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Women's Health - Year 4 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

ECZEMA

  1. what is it?
  2. how does it present?
  3. where does it affect?
  4. what is it associated with?
A
  1. Chronic inflammatory skin condition
  2. Presents as poorly demarcated, itchy red rash
  3. Typically affects skin folds (elbow and behind knees). Infants – scalp, face, flexor
    Adults – chest, neck, flexor
  4. Associated with atopic traits (asthma, hay fevere, allergic rhinitis)
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2
Q

ECZEMA

describe the pathophysiological process of eczema?

A

2 stage process: breakdown/reduced effectiveness of skins natural barrier and subsequent IgE mediated, T cell auto-immune response causing inflammation

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3
Q

ECZEMA

  1. where in the world has higher prevalence of eczema
  2. by what age does eczema usually present?
  3. what can decrease the risk of eczema?
A
  1. developed countries
  2. 5 years
  3. breast feeding
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4
Q

ECZEMA

name some triggers for eczema?

A

soaps, skin infections (staph aureus), extremes of temp, abrasive fabrics, dietary, inhaled allergens, stress, hormonal changes

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5
Q

ECZEMA

name some common complication of eczema and how does it present?

A 
-bacterial infection (Staph)
crusting, weeping, erythema
- eczema hereticum - viral infection characterised by fever and clusters of itchy blisters or punched-out erosions.
-lichenification
- eczema herpeticum
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6
Q

ECZEMA

what is the NICE diagnostic criteria for eczema?

A 
itchy skin plus 3 of
• Itchiness in skin folds
• History of asthma or hay fever
• Dry skin
• Visible patches in skin folds
• Onset in first 2 years
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7
Q

ECZEMA

what investigation may be indicated in eczema not responding?

A

MC+S swab

allergy and RAST test not indicated

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8
Q

ECZEMA

what are the 2 main treatment options?

A

Emollients – improve skins natural barrier

Steroids – reduce inflammation

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9
Q

ECZEMA
describe the use of emollients?
-different types
-when to apply

A
  • creams (water based)
  • lotions (water and oil components)
  • ointments (oil based and most potent
  • The more potent the emollient the more greasy so unpleasant to have on hands
  • Best applied to wet/moist skin
  • Every 4 hours or 3-4x day
  • Use even when no flare ups
  • Avoid soaps
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10
Q

ECZEMA
describe the use of steroids?
- when should they be used?
-when should they be applied?

A
  • Used to bring exacerbation under control,Use at first sign of flare up
  • Apply before emollients
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11
Q 
ECZEMA
describe the use and give examples of...
1. mild steroids
2. moderate steroids
3. very potent steroids
A
  1. Mild – face and neck, mild flare ups eg 1% hydrocortisone or 0.05% clobetasone
  2. Moderate – severe flare ups – axillae and groin eg betamethasone valerate 0.02%, triamcinolone 0.02%
    Potenti – same as moderate – 0.1% betamethasone valerate, mometasone 1%, methylprednisolone acetylate
  3. Very potent – don’t use in children, unless specialist eg clobetasone propionate 0.05%, betamethasone diproprionate 0.05%
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12
Q

ECZEMA

how should staphylococcal infection be treated?

A

flucloxacillin 500mg QID 1-2 weeks

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13
Q

ECZEMA

other than emolients and steroids, what other therapies can be used to treat eczema?

A

Immune modulating agents – pimecrolimus and tacrolimus – severe eczema, alternatives to topical steroids

Phototherapy – UVA/UVB effective in treating disease resistant topical agents

Systemic therapy – rare

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14
Q

PSORIASIS

  1. what is it?
  2. describe the course of the disease
  3. pathophysiology?
  4. what percentage of psoriasis is associated with psoriatic arthritis?
A
  1. Chronic inflammatory skin condition
    Raised, red, itchy, scaly plaques on skin
  2. Follows relapsing remitting course
  3. Strong genetic component
    T cell mediated abnormal immune response – T cells release cytokines resulting in keratinocyte proliferation
  4. 10-15%
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15
Q

PSORIASIS

  1. what age does incidence peak
  2. what ethnicity is it more common in
  3. name some risk factors?
A
  1. 15-25 / 50-60
  2. caucasians
  3. genetic, smoking, obesity, psychological stressors
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16
Q

PSORIASIS

what would skin biopsy show?

A 
parakeratosis
acanthosis
absent granular layer, lengthened rete ridges
thin dermal papillae
dilated tortuous capillaries
munro’s micro-abscences
T cells in upper dermis
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17
Q

PSORIASIS

what are the features of psoriasis?

A
  • Symmetrical
  • Red scaly plaques – white/ silver
  • Often extensor surfaces
  • Scalp, elbows, knees
  • Itchy
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18
Q

PSORIASIS

name different types of psoriasis?

A 
classical
guttate psoriasis
palmoplanar pustular
flexoral
erythrodermic
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19
Q

PSORIASIS

describe classical psoriasis?

A

well circumscribed erythematous plaques with silver scaling, nail changes, auspitzs sign

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20
Q

PSORIASIS

describe guttate psoriasis?

A

young, often follows streptococcal tonsilitis, plaques – multiple discoid erythematous and scaly macules and plaques on trunks. Plaques usually saller than typical psoriasis. Usually <3cm. good prognsosis – often resolve

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21
Q

PSORIASIS

describe palmoplanar pustular psoriasis?

A

yellow brown pustules on palms and soles

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22
Q

PSORIASIS

describe flexoral psoriasis?

A

plaques – erythematous but not scaly, districution – submammary, axillary, anogenital, umbilical. Epidemiology – women, elderly, HIV +ve

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23
Q

PSORIASIS

describe erythrodermic psoriasis?

A

acute onset of erythroderma and pustular plaques, managed with methotrexate

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24
Q

PSORIASIS

describe nail changes?

A

pitting, onycholysis, subungal hyperkeratosis, beaus lines

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25
Q

PSORIASIS

name some precipitating factors?

A

trauma, infection, drugs, emotional stress, sunlight, puberty, menopause, alcohol, obesity, smoking

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26
Q

PSORIASIS

name some associated disorders?

A

psoriatic arthritis, IBD, uveitis, coeliac disease, metabolic syndrome (T2DM, hypertension, hyperlipidaemia, gout, cardiovascular disease

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27
Q

PSORIASIS

what lifestyle changes may be used to manage psoriasis?

A

Minimise risk factors – smoking cessation, reduction of alcohol, weight loss, avoidance of sun exposure, management of stress

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28
Q

PSORIASIS

what topical agents can be used in management?

A
  • Emollients
  • Corticosteroids – start with potent agent eg betamethasone 0.1% / morning applicaton of steroid and evening application of vitamin D analogue – combined agents eg daivobet or Enstilar foam
  • Vit D analogues – calcipotriol, tacalcitol, calcitriol – decrease cell proliferation, side effects -skin irritation, hypercalcaemia if overuse
  • Coal tar preparations – inhibits DNA synthesis, yet it is smelly and messy, used especially in scalp psoriasis
  • Dithranol – anthralin, decreases cell proliferation, side effects- irritates neighbouring normal skin and stains clothes purple
  • Keratolytics – salicyclic acid
  • Retinoids – tazarotene
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29
Q

PSORIASIS

what systemic treatments can be used for management of psoriasis?

A
  • Usually initiated in secondary care setting
  • Phototherapy – UVB / PUVA
  • Retinoids – acitretin, therapeutic effect after 4-6 weeks and used <6 months. Side effects – teratogenic for upto 3 years, dry mucous membranes, hepatotoxicity, deranged lipid profile
  • Immunosuppresants- methotrexate, ciclosporin, azathioprine, hydroxyurea
  • Biological agents – when everyting else has failed eg etanercept, adalimumab, infliximab
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30
Q

PSORIASIS

describe a typical treatment pathway for psoriasis?

A

1st line – vit D analogues +/- topical steroids + tar or salicylic acid +/- UVB
2nd line – retinoids, PUVA, UVB, immunosuppresants
3rd line- dithranol
Goekerman regime – Tar +UVB
Ingram regime – goekerman +dithranol

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31
Q

PSORIASIS

when should a referral be made?

A
  • > 10% body surface
  • Not responding to topical treatment
  • Children
  • Major impact on psychological health
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32
Q

URTICATIA AND ANGIO-OEDEMA

  1. Prevelance
  2. Description
  3. Where does it occur
  4. Cause
A
  1. 20% of people at some point in their life
  2. Itchy, raised skin reactions – weals (hives)
  3. Anywhere on skin. Angio-oedema usually occrs in soft areas of skin such as eyelids, lips, inside mouth
  4. Caused by release of histamine from mast cells. Usually not due to allergy
    Allergens can cause acute Urticaria
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33
Q

URTICARIA AND ANGIO OEDEMA

Management?

A

Aim to suppress symptoms until becomes better
In chronic may last 6-12 months and then gradually disappear
Antihistamine
Monteleukast
Oral steroids – rescue treatment for severe flares
Ciclosporin
Adrenaline injection – if breathing affected
omalizumab

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34
Q

PITYRIASIS ROSEA

  1. What is it?
  2. Describe it?
  3. Who it affects?
A
  1. Viral rash lasting 6-12 weeks
  2. Herald patch followed by similar, smaller oval red patches located on chest and back. Most don’t itch
  3. Teenagers and young adults
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35
Q

PITYRIASIS ROSEA

What are the potential causes?

A

Associated with reactivation of herpesvirus 6 and 7 causing primary rash in inants
Caused by medications such as ACE inhibitors, NSAIDS, hydrochlorothiazide, imatinib, clozapine, metronidazole, terminafine, gold, atypical antipsychotics
Usually lasts 6-12 weeks
Linked to miscarriage

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36
Q

PITYRIASIS ROSEA

Management

A 
Bath or shower with plain water and bath oil or aquesous cream
Moisturise
Expose to sunlight
7 day course of acyclovir
2 week course or oral erythromycin
Topical steroid
phototherapy
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37
Q

LICHEN PLANUS

  1. What is it
  2. Mechanism
  3. Who it affects
  4. Causes
A
  1. Chronic, inflammatory, pruritic skin disorder, on limbs, mucous membranes and genitals
  2. Likely T cell mediated autoimmune disorder
  3. Adults over age of 40
  4. Genetic predisposition, physical and psychological stress, skin trauma, systemic viral infection (hep B, C), contact dermatitis
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38
Q

LICHEN PLANUS

Describe the presentation

A

flexor on first presentation, itchy, not typically painful, may affect genitals, mucous membranes, often round, purpuric, raised lesions, occasionally lesions blister, as initial lesion heals – often leave small flat brown discoloured circles
On mucous surfaces – white, slightly raised lesions, small ulcers or white streaks, tongue or inside cheeks, can be asymptomatic or painful, difficult to treat
Nails – 10% population, longitudinal lines, may involve nail bed
Scalp – usually spared, can cause severe scarring and alopecia

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39
Q

LICHEN PLANUS

What are the subtypes?

A

hypertrophic LP (thick, raised lesions, hyper pigmentation) erosive, ulcerative (painful, mucosal surfaces)

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40
Q

GRANULOMA ANNULARE

  1. What is it?
  2. Who gets it
  3. Pathophysiology
  4. Triggers
A
  1. Inflammatory skin condition typified by annular, smooth, discouloured papules and plaques
  2. Most common in children, teenagers, young adults
    More common in women
  3. May be due to delayed hypersensitivity
  4. skin infections, skin trauma, association with autoimmune thyroiditis, diabetes mellitus, hyperlipidaemia, HIV infection
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41
Q

GRANULOMA ANNULARE

  1. How is a diagnosis made?
  2. Management
A
  1. Clinically
    Skin biopsy - show necrobiotic degeneration of dermal collagen
  2. Treatment not required - disappears on own within a few months
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42
Q

LICHEN SCLEROSUS

  1. What is it
  2. Who does it affect
  3. What conditions is it associated with
  4. What is there an increased risk of?
A
  1. Common chronic autoimmune skin disorder involving anogenital region
  2. Women >50
  3. increased BMI, coronary artery disease, smoking, preceding infections, preceeding trauma increased BMI, coronary artery disease, smoking, preceding infections, preceeding trauma
  4. Increased risk of squamous cell carcinoma
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43
Q

LICHEN SCLEROSUS

  1. Where does it affect
  2. What are the symptoms
  3. Describe the conditions presentation in men
A
  1. Affect non hair bearing areas of vulva and perineum – figure of 8 around genitals and anus. Never affects vaginal mucosa
  2. itch, worse at night, dysuria, dyspareunia, pain when passing stool due to anal fissures, adhesions and scarring (permanent and destructive, reduced size of opening of vagina, reduced size of labia minora, phimosis of clitoris
  3. affects glans of penis, glans can become white, firm and scarred, painful erections, urethra strictures
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44
Q

LICHEN SLEROSUS

describe supportive management?

A
  • Wash gently
  • Use non soap cleanser
  • Avoid tight clothing
  • Avoid synthetic fibres
  • Avoid activities like cycling or horse riding
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45
Q

LICHEN SCLEROSUS

describe topical therapies?

A
  • Emollients
  • Topical steroids
  • Follow up after one month to assess
  • Extra genital lesions
  • Topial oestrogen
  • Oral theraies – reserved for resistant cases, specialist, steroids, retinoids, methotrexate, ciclosporin
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46
Q

LICHEN SCLEROSUS

describe surgical management?

A
  • Excision of SCCs or suspected SCCs
  • Circumscision iin men
  • Surgery to release adhesions and excise scar tissue in women
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47
Q

ACNE VULGARIS

  1. what is it?
  2. who gets it?
  3. cause?
A
  1. Disorder of pilosebaceous follicles (oil glands)
  2. Common – almost universal in second decade of life. Rare before 10yrs
    Peaks in teens (girls 13-14 / boys 18-19). slight male tendency
  3. Initially the result of sebum production – related to androgen levels. Excessive sebum production – leakage into surrounding dermis – excessive colonisation or infection
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48
Q

ACNE VULGARIS

1. associated conditions

A

Associated with depression, anxiety and social phobia
PCOS, steroid use, certain skincare products increase oil load on skin
Potential link with diet

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49
Q

ACNE VULGARIS

what lesions are seen?

A
  • Open comedones (blackheads)
  • Closed comedones (whiteheads)
  • Papules
  • Nodules
  • Cysts
  • Atrophic scars
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50
Q

ACNE VULGARIS

what are the principles of treatment?

A
  • Unblock pores – comedolysis – topical benzoyl peroxide, isotretinoin gel, adapalene lotion
  • Decrease bacterial load in sebum – topical or oral antibiotics
  • Decrease sebaceous gland activity – isotretinoin, COCP, spironolactone
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51
Q

ACNE VULGARIS

conservative management

A
  • Advice
  • Washing
  • Sunlight
  • Avoid oily products
  • Most people tried basics before presenting to GP
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52
Q

ACNE VULGARIS

medical management

A
  • Topical – encourage skin peeling, reduce inflammation, antibiotic effect, apply to all areas
  • Benzoyl peroxide-first line, can cause dryine and irritation, different strengths and can be increased
  • Topical antibiotics – clindamycin or erythromycin, don’t use alone, give in combination with benzoyl peroxide
  • Topical retinoids – adapeline, reduce inflammation, irritating, 12 weeks to be effective, used with other agents, comes in combination with benzoyl perozide as Epiduo
  • Systemic – several months to act, 4 months to assess, combined with topical treatment, useful fro-trunkal acne
  • Oral antibiotics – tetracyclines, clindamycin, rythromycin
  • Isotretinoin – retinoid reduces sebum secretion, teratogenic, dry skin, lips and eye problems, cause myalgia, contraindicated with tetracycline
  • Antiandrogens – COCP in women, reduce oil load on skin, reduces free testoternoe, 3-6 months to have effect,. spironolactone
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53
Q

ROSACEA

  1. what is it
  2. who does it affect
A
  1. Common facial rash
    Chronic and persistent
    Sterile inflammatory papulae, pustule and nodes
    Mistaken for acne
  2. Ages 30-50
    Mainly women
    Celtic ethnic origin – fair skin, blue eyes
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54
Q

ROSACEA

describe the presentation

A

Red rash often with inflammatory papules – often begin as increasing tendency for facial flushing before progressing to papules, pustules and nodules
Rash on cheeks, forehead, nose and chin
Worse when flushed or brushing
Periorbital and perioral areas spared
Associated with increased skin sensitivity and stinging sensation
Accompanies by telangectasia, facial oedema, seborrheic dermatitis, sensitive skin

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55
Q

ROSACEA

describe the management

A
  • Sun protection
  • Gentle soap free cleanser
  • Avoid oil based creams – water based makeup and suncream
  • Avoid factors causing facial flushing – heat, wind, changes in environment temp, alcohol, excessive exercise, hot baths, spicy foods, hot drinks
  • Cool packs
  • Medications – topical metronidazole cream 0.75% OD or BD / oral antibiotics – doxycycline 100mg OD or erythromycin 250-500mg BD for 4-8 weeks
  • Laser treatment for telangectasia
  • Surgical correction for rhinophyma
  • Avoid topical steroids
56
Q

PERIORAL DERMATITIS

  1. what is it
  2. where does it affect and where is spared
A
  1. Groups of itchy or tender small red papules
  2. Around eyes, nostrils, mouths, genitals. Unilateral or bilateral eruption of chin, upper lip and eyelids in perioral, perinasal and periocular distribtison. Sparing of skin bordering lips
57
Q

PERIORAL DERMATITIS

  1. pathology
  2. describe clinical presentation
A
  1. Cause related to: epidermal barrier dysfunction, activation of innate immune system, altered cutaneous microflora, follicular fusiform bacteria
  2. Clusters of 1-2mm erythematous papules or papulopustules. Dry, flaky skin surface. Burning irritation
58
Q

PERIORAL DERMATITIS

describe the management

A
  • Stop face creams, steroids, cosmetics, suncreams
  • Wash face with warm water alone while rash is present
  • Topical therapy – erythromycin, clindamycin, metronidazole, pimecrolimus, azelaic acid
  • Oral therapy – oral antibiorics 6-12 weeks / tetracycline, erythromycin in pregnancy and pre-pubertal, oral low dose isotretinoin
59
Q

FOLLICULITIS

  1. What is it?
  2. causes
A
  1. Inflamed hair follicles. Tender red spot, often with surface pustule
  2. Can be due to infection, occlusion, irritation from regrowing hair, skin disease
    • Bacteria – staph aureus
    • Yeasts – pityrosporum ovale
    • Fungi – ringworm of scalp
    • Viral - herpes simplex, herpes zoster, molluscum contagiosum
    • Parasitic infection
    •regrowing hairs – after regrowth following shaving, waxing electrolysis, plucking
    • Contact reactions – occlusion, chemicals, topical steroids
    • Can be due to immunosuppression, drugs, inflammatory skin diseases
60
Q

IMPETIGO

  1. what are the causes
  2. who gets it
A
  1. Staph aureus / Strep pyogenes

2. outbreaks in schools and famillies

61
Q

IMPETIGO

  1. describe the appearance
  2. what can cause infection?
A
  1. Causes pustules and yellow/golden coloured crust

2. Typically requires skin defect to cause infection eg scratch or abrasion

62
Q

IMPETIGO

what are the 2 types of impetigo?

A
  • Bullous impetigo – pustules and blisters, always staph, blisters due toxins, not often painful, often leave brown crust when burst
  • Non bullous impetigo – staph aureus, strep pyogenes, not usually painful, itchy or irritating
63
Q

IMPETIGO

describe management

A
  • Topical antibiotics eg mupirocin cream TDS
  • Oral antibiotics – complex cases – PO flucloxacilln 500mg QID adults, 12.5mg/kg, max 250mg in children
  • Cover lesions to reduce transmission
  • If cannot be covered – time off school
  • Antiseptic to clean
  • Avoid towel sharing
  • Nose picking can be source of infection so avoid
64
Q

CELLULITIS

  1. what is it?
  2. where is usually affected
A
  1. Bacterial infection of dermis layer and deeper subcutaneous tissues. Often due to break or puncture to skin allowing bacteria to enter
  2. legs and face (often lower limb)
65
Q

CELLULITIS

  1. risk factors
  2. bacterial causes
A
  1. wound, diabetes, old age, insect bites, obesity, fungal infectin between toes, skin conditions, chronically swollen legs, chronic venous insufficiency, varicose veins, IV drug user, immunosuppression, previous cellulitis
  2. Group A beta haeolytic streptococci / staph aureus. Less common – strep pneumonia, haemophilus influenzae, gram negative bacilli, anerobes
66
Q

CELLULITIS

1. describe presentation

A
  • Symptoms spread quickly
  • Erythema blends into surrounding skin
  • Pain
  • Swelling
  • Warmth
  • Often site of skin damage
67
Q

CELLULITIS
investigations in
1. primary care
2. secondary care

A
  1. Not usually required. Clinical history and examination. If no obvious wound – swab
  2. Bloods – raised WCC, CRP, fasting glucose, lipids, cholesterol
    Blood cultures – target antibiotics
    X-ray, CT, MRI
68
Q

CELLULITIS

1. when should you admit to hospital?

A
  • Significantly unwell – tachycardic, tachypnoea, hypotension, vomiting, acute confusion
  • Unstable co-morbidities eg diabetes
  • Contaiminated wound
  • Limb threatening infection
  • Sepsis or life threatening compication eg necrotising fasciitis
  • Very young or frail
  • Immunocompromised
  • Gross limb swelling
  • Facial cellulitis
  • Periorbital cellultis
69
Q

CELLULITIS

  1. management of minor/mild
  2. hospital management
  3. other components of management?
A
  1. PO flucloxacillin 500mg QDS for 7 days
  2. Flucloxacillin 1g QDS IV 48 hrs
  3. Analgesia, Elevate leg, Tetanus vaccination
70
Q

ECTHYMA

  1. what is it
  2. causes
  3. who gets it
  4. where does it affect
A
  1. Skin infection, Crusted sores beneath which ulcers form, Deep form of impetigo
  2. Strep pyogenes and staph aureus
  3. Higher in children, older people and immunocompromised. Higher risk – poor hygiene, high temp and humidity, minor injuries or other skin conditions, untreated impetigo
  4. Most often affects buttocks, thighs, legs, ankle, feet. Usually begins as vesicle or pustule
71
Q

ECTHYMA

describe management

A
  • Depends on extent and severity
  • Soak crusted areas
  • Topical antiseptics or antibiotics – fusidic acid
  • Oral antibiotics – penicillin
  • hygiene
72
Q

ERYTHRASMA

  1. where does it affect
  2. who is more at risk
  3. causative agent
A
  1. affects skin folds under arms, in groin and between toes. more common in groin of males and between toes of females. widespread infections associated with diabetes mellitus. mild itching
  2. more prevelant in; warm climate, excessive sweating, diabetes, obesity, poor hygiene, advanced age, immunocompromised
  3. gram positive, non spore forming, aerobic or facultative bacilli (Corynebacterium minutissimum)
73
Q

ERYTHRASMA

  1. Describe its appearance
  2. what are the 3 types
  3. investigations
A
  1. well defined pink or brown patcheswith fine scaling and superficial fssures
  2. interdigital, intertriginous, generalised/disciform
  3. wood lamp- coral pink colour / swab or skin scrapings
74
Q

ERYTHRASMA

management

A 
Fusidic acid
Clindamycin
Benzoyl peroxide
Whitfield ointment
Oral antibiotics – erythromycin or tetracycline
75
Q

BOILS (FURUNCLES)

  1. what is it?
  2. how does it present
  3. causative organism
  4. related conditions
A
  1. Deep form of bacterial folliculitis.
  2. Present as one or more tender red spots, lumps or pustules. Centred on hair follicle
  3. staph aureus
  4. Can be related to immune deficiency, anaemia, diabetes, smoking, iron deficiency
76
Q

BOILS (FURUNCLES)

  1. management
  2. prevention
A
  1. Antiseptic of antibacterial soap. Hand sanitiser. Topical antiseptic eg povidone iodine or chlorhexidine . Oral antibiotic e penicillin
  2. Weight loss, Diet, Smoking, Wash regularly, • Don’t share towel/flanner, Don’t pick nose, Change underclothes and night attire
77
Q

HIDRADENITIS SUPPURATIVA

  1. what is it?
  2. where does it affect?
  3. who gets it?
A
  1. Inflammatory skin condition. Recurrent boil like nodules
  2. Inflammatory skin condition. Affect apocrine gland bearing skin in axillae, groin, under breasts
  3. Common in; family istory, obesity, insulin resistance, smoking, follicular occlusion disorder, IBD, rare autoinflammtory syndromes
78
Q

HIDRADENITIS SUPPURATIVA

  1. causes
  2. signs
  3. describe severe
A
  1. friction from clotehs, immune response to commensal bacteria, abnormal cutaneous or follicular microbiome, follicular occlusion, release of proinflammatory cytokines, secondary bacterial infection
  2. open and closed comedones, painful firm papules, pustules, pyogenic granulomas, draining sinuses, hypertrophic and atrophic scars
  3. (hurley stage 3) associated with – male, axillary and perianal involvement, obesity, smoking, higher risk of stroke, disease duration
79
Q

HIDRADENITIS SUPPURATIVA

1. management

A
  • Weight loss
  • Smoking cessation
  • Loose fitting clothes
  • Un-fragranced antiperspirants
  • Wash with antiseptics
  • Hydrogen peroxide
  • Peeling agents (resorcinol 15% cream)
  • Simple dressings
  • Analgesics
  • Topical clindamycin
  • Oral antibiotics
  • Anti-androgens – long term COCP, antiandrogenic progesterones, spironolactone and finasteride,
  • Immunomodulatory treatment -systemic corticosteroids, intralesional corticosteroids, methotrexate, ciclosporin, azathioprine, TNF alpha inhibitor adalimumab
  • Metformin – insulin resistance
  • Acitretin
  • Isotretinoin
  • Colchiiine
  • Surgical – drainage, curettage, laser ablation, wide local excision, radical excisional surgery
80
Q

PITTED KERATOLYSIS

  1. what is it?
  2. causative organisms?
  3. who is at risk?
A
  1. Superficial bacterial skin infection. Soles of feet. Causes smelly feet. Whitish skin and clusters of punched out pits
  2. Dermatophilus congolensis, kytococcus sedentarius, actinomyces, streptomyces
  3. farmers, athletes, sailors or fishermen, industrial workers, military personel
81
Q

PITTED KERATOLYSIS

  1. factors leading to development
  2. when is the appearance more dramatic
A
  1. hot, humid weather, occlusive footwear, excessive sweating of hands and feet, thickened skin of palms and soles, diabetes mellitus, advanced age, immunodeficieny
  2. Appearance more dramatic when feet wet
82
Q

PITTED KARATOLYSIS

making a diagnosis

A
  • clinical diagnosis
  • Swabs rare
  • Skin scrapings to rule out fungal infection
83
Q

PITTED KERATOLYSIS

management

A
  • Topical antibiotics and antiseptics (erythromycin, clindamycin, mupirocin, fusidic acid, benzoyl peroxide)
  • Prevention – wear boots for short period, wear socks absorbing sweat, open toed sandals, wash feetm apply antiperspirant, don’t wear sam shoes 2 days in a row (dry them out), don’t share footwear or towels
84
Q

HERPES SIMPLEX

  1. what is it
  2. what are the types
A
  1. Viral, Localised blistering, Cold sores/fever blisters
  2. Type 1 – infants/children
    Type 2 – after puberty, often sexually transmitted
85
Q

HERPES SIMPLEX

management

A

Antiviral

  • 200mg 5 times daily 5days
  • valaciclovir 1g 3times daily for 7 days
  • famciclovir – single dose 3x500mg
86
Q

VARICELLA ZOSTER

  1. how is it spread
  2. clinical presentation
A
  1. airborn
  2. Itchy red papules progressing to vesicles on stomach, back and face then spreading to other parts of body. High fever,headache, cold like symptoms, vomiting and diarrhoea
87
Q

VARICELLA ZOSTER

management

A
  • Minimise scratching
  • Warm bath, moisturise
  • Paracetamol
  • Calamine lotion
  • Oral acyclovir
  • Prevent spread – contagious 1-2 days before rash appears and until all blisters have formed (may take 5-10 days)
  • Can take 10-21 days from contact with infected person to develop
  • vaccination
88
Q

HERPES ZOSTER (SHINGLES)

  1. what is it
  2. who gets it
  3. triggering factors
A
  1. localised, blistering, painful rash, reactivation of varicella zoster, dermatomal distribution
  2. more common In adults (older)
  3. pressure on nerve roots, radiotherapy at level of nerve root, spinal srery, infection,injury, contact with someone with varicella or herpes zoster
89
Q 
HERPES ZOSTER (SHINGLES)
describe presentation
A
  • first sign usually pain, may be in one spot or may spread
  • fever and headache
  • within 1-3 days of pain, blistering rash appears in painful area of skin
90
Q 
HERPES ZOSTER (SHINGLES)
management
A
  • antivirals reduce pain and duration of symptoms if started 1-3 days after onset of herpes zoster
  • acyclovir 800mg 5 times a day for 7 days
91
Q

HPV

  1. describe appearance
  2. who gets it
  3. how is it transmitted
A
  1. Anogenital wart, Suprficial skin lesion, Close skin contact
  2. 15-30yrs, rare in those vaccinated
  3. Transmitted via sexual contact, fomites, vertical (mother to baby)
92
Q

HPV

management

A
  • Prevent with condoms
  • Self applied treatments – podophyllotoxin solution or cream, imiquimod cram, sinecatechins ointements
  • Clinic treatment – cryotherapy, podophyllin resin, trichloroacetic applications, electrosurgery, curettage, laser ablation, 5% fluororacil cream
93
Q

MOLLUSCUM CONTAGIOSUM (WATER BLISTERS)

  1. What is it?
  2. appearance
  3. where does it affect
A
  1. Common viral skin infection of childhood
  2. localised clusters of epidermal papulae (mollusca). Cluster of small round papules. Waxy, shiny look with small central pit
  3. More preelan in warm climates, overcrowded enviroments
94
Q

MOLLUSCUM CONTAGIOSUM (WATER BLISTERS)

  1. causative organism
  2. how is it spread
A
  1. poxvirus
  2. skin to skin contact, indirect contact via shared towels, auto inoculation into another site by scratching, sexual transmission
95
Q 
MOLLUSCUM CONTAGIOSUM (WATER BLISTERS)
management
A
  • Physical treatments – picking out soft white core, cryotherapy, gentle curettage, laser ablation
  • Medical treatments – antiseptics, podophyllotoxin cream, wart paints,cantharidine
  • Prevention – hand clean, avoid scratching, cover visible lesions, dispose used bandages, don’t share towels, safe sex
96
Q

TINEA CORPORIS

  1. what is it
  2. types
A
  1. Ringworm. Infection of trunk, leg or arms with dermatophyte fungus
  2. Acute - inflamed red patches, can be pustular
    Chronic – prominent in body folds, prone to recurrence, due to decreased natural skin resistance to fungi
97
Q 
TINEA CORPORIS (RINGWORM)
management
A 
Topical antifungals
Oral antigungals (terbinafine and itraconazole) if topical unsuccessful
98
Q

TINEA CRURIS

  1. what is it?
  2. who gets it
  3. describe appearance
A
  1. Jock itch. Infection of groin with dermatophyte fungus. similar to ringworm
  2. adult men
  3. Scaly raised red border spreads down inner thigh from groin
99
Q

TINEA CRURIS

management

A
  • Reduce chance of infection – treat feet if necessary, dry properly after bathing using separate towel, don’t share towels, avoid occlusive or synthetic clothing , lose weight
  • Topical antifungal agents
  • Oral antifungals – terbinafine and itraconazole
100
Q

TINEA PEDIS

  1. what is it
  2. causative organism
  3. who gets it
A
  1. Foot infection due to dermatophyte fungus. Hot tropical, urban environment. Interdigital
  2. Trichophytoin rubrum
    T. interdigitale
    Epidermophytoin floccosum
  3. males/adolescents
101
Q

TINEA PEDIS

  1. risk factors
  2. appearance
A
  1. occlusive footwear, excessive sweating, underlying immunodeficiency, systemic corticosteroirs, poor peripheral circulation
  2. Itchy, between toes. Scale covering soles and sides of feet. Small to medium sized blisters
102
Q

TINEA PEDIS

management

A
  • Topical antifungal - azoles, allylamines, butenafine, cicloprox, tolnaftrate
  • Oral antifungal – terbinafine, itraconazole, fluconazole, griseofulvin
103
Q

TINEA MANUUM

  1. what is it
  2. what causes it
A
  1. Misdiagnosed as it is similar to hand dermatitis, psoriasis, keratolysis exfoliative. Acute inflammatory rash like tinea corporis. Usually border and clearing in the middle
  2. contact with another site of infection, contact with another person, direct contact with infected animal, contact with contaminated object
104
Q

TINEA MANUUM

management

A
  • Topical antifungal agents

* Oral antifungals if unsuccessful (terbinafine, itraconazol

105
Q

TINEA CAPITIS

  1. what is it
  2. causative organism
  3. how is it spread
A
  1. Fungal infection of scalp. Involves skin and hair
    Known as scalp ringworm
    Preadolescent children (3-7yrs), immunocompromised
  2. Due to dermatophytic fungi
  3. Spread via infeced people, contaminated objects, fomites in hairbrushes, hats, towls, bedding, couches, toys, fungal spores can be viable for months, infected animals
106
Q

TINEA CAPITIS

What are the 2 types?

A
  • Non inflammatory varients – grey patch, black dot, diffuse scale
  • Inflammatory variants – diffuse pustular, kerion, favus
107
Q

TINEA CAPITIS

management

A
  • 4 weeks of systemic medication as topical agents cannot penetrate root of hair follicle
  • Terbinafine,itraconazole, fluconazole
  • Topicl agents can be used to reduce spore transmission eg ketoconazole
108
Q

TINEA UNGUIUM

  1. causative organism
  2. who gets it
  3. where does it affect
  4. how does it present
A
  1. Trichophyton rubrum and T. interdigitale
  2. Increasingly prevelant with age
  3. one or more toenails
  4. Can present as several different patterns – lateral onychomycosis, subungual hyperkeratosis, distal onycholysis, superficial white onychomycosis, proximal onychomycosis, complete destruction of nail
109
Q

TINEA UNGUIUM

management

A
  • If mild – topical antifungal – 6-12 months – amorolfine, ciclopirox
  • Usually require oral antifungal – terbinafine, itraconazole
  • Fingernail infection cured more quickly than toenail
110
Q

CANDIDA

  1. what is it
  2. what are the causative organisms
  3. give examples of infections
A
  1. Group of yeasts infecting skin
  2. C. tropicalis, C. parapsilosis, C,glabrate, C. guilliermondii
  3. oral candidiasis, angular cheilitis, vulvovaginal candidiasis, balantis, intertrigo, napkin dermatitis, chronic parenchia, onychomycosis, chronic mucocutaneous candidiasis
111
Q

CANDIDA

predisposing factors

A

infancy, old age, warm climate, occlusion, broad spectrum antibiotics, high oestrogen cocp or pregnanc, DM, cushings, iron deficiency, underlying skin disease, immunodeficiency, chemo

112
Q

PITYRIASIS VERSICOLOR

  1. what is it
  2. who gets it
  3. where does it affect
A
  1. Yeast infection of skin. Flaky discoloured patches on chest and back
  2. Slightly more commen in men. More common in hot,humin climates. Affects people that perspire heavity. More common to occur in summer
  3. Trunk, neck, arms
113
Q

PITYRIASIS VERSICOLOR

appearance

A

Patches are coppery brown, paler than surrounding skin or pink
Pale patches more common In darker skin

114
Q

PITYRIASIS VERSICOLOR

management

A
  • Mild – topical – azole, selenium sulfide, terbinafine gel, ciclopirox cream, propylene glycol solution, sodium thiosulphate
  • Oral antigungals – itraconazole and fluconazole – used when topical fail
115
Q

SCABIES

  1. what is it?
  2. who gets it?
  3. how does it spread
A
  1. Itchy rash caused by parasitic mite that burrows in skin surgance
  2. More common in children,young adults, older people
  3. poverty and overcrowding, institutional care, refugee camps, immunde deificinecy
    Causes – skin to skin contact with infected person
116
Q

SCABIES

  1. what should you look for
  2. describe the itch
  3. describe the rash
A
  1. Look for burrows carefully in patient with severe itch
  2. 4-6 weeks after transmission of mite, more severe at night, trunk and limbs and spares calp, can persist for weeks after treatment
  3. hypersensitivity reaction several weeks after initial infestation. Erythematous papules, diffuse of nummular dermatitis, urticated erythema, vesicles on palms and soles, acropustulosis, papulae or nodules in armpits groin, buttocks, scrotum, rare for face and scalp involvement
117
Q

SCABIES

management

A
  • Oral antibiotics for secondary infection
  • Scabicides – 5% permethrin cream
  • Oral ivermectin 200mcg/kg
118
Q

VIRAL WARTS

  1. cause
  2. who gets it
  3. how is it spread
A
  1. Caused by infection with HPV (DNA virus).
  2. School aged children, eczema, immunosuppressed
  3. skin to skin contact
119
Q

VIRAL WARTS

name and describe the types of wart?

A
  • Common wart – papules with rough, papillomatous and hyperkerartic surfaces
  • Plantar wart – tender inwardly growin and painful ‘myrmecia’ on sole
  • Plane wart – flat surface – face, hands shins
  • Filiform wart – long stalk like thread
  • Mucosal wart – lips and inside cheeks
120
Q

VIRAL WARTS

management

A
  • Topical – salicyclic acid
  • Cryotherapy – repeated at 1-2 week intervals
  • Electrosurgery – large and resistant warts
121
Q

SEBORRHOEIC KERATOSIS

  1. what is it
  2. who gets it
  3. appearance
A
  1. Harmless, warty spot appearing during adult life as common sign of skin ageing
  2. older adults
  3. Variable appearance. Flat or raised papule or plaque. 1mm to several cm diameter. Skin coloured yellow, grey, light brown, dark brown, black, mixed colours. Smooth, wacy, warty surface. Solitary or grouped in certain areas
122
Q

SEBORRHOEIC KERATOSIS

management

A
  • Can be removed if unsightly, itchy or catches on clothes
  • Cryotherapy
  • Curettage
  • Ablative laser surgery
  • Shave biopsy
  • Focal chemical peel
123
Q

DERMATOFIBROMA

  1. what is it
  2. who does it affect
  3. causes
  4. descriptin
A
  1. Common benign fibrous nodule usually on skin of lower legs
  2. mainly adults
  3. Sometimes attributed to minor trauma eg insect bites, injections, rose thorn. Solitary firm papule or nodule on limb. Anywhere on skin. 0.5-1.5cm. Tethered to skin and mobile over subcutaneous tissue. Can be painful, tender or itchy
124
Q

LIPOMA

  1. what is it
  2. when does it occur
  3. where does it occur
A
  1. Non cancerous tumour made up of fat cells
  2. Tend to develop in adulthood, most noticeable in middle age. Usually go unnoticed until large enough to become visible and palpable
  3. Slowly grows under skin in subcutaneous tissue
125
Q

LIPOMA

describe the features of lipoma

A
  • Dome shaped or egg shaped lump about 2-10cm in diameter
  • Feels soft and smooth
  • Rubbery or doughy consistency
  • Most common on shoulders, neck, trunk and arms
126
Q

LIPOMA

management

A
  • Usually not needed
  • Simple surgical excision
  • Squeeze technique
  • liposuction
127
Q

MELANOMA

7 point checklist

A
  • size >7mm
  • recent change in size of lesion
  • irregular pigmentation
  • itch or irritation
  • inflammation
  • oozing or crust of lesion
  • asymmetry
  • ugly duckling – stands out compared to other lesions
128
Q

MELANOMA

  1. risk factors
  2. outcome
A
  1. sun exposure (not as important), male, >50, Fhx melanoma, fair complexion, smoking
  2. most dangerous type of skin cancer. most likely to metastasise
129
Q

MELANOMA

name and describe the different types?

A
  • lentigo maligna melanoma – usually face in eldery patints, large flat dark lesion
  • superficial spreading melanoma – legs of women and torso/back of men, slightly raised plaque
  • nodular melanoma – anywhere, dark coloured, may peel or lack pigment, rarely metastasise
  • acral and subungal melanoma-rare, most common in blak africas, palms or soles or subungal skin
130
Q

MELANOMA

management

A
  • Excision
  • Margins guided by extent of spread on histology
  • 2mm margin
  • If metastasis – 5yr survivcal 10%
131
Q

SQUAMOUS CELL CARCINOMA

1. risks

A

smoking, sun exposure, presence of premalignant lesions, age, skin trauma, exposure to carbon containing compounds, asbestos, arsenic, ionising radiation, metals, non solar UV radiation, mre, occupational eg builder/farmer

132
Q

SQUAMOUS CELL CARCINOMA

describe

A
  • Solitary papule/nodule, often eroded at centre or crusty, purulent or bleeding
  • Fleshy lesion
  • Like a giant wart
  • Sun exposed area
  • Hard, scaly dome like structure
  • Can bleed or itch
  • Related to smoking
  • Bowens diseasde – SCC in situ
133
Q

SQUAMOUS CELL CARCINOMA

management

A
  • Surgical excision with minimum 2mm margin
  • Topical creams – 5-fluoracil , imiquimod
  • Rare metastases
134
Q

BASAL CELL CARCINOMA (rodent ulcer)

  1. describe features of disease
  2. risk factors
  3. appearance of lesion
A
  1. Most common form of skin cancer. Rare metastases. Locally destructive. Arise from epidermal basal cells
  2. fair skin, sun exposure
  3. Pearly nodule with raised, red, edge, often on face
135
Q

BASAL CELL CARCINOMA

management

A
  • Surgical excision – 3mm margin

* Topically - imiquimod

Women's Health - Year 4 (15 decks)

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