vaginal dryness in post-menopausal women
AV presentation
- vaginal dryness
- dyspareunia
- occasional spotting.
- On examination, the vagina may appear pale and dry.
Causes of Pruritus vulvae
- Irritant contact dermatitis (e.g. latex condoms, lubricants): most common cause
- atopic dermatitis
- seborrhoeic dermatitis
- lichen planus
- lichen sclerosus
- psoriasis: seen in around a third of patients with psoriasis
Managment of women with Pruritis vulvae
- women should take showers rather than baths
- clean vulval area with emoilent
- clean only once a day
- topical steroids
- Seborrhoeic dermatitis- use steroid-antifungal
What is acne?
disease of the pilosebaceous unit.
What lesions are seen in acne?
- white heads
- black heads
- papules
- pustules
- nodules
- cysts
- ice-pick scars
- hypertrophic scars
Drugs associated with acne?
- steroids
- lithium
- Phenytoin and carbamazepine
- Isoniazid
- Cyclosporine
- Halogens
Acne fulminan
Very severe acne associated with systemic upset (e.g. fever).
Hospital admission is often required and the condition usually responds to oral steroids
classification of mild acne
open and closed comedones with or without sparse inflammatory lesion
moderate acne classification
widespread non-inflammatory lesions and numerous papules and pustules
Severe acne classification
xtensive inflammatory lesions, which may include nodules, pitting, and scarring
mild to moderate acne managment
- 1st line: 12-week course of topical combination therapy
- fixed combination of topical adapalene with topical benzoyl peroxide
- fixed combination of topical tretinoin with topical clindamycin
- xed combination of** topical benzoyl peroxide with topical clindamycin**
monotherapy topical benzoyl peroxide if options are contraindicated or the person wishes to avoid using a topical retinoid or an antibiotic
When to avoid tetracyclines?
- pregancy
- under 12
- use erythromycin instead
minocycline contradiction reason
Not appropriate due to pigmentation
Gram-negative folliculitis managment
high-dose oral trimethoprim
Dianette
- anti-androgen properties.
- However, it has an increased risk of venous thromboembolism compared to other COCPs,
Reducing antibiotic resistance
- monotherapy with a topical antibiotic
- monotherapy with an oral antibiotic
- a combination of a topical antibiotic and an oral antibiotic
acne
when to refer to derm?
- patients with nodulo-cystic acne
- conglobate acne:
Acne conglobate
*Extensive inflammatory papules, suppurative nodules (that may coalesce to form sinuses)
* cysts on the trunk
* most common in men
acne
when to consider referral to derm
- mild to moderate acne has not responded to two completed courses of treatment
- moderate to severe acne has not responded to previous treatment that includes an oral antibiotic
- acne with scarring
- acne with persistent pigmentary changes
- acne is causing or contributing to persistent psychological distress or a mental health disorder
main types of skin cancer
How many types of skin cancer are there?
three
Main types of skin cancer
- Basal cell carcinoma (BCC)
- squamous cell carcinoma (SCC)
- melanoma
What is this?
BCC
Features of BCC
- sun-exposed sites, especially the head and neck account for the majority of lesions
- initially a pearly, flesh-coloured papule with telangiectasia
- may later ulcerate leaving a central ‘crater
- Metastases are extremely rare
What is BCC
- Basal Cell Carcinoma (BCC) is the most common type of skin cancer
- originating from the basal cells of the epidermis.
Risk factors for BCC
- Sun exposure
- Fair skin
- history of sunburns
- genetic predisposition
Description of BCC
BCC often presents as a pearly or waxy bump, a flat, flesh-colored
brown scar-like lesion, or a pinkish patch of skin. It may bleed easily or develop a crust.
Managment of BCC
- Surgical excision is the primary treatment
- Mohs micrographic surgery
- Cryotherapy,
- imiquimod or 5-fluorouracil.
Mohs micrographic surgery
visible tumor and a thin layer of tissue around it is removed.
Prognosis of BCC
- Excellent prognosis with early detection and appropriate treatment.
- Recurrence is possible, emphasizing the importance of regular follow-ups.
Squamous Cell Carcinoma (SCC)
Common skin cancer originating from squamous cells of epidermis.
Risk factors for skin cancer
- Sun exposure
- fair skin
- history of sunburns
- immunosuppression.
Appearance of SCC
- Reddish, scaly patch, wart-like growth, ulceration.
- Typically found in sun exposed areas#
- growth is faster than BCC
Managment of SCC
Surgical excision, Mohs surgery, radiation therapy, topical medications.
Melanoma
Aggressive skin cancer from melanocytes.
Risk factors for melanoma?
- Sun exposure
- family history
- fair skin
- multiple moles
- blistering sunburns.
Appearance of melanoma
- Irregularly shaped mole, asymmetrical, border irregularity, color variation, diameter >6mm.
- can occur in non-sun exposed skin
- Extremly rapid growth
Managment of melanoma
Surgical excision, lymph node biopsy, immunotherapy, targeted therapy.
Metastasize of melanoma
common locations which it spreads to
- regional lymph nodes
- skin
- liver
- lungs
- brain
- bone
What is this?
squamous cell carcinoma
What is this?
melanoma
Bowen’s disease
A type of squamous cell carcinoma in situ, also known as squamous cell carcinoma in situ (SCCIS).
Risk factors for Bowen’s disease
- Sun exposure
- fair skin
- immunosuppression
- human papillomavirus (HPV) infection
Apperance of Bowen’s disease
- Red, scaly patch or plaque, well-defined borders, often mistaken for eczema or psoriasis.
- Any sun-exposed area, commonly found on the legs, arms, face, and neck.
- slow growing, doesn’t invade deeper tissues or metastasize
Managment of Bowen’s disease
- Surgical excision
- cryotherapy,
- topical medications 5-fluorouracil, imiquimod
Melanoma vs Bowen’s disease
- B has well defined borders compared to M
- B on skin exposed skin, M anywhere
- B slow growth, M quick
- B no invasion into dermis
cellulitis
Bacterial infection of the skin and underlying tissues.
Risk factors for cellulitis (4)
- Skin wounds or breaks
- compromised immune system
- obesity
- diabetes.
Symptoms of Cellulitis (6)
- Red (well-defined margins)
- swollen
- warm
- tender skin
- fever+ chills
- fatigue
What is the classification used for cellulitis
Eron classification
class and features of cellulitis
cellulitis and when to use IV antibiotics
Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromized.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.
Class I cellulitis managment
- oral antibiotics
- oral flucloxacillin as first-line treatment for mild/moderate cellulitis
- oral clarithromycin, erythromycin (in pregnancy) or doxycycline is recommended in patients allergic to penicillin
Cellulitis III and IV managment
- admit
- NICE recommend: oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone
Cellulitis class II managment
- NICE recommend: ‘
- Admission may not be necessary if the facilities and expertise are available in the community
- give intravenous antibiotics and monitor the person
- check local guidelines
Complications of cellulitis
Abscess formation, lymphangitis, sepsis
Eczema herpeticum
severe primary infection of the skin by herpes simplex virus 1 or 2.
Epidemiology and presentation of eczema herpeticium
- commonly seen in children with atopic eczema and often presents as a rapidly progressing painful rash.
- monomorphic punched-out erosions (circular, depressed, ulcerated lesions) usually 1-3 mm in diameter are typically seen.
pityriasis versicolor treatment
Ketoconazole shampoo
Pityriasis versicolor predisposing factors
occurs in healthy individuals
immunosuppression
malnutrition
Cushing’s
Managment of Pityriasis versicolor,
topical antifungal. NICE Clinical Knowledge Summaries advise ketoconazole shampoo as this is more cost effective for large areas
if failure to respond to topical treatment then consider alternative diagnoses (e.g. send scrapings to confirm the diagnosis) + oral itraconazole
Pityriasis versicolor features
most commonly affects trunk
patches may be hypopigmented, pink or brown (hence versicolor). May be more noticeable following a suntan
scale is common
mild pruritus
Anti-tissue transglutaminase antibody.
Dermatitis herpetiformis
associated with coeliac disease, and it often presents as a pruritic, blistering rash on extensor surfaces such as the elbows, knees, and buttocks.
Anti-mitochondrial antibody
associated with primary biliary cholangitis (PBC), a chronic liver disease characterised by destruction of intrahepatic bile ducts.
Anti-nuclear antibody (ANA)
systemic lupus erythematosus (SLE) or Sjogren’s syndrome. Although these conditions can present with skin manifestations like rashes, they do not typically present with the characteristic vesicular rash seen in dermatitis herpetiformis.
, Anti-Jo-1 antibody
polymyositis and dermatomyositis
Anti-tissue transglutaminase antibody
haracteristic presentation of dermatitis herpetiformis
What is the scientific name for head lice?
Pediculus capitis
Head lice are also referred to as ‘nits’.
What do head lice feed on?
Human blood
What is the size and appearance of head lice eggs?
Grey or brown, about the size of a pinhead
How long does it take for head lice eggs to hatch?
7 to 10 days
What are nits?
Empty egg shells of head lice, white and shiny
How are head lice primarily spread?
Direct head-to-head contact
What are the symptoms of head lice after initial infection?
Itching and scratching on the scalp
What is the incubation period for head lice?
None
What is the primary method to diagnose head lice?
Fine-toothed combing of wet or dry hair
When is treatment for head lice indicated?
Only if living lice are found
What are some treatment options for head lice?
- Malathion
- Wet combing
- Dimeticone
- Isopropyl myristate
- Cyclomethicone
Are household contacts of patients with head lice required to be treated?
No, unless they are also affected
Is school exclusion advised for children with head lice?
No
What is urticaria?
Local or generalized superficial swelling of the skin
What is the most common cause of urticaria?
Allergy
What are the features of urticaria?
- Pale, pink raised skin
- Known as ‘hives’, ‘wheals’, ‘nettle rash’
- Pruritic
What are the first-line treatments for urticaria?
- Non-sedating antihistamines
- Example: loratadine or cetirizine
How long should non-sedating antihistamines be continued after an episode of acute urticaria?
Up to 6 weeks
What is tinea?
Dermatophyte fungal infections
What are the three main types of tinea infections?
- Tinea capitis (scalp)
- Tinea corporis (trunk, legs, arms)
- Tinea pedis (feet)
What is tinea capitis and its primary cause?
Scalp ringworm, most commonly caused by Trichophyton tonsurans
What may form if tinea capitis is untreated?
A kerion, a raised, pustular, spongy/boggy mass
How can tinea capitis be diagnosed?
Scalp scrapings; lesions due to Microsporum canis may fluoresce under Wood’s lamp
What are the management options for tinea capitis?
- Oral antifungals: terbinafine for Trichophyton tonsurans and griseofulvin for Microsporum
- Topical ketoconazole shampoo for the first two weeks
What are the features of tinea corporis?
Well-defined annular, erythematous lesions with pustules and papules
What is the treatment for tinea corporis?
Oral fluconazole
What characterizes tinea pedis?
Itchy, peeling skin between the toes
What causes scabies?
The mite Sarcoptes scabiei
How is scabies spread?
Prolonged skin contact
What is the primary symptom of scabies?
Widespread pruritus
What are the management options for scabies?
- Permethrin 5% (first-line)
- Malathion 0.5% (second-line)
What should be done to prevent the spread of scabies during treatment?
Avoid close physical contact with others until treatment is complete
What is crusted (Norwegian) scabies?
Severe scabies seen in patients with suppressed immunity, especially HIV
What is the treatment of choice for crusted scabies?
Ivermectin
What is a key feature of crusted scabies?
Skin teeming with hundreds of thousands of organisms
What is the recommended application time for permethrin in scabies treatment?
8-12 hours before washing off
What is the recommended application time for malathion in scabies treatment?
24 hours before washing off
What does eczema herpeticum describe?
A severe primary infection of the skin by herpes simplex virus 1 or 2
Most commonly seen in children with atopic eczema.
What are the typical features of eczema herpeticum?
Rapidly progressing painful rash, monomorphic punched-out erosions (1-3 mm in diameter)
Erosions are circular, depressed, and ulcerated lesions.
What percentage of children are affected by eczema?
15-20%
Typically presents before 2 years but clears in around 50% by 5 years and 75% by 10 years.
What are common features of eczema?
- Itchy, erythematous rash
- Repeated scratching may exacerbate affected areas
- In infants, the face and trunk are often affected
- In younger children, occurs on extensor surfaces
- In older children, affects flexor surfaces and creases of the face and neck
What is the recommended management for eczema?
- Avoid irritants
- Use simple emollients
- Apply topical steroids
- Consider wet wrapping
- Oral ciclosporin in severe cases
What is the fingertip unit (FTU) in relation to topical steroids?
1 FTU = 0.5 g, sufficient to treat a skin area about twice that of the flat of an adult hand
What types of contact dermatitis exist?
- Irritant contact dermatitis
- Allergic contact dermatitis
What is chronic plaque psoriasis?
The most common form of psoriasis, accounting for around 80% of presentations
Features include erythematous plaques covered with silvery-white scale.
What are the features of guttate psoriasis?
- Tear drop papules on the trunk and limbs
- Often precipitated by a streptococcal infection
- Typically presents with pink, scaly patches
What are the recommended first-line treatments for chronic plaque psoriasis?
- Potent corticosteroid applied once daily
- Vitamin D analogue applied once daily
What is Auspitz’s sign?
Red membrane with pinpoint bleeding points seen when the scale is removed from psoriasis plaques
What factors may exacerbate psoriasis?
- Trauma
- Alcohol
- Certain drugs (e.g., beta blockers, lithium)
- Withdrawal of systemic steroids
What is the prevalence of psoriasis?
Around 2%
Patients with psoriasis are at increased risk of arthritis and cardiovascular disease.
What is the primary treatment for scalp psoriasis?
Potent topical corticosteroids used once daily for 4 weeks
If no improvement, consider different formulations or agents to remove adherent scale.
What are the adverse effects of topical corticosteroids?
- Skin atrophy
- Striae
- Rebound symptoms
- Systemic side-effects when used on large areas
What are the main agents used for non-biological systemic therapy in psoriasis?
- Methotrexate
- Ciclosporin
What are the criteria for initiating non-biological systemic therapy?
- Cannot be controlled with topical therapy
- Significant impact on physical, psychological or social wellbeing
- Extensive psoriasis or significant functional impairment
What types of biological agents are used in psoriasis treatment?
- Adalimumab
- Etanercept
- Infliximab
- Ustekinumab
What are vitamin D analogues used for in psoriasis management?
They work by reducing cell division and differentiation, thus decreasing epidermal proliferation
What is the recommended management for flexural psoriasis?
Mild or moderate potency corticosteroid applied once or twice daily for a maximum of 2 weeks
True or False: Psoriasis can lead to increased risk of cardiovascular disease.
True
Fill in the blank: The alkaline nature of _______ may cause irritant contact dermatitis.
cement
What is the typical appearance of allergic contact dermatitis?
Acute weeping eczema, predominantly affecting the margins of the hairline
Often triggered by hair dyes.
most common malignancy associated with acanthosis nigricans
gastrointestinal adenocarcinoma
What skin condition is commonly associated with rheumatoid arthritis
Pyoderma gangerousum
