Derm 2 (weblearn) Flashcards
(105 cards)
1
Q
What eponymous name is given to the rash over the knuckles?
A
Gottron’s papules (dermatomyositis)
2
Q
How would you confirm a diagnosis of dermatomyositis?
A
Raised serum muscle enzymes: ALT, AST, CK, LDH
EMG shows fibrillation potentials
Muscle biopsy
Autoantibody associations: anti-Mi2, anti-Jo1
3
Q
Which cancers are associated with dermatomyositis?
A
lung, ovary, breast, stomach or cervix.
4
Q
How do you treat dermatomyositis?
A
Immunosuppression.
Start prednisolone. Consider azathioprine, methotrexate etc in resistant cases.
5
Q
What treatments are available for psoriasis?
A
topical treatments including dithranol, steroids and vitamin D anologues
Enstilar foam (vit D analogue calcipotriene and betamethasone dipropionate) Dovobet gel (Calcipotriol, a derivative of vitamin D, works by reducing the production of skin cells. Betamethasone, a corticosteroid, helps reduce inflammation.) Exorex Lotion 1% contains 1% prepared coal tar in the bast of esterified fatty acids. OK to get on normal skin
PUVA (oral psoralens followed by UVA treatment two or three times a week)
UVB 311-312 nm 3 x weekly for 8 weeks
Methotrexate
Ciclosporin
Oral retinoids
6
Q
A 3-year-old boy, who has suffered with eczema in the past, presents with a fever and an area of rapidly worsening, painful eczema on his face. There are extensive crusted papules, blisters and erosions. What’s the diagnosis?
A
Eczema herpeticum
7
Q
Which pathogen is the likely cause for eczema herpeticum?
A
Herpes simplex virus
8
Q
What are the complications of eczema herpeticum?
A
Herpes hepatitis
Herpes encephalitis
Disseminated intravascular coagulation (DIC)
9
Q
What features would make you worry about malignant melanoma?
A
Asymmetry
Borders - irregular
Colour - more than 1
Diameter - > 6mm
Evolution - lesion has changed over time
10
Q
What is the most important prognostic indicator for malignant melanoma?
A
Breslow thickness - the depth of local invasion (Breslow’s thickness = from granular cell layer to deepest part of invasion.)
Less than 1 mm : 5 year survival 95–100%
1–2 mm : 5 year survival 80–96%
2.1–4 mm : 5 year survival 60–75%
Greater than 4 mm : 5 year survival 50%
In Oxford any melanoma greater that 2mm would be referred for sentinel node lymph node biopsy. If this is positive then patients can be entered onto clinical trial.
11
Q
What is a DLQI?
A
dermatology life quality index
12
Q
What facts are key in determining a dermatological history?
A
Duration
How does it affect you? (Quality of life assessment)
How bad is it today?
What has been tried and for how long?
How are topical preparations being applied?
Occupation: history of long term sun exposure (e.g. lived abroad, gardening), exposure to chemicals at work
PMHx/medication
FHx of Atopy or Skin tumours if appropriate
13
Q
What information must be specified when prescribing topical corticosteroids?
A
Base e.g. gel, cream, ointment
Size of tube e.g. 30g
Where to apply it
How often to apply it
How long to continue for
Discuss likely outcome of treatment reduce scale, redness and itch
Advice re side effects of inappropriate long term use
14
Q
What are the differentials of itch?
A
Skin – Dermatitis, allergic or atopic, infection(fungal), scabies, other eg lichen planus
Renal – chronic renal failure
Liver – cirrhosis, any cause of cholestasis and increased bilirubin
Haematological – Fe deficiency anaemia, polycythaemia
Thyroid – hypo and hyperthyroid
Malignancy – lymphoma, leukaemia
Psychiatric – anxiety, depression, obsessive compulsive
Drug- eg ACE inhibitors
15
Q
List the most important types of psoriasis. Briefly describe the morphology and/or distribution of each
A
- Chronic plaque psoriasis (most common) – well demarcated erythematous plaques with thick silvery scale. Common on extensor surfaces, and scalp
- Guttate: raindrop lesions- often reactive eg to streptococcal sore throat. Increased life time risk of chronic plaque
- Flexural/ inverse psoriasis
- Pustular: palmar plantar distribution. Generalised pustular Can be following inappropriate topical steroid use on plaque psoriasis
- Erythrodermic (complication of psoriasis): whole body redness
16
Q
What key features distinguishes psoriasis from other dermatological conditions?
A
- Symmetric
- Affects extensor surfaces
- Non-pruritic, unlike eczema
- Auspitz sign: gentle scratching of scale causes capillary bleeding
- Koebener phenomenon seen on trauma
- 50% have nail pitting
- May have associated arthropathies due to HLA association of psoriasis
17
Q
What is known of the pathophysiology underlying psoriasis?
A
- Chronic inflammatory skin disease due to keratinocyte hyperproliferation and inflammatory cell infiltration.
- Cause unknown. Complex interaction of genetic, immunological and environmental factors.
- Triggers: trauma (friction, inflammation), infection esp streptococcal, drugs (lithium, antimalarials, ACEi, beta blockers), stress and alcohol and UV light in 6%.
18
Q
How is psoriasis managed?
A
- General avoidance of triggers
- Regular emollients, soap substitutes
- Topical: vitamin D analogues (calcipitriol), corticosteroids, retinoids (tazarotene), keratinolytics (coal tar) and scalp preparations
- Phototherapy for extensive disease e.g. UVB, and photochemotherapy (PUVA – psoralen and UVA)
- Oral therapies for extensive and severe psoriasis: methotrexate, oral retinoids, cyclosporin, mycophenolate mofetil, fumaric acid esters, biological agents if PASI >= 10 (infliximab (anti-TNF), etanercept, efalizumab, ustekinumab (anti-IL12/23))
PASI = Psoriasis area and severityindex
19
Q
What are the main risk factors associated with the development of squamous cell carcinomas?
A
SHIT
Sunlight Scars, burns,venous ulcers Human papilloma virus Immunosuppression Ionising radiation Industrial carcinogens – pitch, tar, creosote, crude paraffin oil, fuel oil Toxins- Arsenic
20
Q
What is the management for SCC?
A
- Surgical excision is the treatment of choice
- Moh’s micrographic surgery is indicated in high risk, recurrent tumours and involves excision of the lesion and tissue borders until specimens are microscopically free of tumour
- Radiotherapy may be indicated for large, non-resectable tumours
- Chemotherapy may be appropriate for metastatic disease
21
Q
What are the characteristic features of a BCC?
A
- A nodule or ulcer on an exposed site with a rolled pearly edge and telangiectasia.
- It can expand to cause necrosis and ulceration causing local destruction of tissues but does not metastasise.
22
Q
Which 4 clinical types of BCC exist?
A
Nodulo-cystic
Superficial
Pigmented
Morphoeic
23
Q
What treatments are available for BCC?
A
MOHS surgery
Radiotherapy
Cryotherapy and curettage and cautery can be used for small and low risk lesions.
24
Q
What are the risk factors that are particularly associated with the development of melanoma?
A
- Atypical moles
- Having numerous moles and naevi (>100)
- Skin phototypes I and II (red hair and freckling)
- Sunburn – especially severe burning during childhood
- Family history of MM
- Previous cutaneous MM
- Immunosuppression
25
What are the'red flag' characteristics of moles that suggest malignancy?
```
Asymmetry
Border irregularity
Colour heterogeneity
Diameter >7mm
Evolution over time, incl symptoms such as bleeding, itching
```
26
What types of benign melanocytic naevi are there?
- Benign moles that can either be intradermal, compound or junctional
- Congenital naevi
- Halo naevi (have an area of surrounding depigmentation)
- Spitz naevi (found on Children’s faces)
- Blue naevi (e.g. Mongolian blue spots)
- Clinically atypical or dysplastic naevi – these are concerning as there is an increased risk of melanoma
27
What is a keratoacanthoma?
It is a common, benign, non-melanocytic tumour. It is a well-differentiated SCC. The normal progression is intially a period of rapid growth, followed by persistance for 2-3 mo, then involution over 4-6 mo. They may be removed surgically.
28
What is Bowen's disease and how does it present?
Bowen's disease is full thickness dysplasia and is an SCC in situ. It presents as a solitary scaly plaque, usually on a light exposed site and is asymmetrical. It rarely develops into SCC.
29
What is the differential diagnosis for Bowen's disease?
Superficial BCC
Fungal infection
Psoriasis
30
How is Bowen's disease treated?
- surgery
| - topical 5-fluorouracil or imiquimod
31
What are the risks associated with solar keratoses and subsequently, what is the management strategy?
They are premalignant tumours which arise from dysplasia in the epidermal basal cell layer. They are an indicator that a patient is at risk of skin cancer. About 20% regress spontaneously, and progression to SCC is rare.
Treatment is only required if they are troublesome, otherwise advice should be for patients to be vigilant for the development of cancers, and to take necessary precautions e.g. sun protection.
32
What are seborrhoeic keratoses?
They are a benign proliferation of epidermal keratinocytes of unknown aetiology
33
What are the clinical features of seborrhoeic keratoses?
- These are benign, warty lesions that can be solitary or multiple.
- They are pigmented and flat-topped with surface pits and irregularities.
- They have a "stuck-on" appearance.
34
What are the side effects of methotrexate that must be discussed with patients and what must be monitored in patients taking this drug?
Taken once weekly for psoriasis. Avoid alcohol
- Anorexia, nausea
- Low WBC: regularly check FBC. Need to monitor for infection
- Hepatitis, liver fibrosis, rarely cirrhosis (urea and electrolytes and LFTs done pre treatment, then weekly until therapy stabilised, then monthly)
- Interstitial pneumonitis/pulmondary fibrosis (seen in rheumatoid arthritic not psoriasis) – SOB, cough, fever
- Teratogenic – males and females should avoid conception for at least 3 months after stopping
35
When is isotretinoin used? What are the side effects of isotretinoin and what monitoring is required?
Isotretinoin is a drug used to treat severe acne vulgaris. Give for at least 16 weeks
Minor side effects: dry skin and mucous membranes, nose bleeds, cheilitis, temporary elevation of serum lipids (reverts to normal at end of course), headache, arthragia, hairloss
Reports of depression and suicide but causal link never proved.
Major side effects: teratogenic (written consent form, continue contraceptive treatment for 1 month after stopping), liver dysfunction (raised liver enzymes)
Monitoring: pregnancy test before starting therapy and also start patient on oral contraceptives. Pre-treatment test liver function and fasting lipids. Recheck liver function tests and fasting lipids during treatment.
36
What is the main use for ciclosporin in dermatology?
Ciclosporin is effective for treating severe psoriasis
37
What requires monitoring in patients on ciclosporin and why?
The main problem is renal toxicity and so blood pressure and renal function should be measured. Ciclosporin interacts with a number of drugs (e.g. trimethoprim, NSAIDs).
38
When are antihistamines used in dermatology?
- Management of Urticaria. Chlorpheniramine can also be used alongside adrenaline and hydrocortisone in the management of anaphylaxis and angioedema.
- Sedating antihistamines e.g. chlorpheniramine may also be used to therefore stop night time scratching. e.g. atopic dermatitis. Care must be taken in the elderly due to falls risk.
39
What are the different types of topical steroid available?
Mildly potent – hydrocortisone acetate
Moderately potent (2-25 times stronger than hydrocortisone)
– clobetasone butyrate (eumovate)
– triamicinolone acetonide
Potent (100-150 times stronger than hydrocortisone)
– betamethasone valerate (betnovate)
– hydrocortisone 17-butyrate
– methylprednisolone aceponate
Very potent (600 times stronger than hydrocortisone)
– clobetasone propionate (dermovate)
– betamethasone dipropionate
40
What are the side effects of topical steroids that patients must be warned about?
Skin atrophy, telangiectasia, striae
They may mask, cause or exacerbate skin infections, acne or perioral dermatitis and allergic contact dermatitis
41
What are the different types of eczema/dermatitis?
Primarily exogenous
- Irritant contact (e.g. occupational)
- Allergic contact (type IV hypersensitivity)
Primarily endogenous
- Atopic (often in childhood, resolves in teenage years)
- Seborrheoic
- Discoid
- Pompholyx
- Asteototic
- Stasis (venous)
42
What are key questions in a history of atopic eczema?
Duration?
Triggers/exacerbants (infections, allergens, heat, stress)?
Sites affected?
How does it affect your life?
What has been tried already? Has it worked?
Personal or Fhx of atopy e.g. hayfever, asthma, allergic rhinitis?
43
What would be found on examination of atopic eczema?
- Intensely pruiritic dry rash: 'papules and vesicles on an erythematous base'
- In a baby: face and extensor surfaces
- In a child and adult: flexures affected, especially the neck, wrists, behind the knees
- Erythema not clearly demarcated
44
What are the possible complications of eczema?
- Lichenification when chronic
- Secondary viral infection e.g. moluscum contagiosum, warts, eczema herpeticum
- Secondary bacterial infection
- Erythroderma
45
List the ways in which eczema can be managed
- Avoid exacerbants, Irritants e.g. soaps , allergens (if possible) eg Pets, house dust mite
- Emollients: cream base if weeping, ointment base if dry
- Topical steroids for flare-ups (potency varies from weakest to strongest: hydrocortisone, eumovate, betnovate, dermovate)
- Treat infective exarcebations- eg antibiotics, antivirals for eczema herpeticum
- Topical immunmodulators e.g. tacrolimus as steroid-sparing agents
- 'Weekend therapy': 2 day weekly anti inflammatory to prevent flares
- Oral therapies: antihistamines to relieve itch
46
What is alopecia areata and how does it present?
A condition in which there is either generalised or localised hair loss commonly presenting with well demarcated bald areas. Exclamation mark hairs (thinner at proximal end) are diagnostic. The nails are often affected and have pits and ridges. The condition is non-scarring and spontaneous regrowth usually occurs within 2-6 months.
47
What are the risk factors for alopecia areata?
Some people have a genetic predisposition. Alopecia areata can be seen more commonly in atopic individuals and in those with autoimmune disorders such as diabetes and vitiligo.
48
What are the main differentials of a red swollen leg? Explain how they can be investigated. In the order of (importance? severity? Occurrence)
History is always key: risk factors, nature of symptoms, duration and systemic wellness
- Cellulitis (diffuse edge)/erysipelas (well-defined edge) – systemically unwell, site of injury, painful and spreading redness, do anti-streptococcal O titre and skin swab
- VTE – assess for risk factors e.g. long haul flights or bed rest, family or personal history; calculate pre-test probability and conduct D-dimer test if necessary, may go on to do ultrasound
- Chronic venous insufficiency – postural effect on symptoms – worse on standing, relieved on walking; doppler ultrasound and/or venography, ABPI
- Venous stasis eczema- unknown pathology inflammatory eczema secondary to venous stasis. Treat with topical emollients/ steroids +/- support
- Contact dermatitis – patch test may be needed
- Trauma – history; examine, may need further x-ray
49
What do urticaria, angioedema, and anaphylaxis have in common?
They are on a spectrum with urticaria being the mildest, then angioedema, and anaphylaxis being the most life threatening. They are thought to be due to either immune mediated (allergic) or non immune stimulation. The former being either IgE mediated, complement mediated or via immune-complex formation e.g. penicillamine. Non-immune causes include ACEi and drugs that inhibit or block COX in prostaglandin synthesis.
Causes: idiopathic, food (nuts, sesame seeds, dairy), drugs (penicillin, contrast media, NSAIDs, morphine, ACEi), insect bites, contact (latex), viral or parasitic infection, autoimmune and hereditary (in some cases of angioedema, a deficiency of C1q inhibitor is to blame).
50
What is urticaria, what causes it and how is it usually treated?
- 'Wheals' – Pruritic oedematous swellings of the superficial dermis, causing raising of the epidermis.
- Lasts <24 hours.
- Caused by local increase in permeability of capillaries and small venules, mediated mainly by histamine from skin mast cells. Release may be induced by non- or immunological factors.
- Treated with antihistamines. If severe may need immunosuppressant tx eg ciclosporin.
51
Describe the difference between anaphylaxis and angioedema
Angioedema: deeper swelling than urticaria; painful, involving dermis and subcutaneous tissues. Manifests clinically as swelling of tongue and lips. Assess patients airway: are they able to speak, any voice changes, is it difficult to swallow, difficulty in breathing, wheeze, stridor. Check O2 saturations.
Anaphylaxis (anaphylactic shock): bronchospasm, facial and laryngeal oedema, hypotension. May initially present with urticaria and angioedema.
52
How are anaphylaxis and angioedema treated?
Unlike urticaria, either of these can lead to asphyxia, cardiac arrest and death.
Angioedema: corticosteroids (may need to treat as anaphylaxis if severe)
Anaphylaxis: IM adrenaline, corticosteroids and antihistamines, supportive care
Investigate potential triggers through careful history and allergy testing (IgE and prick testing)
Provide education and Epi Pen plus antihistamines for future attacks
53
What is erythroderma?
Erythroderma is also known as exfoliative dermatitis, and is defined as affecting >90% of the body's surface areas.
54
Why is erythroderma a medical emergency?
- life-threatening
- mortality ranges from 20-40%
- prognosis depends on the underlying cause, which could be any one of: previous skin disease e.g. dermatitis of any variety, psoriasis, drugs e.g. sulphonamides, penicillin, alluopurinol, captopril, Cutaneous T-cell lymphoma or leukaemia, or Idiopathic.
Risks (similar to a burns patient) come from:
- Fluid loss
- Electrolyte imbalance
- Hypothermia
- High-output cardiac failure
- Capillary leak syndrome (most severe)
- Secondary infection
55
How do you manage erythroderma?
- Investigate and treat the underlying cause, stop all unnecessary drugs
- May need iv fluids and resuscitation (may include high calorific foods and protein supplements), monitor core body temperature
- Take swabs and monitor for any secondary infections
- Consider the need for analgesics, sedating antihistamines and VTE prophylaxis (especially as decrease mobility and dehydrated)
- Emollients and wet wraps to maintain skin moisture
- Take care to avoid pressure sores
- Topical steroids may help relieve inflammation
56
What is eczema herpeticum? What causes it? What are the symptoms? How do you manage it?
- Life threatening.
- Often seen in children.
- It is a complication of atopic eczema, though can occur in other conditions (such as burns and pemphigus, Darier’s disease, ichthyosis).
- It presents as a widespread eruption of extensive crusted papules, blisters and erosions caused by herpes simplex 1 infection.
- There is pain and intense itching. Systemic illness is present, with fever and malaise.
- Management is with antivirals (aciclovir), may need to be IV in severe cases.
- Antipyretics, parenteral fluids and pain relief may all be needed.
Complications include secondary bacterial infection (so antibiotics may be needed), herpes encephalitis, DIC and rarely, death.
57
List some causes of purpura and describe their distinguishing features (in order of increasing severity)
Senile purpura = Elderly patient, otherwise well, non palpable purpura seen in the context of thin papery skin, ask if pt is taking any anticoagulant or antiplatelet.
Small vessel cutaneous vasculitis (may be secondary to infection, drugs or systemic vasculitis) = palpable purpura
Meningococcal septicaemia = acute onset, progressive, triad of symptoms.
DIC = seriously systemically unwell, extensive, irregularly outlined ecchymoses, bullae and gangrene.
58
What is the most important differential of a purpuric rash, which must be ruled out? What is the normal cause? What are the symptoms?
Acute meningococcaemia. Septicaemia caused by a gram negative diplococcus, Neisseria meningitis. Most commonly affecting children 6mo-3years.
Presents acutely, as a triad
1. Meningism – headache, fever, neck stiffness
2. Septicaemia – systemically unwell, hypotension, fever, myalgia
3. Typical non-blanching purpuric rash which may begin in a maculopapular rash but progresses to ecchymoses, haemorrhagic bullae and tissue necrosis.
59
What are the characteristic lesions in erythema multiforme and what are the common precipitation factors?
Initially present as erythematous plaques which expand to give annular "targetoid" lesions with central clearing. They may develop into frank blisters.
Precipitants:
- Herpes simplex virus infection
- Mycoplasma pneumonia
- Streptococcal sore throat
- Drugs: penicillins, sulphonamides, phenytoin
60
What is Stevens Johnson syndrome?
A type pf erythema muliforme with severe involvement of the eys and mucosal surfaces. There are target lesions, mouth and genital ulcers, fever and systemic illness.
61
What are the causes of Stevens Johnson syndrome?
- Viral (herpes simplex)
- Bacterial (mycoplasma, TB)
- Drugs (sulphonamides, barbiturates)
62
What is the mortality rate in Stevens Johnson syndrome?
5-12%
63
What is TEN?
Toxic Epidermal Necrolysis (TEN)
A serious and life-threatening variant of erythema multiforme in which there is mucosal necrosis with systemic toxicity. Histopathological analysis of the skin shows full thickness epidermal necrosis with subepidermal detachment. The typical cause is a drug reaction.
64
What is the management for TEN?
- The patient should be managed in adult intensive care.
- Stop any drugs that may have caused the reaction.
- Treat symptomatically with bed rest and topical dressings.
- Consider steroids in severe cases.
65
What is the mortality rate in TEN?
30%
66
Varicella Zoster virus can have two different manifestations in the skin, dependant on whether it is a primary infection, or a reactivation of latent virus. Explain how each presents and how they should be managed, with reference to complications.
a) Primary infection = varicella (chicken pox)
- Transfer by respiratory droplets or direct contact, contagious until crusting over of vesicles (5 days after last vesicle appears).
- Prodrome of malaise, fever, headache and myalgia then crops of pruritic lesions progressing from erythematous macules and papules to grouped central vesicles then crusting over.
- Self-limiting if primary infection in childhood so only supportive care needed; if first infection in adulthood then systemic aciclovir may be indicated to decrease symptoms as it if often more severe and may have systemic complications such as pneumonia and encephalitis.
b) Reactivation of latent infection = herpes zoster (shingles). The virus remains dormant in sensory nerve ganglia therefore dermatomal distribution of the rash.
- Initially get intense local pain then clusters of erythematous papules evolving into vesicles then papules. NB in facial zoster look for lesions on the nose as it indicates involvement of the ophthalmic division of the trigeminal nerve and the eye may be affected.
- Risks of secondary infection. May get a more severe disease in those immunocompromised, for example ulceration may occur. Older patients with severe disease may be left with post herpetic neuralgia.
67
How do bacterial infections of the skin present?
Painful spreading rash
Presents with signs of inflammation:
- Swelling (tumour)
- Erythema (rubor)
- Warmth (callor)
- Pain (dolor)
May have associated lymphangitis
Systemically unwell, with fever, malaise or rigors (more common in erysipelas)
Most common in the lower limbs, asymmetrical infection. Often with minor skin injury, especially with lymphoedema, ulcers and venous stasis:
- Cellulitis: involves deep subcutaneous tissues
- Erysipelas: acute superficial form of cellulitis, involves the dermis and upper subcutaneous tissues. Differentiated from cellulitis due to well-defined red border.
Also seen on the face but mainly in children:
- Impetigo: superficial skin infection that may occur on normal skin, or complicate eczema. Characteristically golden, honey-coloured crusting and oozing. Causative organism: Staph aureus or Strep pyogenes in crusted impetigo. May have bullous lesions due to disruption of the superficial layers of the epidermis just below the stratum corneum. Managed with antibiotics: flucloxacillin or benzylpenicillin. NB may differ in immunocompromised pts.
68
What are viral warts caused by?
HPV1 and HPV2
69
In what three ways do viral warts commonly present?
1. Common wart (verruca vulgaris) - found on the hands of children and the immunosuppressed. They demonstrate Koebnerisation.
2. Plane warts - found on the face and the back of the hands.
3. Plantar warts (verruca plantaris) - pressure and friction causes the warts on the sole of the foot to grow inwards towards the dermis. They can be painful. They are found in children, sportsmen and athletes.
70
What are the main methods for treating warts?
- No treatment - some will involute spontaneously
- Salicylic acid or gluteraldehyde paint
- Cryotherapy for persistent warts
- No other therapy has evidence for efficacy
71
Which fungus typically causes skin, hair and nail infections and under what kind of conditions is it likely to grow?
Trycophyton rubrum
This fungus likes hot, humid environments. It grows where there is sweating or maceration of the skin. It can be found between the toes as occlusive footwear creates the right environment. Use of hair greases and oils can encourage its growth. It is more commonly seen in immunosuppressed patients.
The infections caused by the fungus:
```
tinea capitis (scalp)
tinea corporis (body)
tinea cruris (groin)
tinea pedis (feet)
tinea unguium (nails)
```
72
How would you investigate and treat a tinea infection?
- Take sample for microscopy and culture (skin scraping for tinea corporis, cruris and pedis, hair sample and toothbrush scraping for tinea capitus, nail sample for tinea unguium).
- Look for fungal hyphae and spores on microscopy in potassium hydroxide.
- Topical antifungals such as terbinafine and miconazole are first line for cutaneous tinea.
- Oral therapy may be required for severe or persistant infection.
- For tinea capitus oral therapy (terbinafine or griseofulvin or itraconazole) is required.
- Treatment of Tinea Unguium is only necessary with appropriate risk benefit analysis of oral treatment.
73
What is tinea incognito?
When topical steroids are applied to a tinea infection of the skin, its presentation may become atypical. The infection may also worsen when topical steroids are applied. The skin may be less scaly with a less raised margin and there may be pustules.
74
Describe the 4 main changes that occur in the skin that are implicated in the pathogenesis of acne vulgaris.
- Seborrhoea: increased sebum production
- Pilosebaceous duct hypercornification leading to sebum outflow obstruction and comedone formation
- Colonisation of the pilosebacoeus duct with Propionibaterium acnes
- Secondary Inflammation around the sebaceous gland
75
Explain how hormones may play a role in acne vulgaris
- The pilosebaceous glands are sensitive to androgens.
- Women with acne may have increased free testosterone due to decreased sex hormone binding globulin.
- The pilosebaceius gland may have increased androgen sensitivity.
76
Describe the main dermatological features and distribution of lesions in acne vulgaris
Open and closed comedones (blackheads and whiteheads), papules, pustules, nodules and scarring.
Pits and ice-pick scars are characteristic.
Lesions are distributed mainly on the forehead, nose and chin but sometimes the whole face, upper chest and back (where the pilosecceous glands are more numerous). Also look for oily skin and scalp.
77
List 5 variants of acne vulgaris and main aetiological factor involved
- Tropical acne: cause by hot, humid environments
- Steroid acne: caused by systemic steroid therapy
- Chemical acne: caused by cutting oils and chlorinated hydrocarbons
- Chloracne: caused by dioxin and chlorinated hydrocarbons
- Infantile acne: common and resolves. If any other signs of virilisation (development of male features) may need further investigation
78
List 3 different types of topical therapy used for acne
- benzoyl peroxide (apply to whole face, takes 2-3 months to have maximal effect, !! skin irritation, bleaches clothing/towels)
- erythromycin/clindamycin (give with benzoyl peroxide to avoid resistance). erythromycin safe in pregnancy. takes 4-6 months to have maximal effect
- topical retinoids e.g. adapalene. CI pregnancy. !! burning, erythema, stinging, pruritus, dry/peeling skin
Apply once daily unless side effects, then every other day.
Nb combination treatments e.g. retinoid plus antimicrobial or retinoid plus benzoyl peroxide have better efficacy long term.
Epiduo= adapalene 0.1% and benzoyl peroxide 2.5%
79
List 3 systemic treatments available for acne
- antibiotics e.g. tertracycline
- isotretinoin (roaccutane)
- hormonal therapy e.g. cyproterone acetate (Dianette)
80
Describe the clinical features of Acne Rosacea
- Acne Rosacea typically presents in older age group (30-40).
- It has a higher prevalence in women.
- There is often a history of facial flushing.
- Clinically there is facial redness and papules and pustules.
- This may be accompanied by 'rhinophyma' sebaceous hyperplasia of the nose and eye involement
81
How would you manage acne rosacea?
- Soap substitutes minimise irritation of the skin
- Avoid precipitants of flushing (eg hot spicy food)
- Sunprotection as Sunlight may also make things worse
- Topical treatments: metronidazole cream or azelaic acid.
- Cosmetic camouflage may reduce redness.
- An oral antibiotic will control papulopustular disease, but has little impact on redness
- Oral retinoids are sometimes advocated for sebaceous gland overgrowth
- Rhinophyma can be pared down electrosurgically
82
When investigating a patient for systemic causes of generalised itching, what tests should you request and why?
- Check for liver disease e.g. build up of bile salts, primary biliary cirrhosis: liver function tests
- Check for chronic renal failure: urea and creatinine
- Check for polycythaemia rubra vera and iron deficiency anaemia: full blood count
- Check for thyroid disease: TSH
- Pregnancy test (if appropriate)
- Check Medications
83
Name 5 cutaneous causes of itching and describes the characteristic lesions in each condition
- Eczema: erythematous, scaly patches with excoriations and lichenification
- Dermatitis herpetiformis: itchy vesicles over the knees, elbows and buttocks
- Lichen planus: violaceous flat-topped papules over the forearms, wrists and legs
- Urticaria: erythematous wheals that last for less than 24 hours
- Scabies: linear burrows, finger web scale or crusting, excoriations over the body
84
What type of drug is permethrin? What is it used for and how is it administered?
Permethrin is an acaricide which is used to kill the scabies mite. It is painted on the entire body from the neck to the soles of the feet. It is washed off in a hot bath 24 hours later.
85
Name 6 skin signs that you might find in a patient with diabetes mellitus
- Necrobiosis lipoidica
- Disseminated granuloma annulare
- Diabetic rubeosis (diabetic microangiopathy causes redness of the face, hands and feet)
- Candida albicans infection
- Neuropathic foot ulcers
- Vitiligo
86
A 20 year old man presents with an itchy erythematous rash in the groins. He complains of dysuria. He denies urethral discharge and he has a regular sexual partner. He takes no regular medications. A swab is taken which reveals a budding yeast. What is the diagnosis and how should this patient be investigated further. What treatment would you recommend?
The diagnosis is Candida albicans infection.
Candidiasis is rare in young men and could be a sign of immunosuppression. The patient should be examined for signs of lymphadenopathy and a FBC sent to check for signs of haematological malignancy. A fasting glucose measurement should be taken to check for diabetes mellitus and a HIV test should be considered.
The patient could be treated with clotrimazole cream or oral fluconazole.
87
What are the clinical features of dermatomyositis?
Heliotrope rash around the eyes
- Gottron's papules
- Periungal telangiectasia
- Erythematous macules
- Photosensitive rash: typically on the face and dorsum of hands
- Proximal muscle and pharyngeal weakness
- Signs of possible malignancy: weight loss, chronic cough
88
Which malignancies are associated with dermatomyositis?
breast
ovary
lung
GI
89
Describe briefly how you would investigate and manage the patient with dermatomyositis
Investigations: ↑CK, look for ab to striated muscle, muscle MRI shows inflammation, EMG, skin biopsy shows characteristic histology.
Management: high dose systemic steroids and immunosuppressants e.g. azathioprine. Investigate for underlying malignancy.
SLE
90
Describe briefly what systemic lupus erythematosus (SLE) is and what autoantibodies are typically detected
SLE is an inflammatory connective tissue disorder. It affects multiple body systems. It is an autoimmune condition which causes a small vessel vasculitis.
Antinuclear antibodies and anti double stranded DNA antibodies are typically positive.
91
What are the characteristic skin and skin appendage signs seen in SLE and how should they be treated?
- diffuse generalised hair loss
- malar (butterfly) rash over the face
- Photosensitive rash.
Wear protective clothing and use high SPF sunscreen. Treat skin lesions with topical steroids. Systemic treatments include antimalarials.
92
What's the diagnosis?
An 85 year old gentleman who is in hospital with pneumonia. He has noticed blisters appearing over the last few weeks. On examination there are several tense and large blisters on an erythematous and eczematised base over the forearms and one on the right leg.
bullous pemphigoid
93
What's the diagnosis?
A 50 year old man who has multiple erosions over the trunk and some oral ulcers and genital discomfort. You cannot see any intact blisters.
pemphigus vulgaris
94
Describe the differences that can be found histologically and on immunofluorescence in bullous pemphigoid and pemphigus vulgaris.
Bullous pemphigoid:
- the blisters are sub-epidermal and hence more easily remain intact.
- They are usually filled with eosinophils.
- Mucosal involvement is not seen.
- Immunoglobulin and C3 can be seen fixed at the dermo-epidermal junction on immunofluorescence.
Pemphigus vulgaris:
- the blisters are intra-epidermal.
- Individual keratinocytes can be found floating in the blisters.
- Mucosal involvement is common.
- On immunofluorescence immunoglobulin is found between keratinocytes attached to desmoglein.
95
Is bullous pemphigoid or pemphigus vulgaris more serious?
Pemphigus vulgaris is more serious because if untreated the patient can be at risk of disturbance of fluid and electrolyte balance and secondary infection. Raw blisters on mucosal surfaces can turn into ulcers.
96
Autoimmune blistering disorders are rare causes of blisters. List the more common causes of blisters.
- Trauma: burns, pressure
- Bites
- Infection:
Viral e.g. herpes simplex virus
Bacterial e.g. bullous impetigo
- Acute eczema, severe contact dermatitis
97
What features distinguish vascular ulcers from other types of ulcer?
- malleolar area (often the medial) which is affected
- The ulcer is normally large, shallow, irregular edge with an exudative and granulating base.
- The skin is warm with normal peripheral pulses but distinct features which may be seen are:
AVENOUS
- atrophie blanche (white scarring with dilated capillaries)
- varicose veins/ DVT
- eczema (stasis)
- narrow calf (lipodermatosclerosis)
- oedema
- ulceration
- scaring, haemoSiderin deposits
- They are often painful, and made worse by standing.
98
A 70 year old lady presents with a leg ulcer that is failing to heal despite compression bandaging and careful wound management by the district nurses. What differential diagnoses would you consider and how should this be investigated?
A non-healing ulcer may be a malignancy or could be due to an atypical infection such as mycobacteria.
A skin biopsy should be taken to exclude malignancy and swabs for microscopy and culture. Inflamed and irritated skin around the ulcer may be due to contact dermatitis from dressings so patch testing may also be considered.
99
How do neuropathic ulcers usually present?
- in patients with diabetes
- located at pressure points
- surrounded by callous
- foot is warm
- sensory testing there is diminished sensation
- The ulcer can look extremely painful but the patient may be unaware of the lesion.
100
How should neuropathic ulcers be treated?
- Optimise diabetic control including smoking cessation
- Protect ulcer from further injury
- Advise patient on the importance of correctly fitting footwear
- Careful chiropody with good skin and nail care
- Regular foot examination
101
On examination, what features would be seen in pyoderma gangrenosum and what is the underlying aetiology?
- rare type of ulcer
- Clinical features are painful, rapidly growing and preceeded by a tender pustule.
- bluish with an undetermined wound edge
- is neither infectious nor gangrenous, but rather a neutrophilic dermatosis.
- thought to result from an inappropriate immunological reaction, with the stimulus being as yet unidentified.
102
In what kind of patient population might you expect to see pyoderma gangrenosum?
It is associated with:
- rheumatoid arthritis (seropositive and negative)
- inflammatory bowel disease
- myeloproliferative disorders
- but 50% have no underlying cause
103
Which systemic therapies can be used for psoriasis and what are the side effects?
Methotrexate
- 10-25mg weekly (administer alongside Folic acid)
- Immunosuppressant: risk of myelosuppression & hepatitis therefore must
monitor FBC, LFTs (initially weekly)
- Can cause nausea, vomiting, oral ulcers. Teratogenic. Limit EtOH.
Acitretin
- 25mg daily (can reduce dose if poorly tolerated)
- Vitamin A derivative: need to monitor LFTs, lipid profile ~3/12
- Causes mucocutaneous dryness; can cause mood disturbance.
- Teratogenic & no pregnancy for 2 yrs after – only M & post-menopausal F.
Ciclosporin
- 2.5-5mg/kg/day in 2 divided doses; rapid onset action
- Immunosuppressant: can cause renal impairment and hypertension therefore must monitor U+E and BP
- Use only as short-term (<12/12) treatment – agree with patient at outset
104
How do you treat scalp psoriasis?
To descale: Tar based treatments e.g. Cocois, Sebco ointment – apply overnight then comb out the following morning
To treat inflammation: Topical steroids e.g. Dermovate, Diprosalic scalp applications
105
What are the comorbidities of psoriasis?
Psychiatric co-morbidity
- high anxiety scores in 2/3
- depression reported in 60%
Smoking
- high (x2) prevalence of smoking cf. general population
- heavy tobacco use correlates with severe disease
- palmoplantar pustulosis worse/harder to treat if smoke
Alcohol
- excess consumption in patients with severe psoriasis
- may influence suitability of systemic treatments
- arterial hypertension
- coronary heart disease
- hyperlipidaemia
- obesity
- type II diabetes
