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medicine year 3 > Week 10 - Dermatology > Flashcards

Week 10 - Dermatology Flashcards

1
Q

What is a fixed drug rash?

A

Same area, same drug i.e. paracetamol

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2
Q

Describe a lichenoid rash

A
  • Looks similar to the rash ‘lichen planus’
  • Purplish, itchy, flat rash
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3
Q

If a patient with psoriasis complains of joint pains, how would you assess this, what pattern might you expect to see of associated joint problems and what considerations in treatment might you have to give?

A
  • Small joint , digit arthritis, swelling redness, arthralgia. Look for significant nail pitting
  • Axial sacroiliac
  • Certain drugs better for combination skin psoriasis and psoriatic arthritis e.g. methotrexate
  • Anti-inflammatories for joints e.g. Naproxen
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4
Q

What is eczema herpeticum?

A
  • HSV infection with eczema
  • Painful
  • Monomorphic blisters
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5
Q

How is fifth disease treated?

A
  • Self-limited (7-10 days) and resolves without complications or sequelae in children
  • Treatment is generally supportive on a case-by-case basis
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6
Q

Describe the genetic inheritance of psoriasis

A
  • One sibling with psoriasis - risk 24%
  • One parent with psoriasis - risk is 28%
  • One sibling and one parent with psoriasis - risk is 41%
  • Two parents with psoriasis - risk is 65%
  • If both parents and a sibling have psoriasis risk is 83%
  • PSORS genes (e.g. PSORS1, chromosome 6) and HLA - Cw0602 associated in certain subtypes
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7
Q

List the types of psoriasis

A
  • Plaque - most common
  • Guttate - teardrop/raindrop (small patches)
  • Pustular
  • Erythrodermic - red allover
  • Flexural/inverse
    • Most on extensor surface, flexural is unusual variant
  • Palmar/plantar pustulosis?
  • Psoriasis at sites of trauma/scars - Koebner phenomenon
    • E.g. in carpenters/joiners on knees/knuckles
    • Not Auspitz phenomenon - scratch off patch and have pin point bleeding
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8
Q

How is the severity of acne classified?

A
  • The Leeds Acne Grading System - grades 1-12
  • For decisions on therapy and appropriate follow-up, acne assessment is necessary
  • Important to identify the prevalence of types of acne lesion present (comedonal and papulopustular or nodulo-cystic) and the presence of scarring
  • Scale can be useful for tracking improvement from baseline throughout the entire course of treatment
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9
Q

List the types of skin drug reactions

A
  • Maculopapular
  • Urticaria
  • Morbilliform
  • Papulosquamous
  • Photo-toxic
  • Pustular
  • Lichenoid
  • Fixed drug rash
  • Bullous
  • Itch (no rash)
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10
Q

What is the usual causative organism in an SSTI caused by freshwater exposure and which antibiotic should be used?

A
  • Organism - aeromonas hydrophilia
  • Antibiotic - ciprofloxacin
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11
Q

List the types of acanthosis nigricans

A

Three types of acanthosis nigricans have been recognised

  • Type 1 - associated with malignancy
    • Adenocarcinoma, especially of the GI tract (60% gastric), sudden onset and more extensive
  • Type II - familial type, autosomal dominant
    • Very rare, appears at birth, no malignancy
  • Type II - associated with obesity and insulin resistance
    • Most common type
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12
Q

What are the side effects associated with acne treatment?

A
  • Topical agents - irritant, burning, peeling, bleaching
  • Oral antibiotics - gastro upset
  • OCP - possible DVT risk
  • Oral isotretinoin
    • Trivial - dry lips, nose bleeds, dry skin, myalgia
    • Serious - deranged liver function, raised lipids, mood disturbance, teratogenicity
      • Mood disturbance link not proven but often seen if patient has underlying mood disorder
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13
Q

What are the effects of Cushing’s disease systemically?

A

Excessive production of cortisol in the body leads to -

  • Increased central adiposity
  • Moon facies and buffalo hump
  • Global skin atrophy, epidermal and dermal components
  • Striae on abdominal flanks, arms, thighs
  • Purpura with minor trauma - reduced connective tissue
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14
Q

What is seen in scleredema?

A
  • Can’t squeeze skin - loss of elasticity
  • Generalised erythema
  • Often affects upper back
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15
Q

How is shingles treated?

A
  • Treat only high-risk patients (immunocompromised, disseminated) with acyclovir
  • Pain management - NSAIDs, gabapentin
  • Wait for pustular lesions to crust over before they can come out of isolation
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16
Q

Describe the typical distribution of atopic eczema in infants

A
  • Cheeks, chin
  • Skin broken - itchy, hard to stop babies scratching
  • Drool - keeps skin around mouth hydrated, not affected
  • Risk of secondary infection where skin broken
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17
Q

How is eczema herpeticum treated?

A
  • Need hospital admission
  • Anti-viral
  • Secondary bacterial infection - antibiotics
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18
Q

Describe a typical psoriasis patient - appearance, distribution, clinical signs

A
  • Any age, sometimes two peaks - early onset and late onset
  • Symmetrical extensor distribution
  • Scaly plaques
  • Scalp and nails effected
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19
Q

What are the complications of measles?

A

1/5 unvaccinated + measles hospitalised

1/20 children + measles get pneumonia (common cause mortality)

1/1000 children + measles get encephalitis - deaf/intellectual disability

3/1000 children + measles die (respiratory + neurological complications)

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20
Q

What are the consequences of burns?

A
  • Damage to skin compromises resistance to environment
    • Infection
    • Hypothermia - temperature regulation
    • Acid base abnormalities
    • Dehydration - fluid loss
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21
Q

What investigations should be done in immunobullous disorders?

A

Skin biopsy with immunofluorescence

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22
Q

What complications are associated with atopic eczema?

A
  • Bacterial infection - staph. Aureus
  • Viral infection
    • Molluscum
    • Viral warts
    • Eczema herpeticum (HSV infection w/ eczema)
  • Tiredness
  • Growth reduction
  • Psychological impact
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23
Q

How is impetigo managed?

A
  • Remove crust gently
  • Flucloxacillin
  • Prevent secondary infection
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24
Q

How does a squamous cell carcinoma develop?

A
  • May occur in normal skin or skin that has been injured (burns, chronic ulcers, radiation treatment) or chronically inflamed
  • Originates from keratinocytes
  • Pre-malignant variants - actinic keratosis –> Bowen’s disease (squamous cell carcinoma in situ)
  • Most SCC occur on skin that is regulalry exposed to sunlight or other UV radiation
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25
Q

Describe the classification for burn severity

A
  • Superficial (1st) - epidermis only
    • Red/dry
    • Blanches on pressure
    • Painful
    • Heals in 7 days
  • Partial-thickness (2nd) - epidermis and dermis
    • Superficial vs deep
    • Blisters
    • Pain > painless
    • Heal <21 days +/- antibiotics, surgery, grafting
  • Full thickness (3rd) - to subcutaneous tissue
    • Painless - nerve endings destroyed
    • Non-blanching
    • Surgery
  • Fourth degree - fascia, muscle, bone
    • Healing requires surgery
  • Percentage body surface area affected
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26
Q

What investigations/referrals might you make in a patient with psoriasis complaining of joint pains?

A
  • Inflammatory blood markers
  • Plain Film X-rays
  • Autoantibodies e.g. ANA and Rheumatoid factor
  • Consider PEST score assessment of joints and referral to Rheumatologist
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27
Q

What risk factors are associated with cutaneous anthrax?

A
  • Working with animals or animal hides
  • Making, owning or playing animal hide drums
  • Drug use (particularly heroin use) - Glasgow outbreak 2012
  • Travel
  • Working in postal sorting offices or handling large volumes of mail
  • Received threatening letter or package containing white powder
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28
Q

Describe the immune function of the skin

A
  • Langerhan’s cells (LC) are members of the dendritic cells family, residing in the basal layers
  • Specialise in antigen presentation - acquire antigens in peripheral tissues, transport them to regional lymph nodes, present to naïve T cells and initiate adaptive immune response
  • Activated T cells initiate cytokine release cascade
  • Involved in antimicrobial immunity, skin immunosurveillance, induction hypersensitivity and pathogenesis of chronic inflammatory diseases of the skin
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29
Q

What is the usual causative organism in an SSTI caused by saltwater exposure and which antibiotic should be used?

A
  • Organism - vibrio vulnificus
  • Antibiotic - doxycycline
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30
Q

What is the usual causative organism in pus forming typical cellulitis and which antibiotic should be used?

A
  • Organism - S. aureus, MRSA
  • Antibiotic - flucloxacillin, vancomycin
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31
Q

How often do animal bites become infected?

A

15-20% of dog and 50% of cat bites

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32
Q

What causes blistering disorders?

A
  • Drug/infection induced
    • Steven Johnson syndrome
    • Toxic epidermal necrolysis
  • Immunobullous diseases
    • Bullous pemphigoid
    • Bullous pemphigus
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33
Q

How is chickenpox diagnosed?

A

Diagnosed by PCR or vesicle fluid (or serology)

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34
Q

What is urticaria?

A
  • Hives/weals/welts
  • Raised itchy rash
  • Lesions last <24 hours
  • Non-scarring
  • Common skin disorder to present to A&E
  • Acute <6 weeks
  • Chronic >6 weeks
  • Can have some angioodema but not anaphylaxis
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35
Q

Describe the typical appearance of nodular melanomas

A
  • Can look shiny - not at edge
  • Abnormal pigmentation
  • Can look like pigmented basal cell carcinoma
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36
Q

How is HSV diagnosed?

A

Clinical, blood or vesicle fluid for PCR, serology sometimes helpful

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37
Q

What are the complications of eczema herpeticum?

A

If spreads to eye - herpes keratitis

Scarring in eye, need ophthalmology

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38
Q

Describe the development of basal call carcinoma

A
  • The process of creating new skin cells is controlled by a basal cell’s DNA
  • A mutation in the DNA causes a basal cell to multiply rapidly and continue growing when it would normally die, eventually the accumulating abnormal cells may form a tumour
  • Rarely a PTCH mutation may predispose
  • About 80% of basal-cell cancers are found on the head and neck/UV exposed sites
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39
Q

List the features of cutaneous anthrax

A
  • Major features
    • Surrounded by extensive oedema
    • Painless and non-tender
  • Minor features
    • Black eschar
    • Progresses over 2-6 days through papular, vesicular and ulcerated stages before eschar appears
    • Affects hands, forearms, face and neck, site of injection
    • Discharge of serous fluid
    • Local erythema and induration
    • Local lymphadenopathy
    • Associated with systemic malaise including headache, chills and sore throat, but afebrile (vs injectional - more systemic with fever, leads to mediastinal haemorrhage)
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40
Q

List triggers of vasculitis

A
  • Infection
  • Drugs
  • Connective tissue disease i.e. RA
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41
Q

List the risk factors for the development of a melanoma

A
  • Genetic markers e.g. CDKN2A mutations
  • Family history of dysplastic naevi or melanoma
    • 2/3 + first degree relatives affected
  • UV irradiation
  • Sunburns during childhood
  • Intermittent burning exposure in unacclimatised fair skin
  • Number (>50) and size (>5 mm) of melanocytic naevi
  • Congenital naevi
  • Number of atypical naevi (>5)
  • Atypical/dysplastic nevus syndrome
  • Personal history of melanoma
  • High socioeconomic status - more holidays abroad
  • Skin type I, II
  • Equatorial latitudes
  • DNA repair defects e.g. xeroderma pigmentosum
  • Immunosuppression
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42
Q

In chronic plaque psoriasis give a treatment ladder of therapies starting with the mildest to the more systemic and complex 3rd line treatments

A
  • Topicals – Emollients, Corticosteroids, Vitamin D Analogues, Tar / Dithranol
  • Phototherapy – UVB, PUVA
  • Systemics – Retinoids (acitretin), Apremilast, Dimethyl Fumarate
  • Immunosuppressives – Ciclosporin, Methotrexate
  • Biologic immunosuppressives – Adalimumab, Secukinumab, Risankizumab etc
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43
Q

What are the symptoms of hand-food-and-mouth disease?

A
  • Fever, rash, headache, sore throat, oropharyngeal ulcers, and loss of appetite
    • Rash on the palms of hands and soles of feet (+ legs, buttocks)
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44
Q

How is necrolytic migratory erythema treated?

A

Removal of the tumour

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45
Q

Describe the appearance of atopic eczema on darker skin

A
  • Symmetrical distribution
  • Flexural sites
  • Hyperpigmentation - esp. seen in periorbital areas
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46
Q

Which skin lesions are likely to be relevant in an older man with sun damage?

A
  • Seborrhoeic waters
  • Fleshy moles
  • Pigmented dermatofibroma
  • Melanoma
  • BCC
  • Actinic keratosis
  • Irritated haemangioma
  • Bowen’s disease
  • SCC
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47
Q

Describe the management of necrositing fasciitis

A
  • Early suspicion and surgical debridement
  • Antibiotics - 5 used
    • Penicillin
    • Flucloxacillin
    • Clindamycin
    • Gentamicin
    • Metronidazole
  • Clindamycin which switches off exotoxin production improves mortality
  • Activated protein C, evidence in NF is limited and it cannot be used within 24 hours of surgery
  • Immunoglobulin G (IVIG) - unproven no RCT, benefit?
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48
Q

Describe the topical therapies available for psoriasis treatment

A
  • Moisturisers - help reduce dryness, flaking
  • Steroids (reduce autoimmune response, redness, itching, inflammation)
  • Salicylic acid (to dissolve thick dead skin)
  • Slow down keratinocyte proliferation
    • Vitamin D analogues
    • Coal tar
    • Dithranol
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49
Q

Define ulceration

A

Surface of skin broken, integrity of epidermis lost

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50
Q

Which organisms are most commonly the causative agent in bacterial cellulitis?

A
  • Most common cause of bacterial cellulitis = S aureus
    • Carried by 30-40% of population, MRSA prevalence approx. 2%
    • Normally nose, moist areas of skin, type carried is very stable
  • Streptococcus pyrogenes is one of the most frequent pathogens of humans
    • Carriage 5-15% usually in the respiratory tract and vaginal tract
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51
Q

What skin changes are associated with internal malignancy?

A
  • Necrolytic migratory erythema
  • Erythema gyratum repens
  • Acanthosis nigricans
  • Erythema annulare
  • Sweet’s syndrome
  • Sister Mary Joseph nodule
    • Bulging nodule of umbilicus due to metastatic disease of abdomen/pelvis
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52
Q

What is erythema multiforme?

A
  • Self-limiting allergic reaction
  • HSV, EBV, occasionally drug
  • No or mild prodrome
  • Target lesions
  • Never –> TEN
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53
Q

How is the management of psoriasis determined?

A
  • Severity
  • What patient wants
  • What patient can cope with
  • If have arthropathy
  • Use scoring systems to dictate treatment plan
    • DLQI - disease life quality index, patient completes to determine impact of psoriasis on life
    • PASI - psoriasis area severity index, doctor fills out, give score and monitor if getting better with treatment
    • PEST - psoriasis epidemiology screening tool, tells about sore joints, refer to rheumatology if high
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54
Q

List the types of Herpes Simplex Virus (HSV)

A
  • Type 1 - stomatitis ‘cold sore’
  • Type 2 - genital herpes
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55
Q

What causes erythema nodosum?

A
  • Streptococcal infection
  • Pregnancy/oral contraception
  • Sarcoidosis
  • Drug induced
  • Bacterial/viral infection
  • Others
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56
Q

How are bites treated?

A
  • Routine prophylaxis not always recommended
    • Indicated in certain situations - deep, on the hands, splenectomised or immunocompromised patient, crush injury
  • Treatment, gram stain or wound and blood cultures
  • Aggressive debridement and abscess drainage
  • Cover staphylococci, anaerobes, pasteurella and capnocytophaga
  • Rabies immunoglobulin and vaccination if appropriate
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57
Q

What is angioodema?

A

Swelling under the skin or mucous membranes

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58
Q

What is the usual causative organism in cat/dog bites and which antibiotic should be used?

A
  • Organism - pasteurella multocida
  • Antibiotic - co-amoxiclab, doxycycline and metronidazole
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59
Q

Describe the distribution of acne

A
  • Face
  • Chest
  • Back/shoulders
    • Young, athletic men w/ disproportionate acne on shoulders/chest - suspicious of androgen excess/exogenous steroid use
  • Occasionally legs, scalp
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60
Q

How is urticaria treated?

A

Antihistamines, steroids, phototherapy, immunosuppression, omalizumab

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61
Q

What are the causes of urticaria?

A
  • Immune mediated
    • Type 1 IgE response
  • Non-immune mediated
    • Direct mast cell degranulation e.g. opiates, antibiotics, contrast media, NSAIDs
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62
Q

Describe the embryological origin of the skin

A
  • Epidermis is derived from ectoderm
  • 5th week, the skin of the embryo is covered by simple cuboidal epithelium
  • 7th week single squamous layer (periderm), and a basal layer
  • 4th months, an intermediate layer, containing several cell layers, is interposed between the basal cells and the periderm
  • Early foetal period the epidermis invaded by melanoblasts, cells of neural crest origin
  • Hair - 3rd month as an epidermial proliferation into dermis
  • Cells of the epithelial root sheath proliferate to form a sebaceous gland bud, sweat glands develops as down-growths of epithelial cords into dermis
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63
Q

What is the function of skin?

A

Three main functions - protection, regulation and sensation

  • Protection - primary function as a barrier (physical and immunological)
    • Mechanical impacts
    • Protects and detects pressure
    • Detects variations in extreme temperature
    • Barrier to micro-organisms
    • Barrier to radiation/chemicals
  • Regulation - physiological
    • Body temperature via sweat, hair and changes in peripheral circulation
    • Fluid balance via sweat and insensible loss
    • Synthesis of vitamin D
  • Sensation - network of nerve cells that detect and relay changes in the environment (heat, cold, touch and pain)
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64
Q

How is venous dermatitis managed?

A

Emollients

Mild/moderate topical steroid

Compression bandaging/stockings - improves venous drainage

Consider early venous surgical intervention

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65
Q

Describe the use of UV phototherapy in psoriasis treatment

A
  • Non-specific immunosuppressant therapy
  • Can reduce T cell proliferations
  • Encourages vitamin D and reduces skin turnover
  • UV-B light most commonly used
  • UV-A with psoralen photosensitiser
  • Risks - short term burning, longer term skin cancer
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66
Q

How can you objectively and subjectively measure severity of psoriasis disease and impact?

A

Using scoring tools such as PASI and DLQI

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67
Q

What skin changes are seen in vitamin B deficiencies?

A
  • B6 (pyridoxine) - dermatitis
  • B12 (cobalamin) - angular cheilitis
  • B3 (niacin) - pellagra
  • Causes dementia, dermatitis, diarrhoea
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68
Q

What skin changes are seen in steroid insufficiency i.e. Addison’s disease?

A
  • Hyperpigmentation - skin bronzing due to ACTH
  • Acanthosis nigricans
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69
Q

What is the difference between eczema and dermatitis?

A
  • Terms eczema and dermatitis interchangeable
  • Dermatitis - inflammation of the skin
  • Eczema more associated with atopic condition from childhood
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70
Q

What public health and personal holistic preventative measures aim to combat skin cancer?

A
  • British Association of Dermatologists publicity
  • British Skin Foundation research
  • Skin Cancer UK , Sun Awareness week, Drug company and Pharma sunblock advertisement
  • MacMillan Cancer Support, booklets, webpage, leaflets, help lines
  • Campaigns against tanning salons
  • Australian style slip/slap/slop sun protection
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71
Q

What is a mobilliform rash?

A

Rose-red flat (macular) or slightly elevated (maculopapular) eruption

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72
Q

How is chickenpox treated?

A
  • Self-limiting in children
  • Treat at-risk adults within 48 hours of symptoms (pregnant, immunocompromised, pneumonitis) - acyclovir PO/IV
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73
Q

List the types of soft tissue infections which can occur following exposure to water

A
  • Aeromonas spp
    • Fresh water
    • Rapidly developing infection associated with fever and sepsis
  • Edwardsiella tarda
    • Fresh water
    • Cellulitis, occasionally fulminant infection with bacteraemia
  • Erysipelothrix rhusiopathiae
    • Puncture wounds from crabs etc
    • Indolent localised cutaneous eruption, erysipeloid
  • Vibrio vulnificus
    • Salt or brackish water
    • Rapidly progressive necrotising infection, bullous cellulitis, sepsis
  • Mycobacterium marinum
    • Fresh or salt including fish tanks
    • Indolent infection, papules to ulcers, ascending lesions may resemble sporotrichosis
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74
Q

What are the symptoms of fifth disease?

A
  • Fever, headache, runny nose, followed by pruritic rash on face (‘slapped cheek’) as well as the torso and extremities
  • May also result in acute or persistent arthropathy, as well as so-called gloves-and-socks syndrome, characterized by papular, purpuric eruptions on the hands and feet
  • In addition, an acute cessation of red blood cell production may be triggered by the virus, with transient aplastic crisis, chronic red cell aplasia, hydrops fetalis, or congenital anaemia resulting
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75
Q

Which patients may get diagnostic/staging imaging in skin cancers?

A

Usually thicker melanomas e.g. >Breslow 2mm, stage III melanomas, evidence of lymph node involvement, high risk SCC CT scan, PET scan

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76
Q

How is PVL producing staph aureus managed?

A
  • Management involves drainage and treatment according to sensitivity patterns
  • Screen nose, throat, axilla, perineum and skin lesions for carriage
  • Decolonise using standard regimens
  • PCR for the toxin gene
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77
Q

What skin changes are seen in thyroid disorders?

A
  • Hypothyroidism - dry skin (non-specific but sometimes associated)
  • Grave’s disease (more specific signs)
    • Thyroid dermopathy/pretibial myxoedema
    • Thyroid acropachy - nail changes (clubbed fingers due to generalised soft tissue swelling)
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78
Q

List the characteristics of pigmented basal cell carcinomas

A
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79
Q

What skin changes are seen in steroid excess?

A
  • E.g. Cushing’s disease
    • Acne - different to teenage acne
      • Less comedonal, more inflammatory
      • Back and chest, face often spared
    • Striae - exaggerated stretch marks, in unusual areas
    • Erythema
    • Gynaecomastia - excess breast tissue in men
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80
Q

What causes pyoderma gangrenosum?

A
  • Inflammatory bowel disease
    • Crohn’s disease, ulcerative collitis
  • Rheumatoid arthritis
  • Myeloma
  • Others
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81
Q

List the subtypes of acne

A
  • Papulopustular - most common
  • Nodulocystic - more severe
  • Comedonal - just blackheads/whiteheads
  • Steroid induced - oral corticosteroids or exogenous
  • Acne fulminans - severe, sudden onset acne, systemically unwell (fever, inflammatory markers raised)
  • Acne rosacea - ‘adult’ form of acne
  • Hidradenitis (acne inversus)
    • Goes along with acne, affects folds of skin e.g. under arms, buttocks
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82
Q

Describe the features of the varicella zoster virus in shingles

A
  • Reactivation of dormant VZV (dorsal root ganglia)
  • Dermatomal distribution
  • Transmissible- isolate until last crop of vesicles crusted
  • May be very painful
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83
Q

Describe the prognosis of acral melanomas

A
  • Present late, people don’t notice until widespread
  • Poor prognosis
  • Surgical resection difficult
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84
Q

List the types of eczema

A
  • Endogenous
    • Atopic
    • Seborrhoeic
    • Discoid
    • Varicose
    • Pompholyx
  • Exogenous
    • Contact (allergic, irritant)
    • Photoreaction (allergic, drug)
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85
Q

Discuss different skin cancer staging tools and any UK guidelines on skin cancer management

A

SIGN guidelines melanoma

AJCC 8 staging for melanoma

BAD guidelines on management of melanoma

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86
Q

Describe the treatment of melanomas

A
  • Surgical excision - may need skin graft
    • Breslow <1mm - 1cm margin
    • Breslow >1mm - 2cm margin
  • Immunotherapy - ipilimumab, nivolumab
  • Immune check point/MEK inhibitors (trametinib)
  • Biologic antibodies e.g. BRAF genetic defects (dabrafenib)
  • Imaging - CT, MRI, PET
  • Long term follow-up, up to 5 years
  • Assessment for lymph node/organ spread (liver, spleen etc.)
    • Sentinel lymph node biopsy
  • Genetic testing in families, multiple primary melanomas
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87
Q

What is the differential diagnosis in bacterial cellulitis? How can they be differentiated?

A
  • Stasis dermatitis - absence of pain/fever, cricumferential, bilateral
  • Acute arthritis - joint involvement, pain on movement
  • Pyoderma gangrenosum - ulceration on legs, history of IBD
  • Hypersensitivity/drug reaction - exposure to allergens/drug, pruritis, absence of fever and pain
  • DVT - absence of skin changes or fever
  • Necrotising fasciitis - severe pain out of proportion, swelling, fever, rapid progression, systemic toxicity
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88
Q

What is a macule?

A

Flat skin lesion, can’t feel but can see, small (0.5cm)

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89
Q

Give examples of drugs which can cause skin reactions

A
  • Maculopapular rashes e.g. antibiotics
  • Photosensitive rashes e.g. diuretics, antibiotics
  • Severe idiosyncratic reactions e.g. Toxic Epidermal Necrolysis – anti epileptics, antibiotics
  • Urticarial reactions – e.g. antibiotics, opiates, NSAIDs, ACE inhibitors
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90
Q

Describe the epidemiology of basal cell carcinomas

A
  • Most common type of skin cancer
  • Approx. 3/10 Caucasians may develop a basal cell cancer within their lifetime
  • Much less common in darker skin types (type IV+) - genetic component if dark skin with BCC
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91
Q

How are squamous cell carcinomas treated?

A
  • Gold standard - surgical excision 4mm margin
    • May need skin grafts/complicated flap repair
  • Elderly/frail patient w/ comorbidities etc.
    • Curettage and cautery - better tolerated that surgery

Pre-malignant (squamous cell carcinoma in-situ)

  • Topical imiquimod/5-fluorouracil cream
  • Cryotherapy
  • Photodynamic therapy
  • Sun protection
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92
Q

Describe the anatomy of the skin

A
  1. Epidermis - stratum corneum, statum granulosum, stratum spinosum, stratum basale
  2. Basement membrane
  3. Dermis - contains glands, hair follicles
  4. Subcutaneous tissue
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93
Q

What is an erythematous skin lesion?

A

Red, inflamed

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94
Q

Describe the clinical manifestations of necrotising fasciitis

A
  • Remarkably rapid progression
  • Most common on the extremities e.g. legs
  • Initially erythema and swelling without sharp margins
  • Exquisite pain and tenderness
  • Lymphatic involvement is rare
  • Colour changes from red-purple to blue-gray
  • Skin breakdown and bullae with development of anaesthesia
  • Probing of the lesion reveals easy passage through tissues
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95
Q

How prevalent is psoriatic arthritis?

A

Up to 20% of patients with psoriasis develop arthritis - different patterns of sero-negative arthritis

96
Q

What is the usual causative organism in an SSTI in butchers/fish handlers and which antibiotic should be used?

A
  • Organism - erysipelothrix
  • Antibiotic - ciprofloxacin
97
Q

Describe the prognosis of basal cell carcinoma

A

Rarely metastasised or kills - good prognosis

98
Q

What causes necrobiosis lipoidica?

A

Due to microvascular cutaneous dysfunction in diabetes

99
Q

Why is a history of alcohol excess, tuberculosis and/or previous malignancy significant in treatment for psoriasis?

A
  • Systemic therapy often liver toxic
  • Immunosuppressives can resurge pre-existing or unknown tuberculosis
  • Immunosuppression could theoretically cause recurrence of malignancy - certain drugs higher risk
    • Need to know what type of tumour, if high risk tumour, completely resected?
    • Consider non-immunosuppressive
    • Liase with oncologist and surgeon, risks vs benefits, quality of life right now if severe psoriasis
100
Q

How is tinea classified?

A

Classification based on the affected region, such as tinea pedis for feet (“athlete’s foot”), tinea corporis for body, tinea capitis for head/scalp, and tinea cruris for groin (“jock itch”)

101
Q

How often are skin cells renewed?

A

Every 24hr skin sheds layer of dead cells, renewed fully approx. 28 days

102
Q

What is a pustule?

A

Small pus containing skin lesion

103
Q

What is the differential diagnosis for acrodermatitis enteropathica?

A

Nutritional deficiencies, necrolytic migratory erythema

104
Q

Describe the typical appearance of psoriasis (vs eczema)

A
  • Eczema - more diffuse, couldn’t easily draw around with a pen
  • Psoriasis
    • Could draw around edges very clearly
    • Normal skin around/between
    • Symmetrical distribution
    • Truncal component
    • Redness - salmon pink
    • Scaly due to high turnover of skin
    • Central part of back, behind/in ears and around hairline common distribution
    • On dark skin - more white appearance
105
Q

Describe the features of varicella zoster virus (chickenpox)

A
  • Often a self limiting childhood infection
  • Highly infectious - manage in side room
  • Contagious from day 8-21 (i.e. before symptoms on day 10
106
Q

Describe the aetiology of eczema

A
  • Aetiology - combination of genetic, immune and reactivity to a variety of stimuli
    • Inflammation in eczema primarily due to inherited abnormalities in skin, so called ‘barrier defect’ - thinner barrier protective seal of skin
    • Leads to increased permeability and reduces its antimicrobial function
    • An inherited abnormality in Filaggrin expression considered a primary cause of disordered barrier function, filaggrins are proteins which bind to keratin fibres in the epidermal cells
107
Q

Describe the appearance of necrobiosis lipoidica

A
  • Waxy appearance
  • Usually yellow discolouration
  • Often shins
  • Occasionally ulcerates and scars - avoid significant trauma
108
Q

Discuss the prognosis of each type of skin cancer and diagnostic measurements/markers or tests

A
  • Basal Cell Carcinoma – most treatment curative, good prognosis, highest risk separate second new lesion
  • Squamous Cell Carcinoma – most surgical excision curative but risk of recurrence, metastatic spread
    • Staging, risk assessment to guide prognosis, thickness of tumour, size, lymphatic invasion
  • Melanoma – most melanomas in good prognosis category with a thin histological Breslow thickness
    • In high risk, thicker melanomas, may carry out sentinel lymph node studies, CT scans, blood LDH
109
Q

What antibiotics are used to treat pasteurella infections?

A
  • Gram negative
  • Commonest pathogen isolated from bites
  • Treatment
    • Penicillins (fluclox much less active)
    • Cephalosporins
    • Tetracyclines
    • Quinolones
    • Macrolides
  • Clindamycin and erythromycin have high MICs - don’t use
110
Q

How is acrodermatitis enteropathica treated?

A

Zinc supplementation

111
Q

How is tinea treated?

A

Antifungal agents

112
Q

What causes contact dermatitis?

A
  • Precipitated by an exogenous agent
    • Irritant - direct noxious effect on skin barrier
    • Allergic - type IV delayed T cell hypersensitivity reaction
  • Common allergens
    • Nickel - jewellery, zips, scissors, coins
    • Chromate - cement, tanned leather
    • Cobalt - pigment/dyes
    • Colophony - glue, adhesive tape, plasters
    • Fragrance - cosmetics, creams, soaps
113
Q

List risk factors for sun damage to the skin

A
  • Natural UV sun exposure
  • Sunbeds
  • Photosensitising drugs
  • Radiotherapy
  • Immunosuppression
  • Occuptation
    • Outdoor workers
    • Pilots
    • Armed forces
    • Gardeners
114
Q

What are the complications associated with chickenpox?

A
  • Congenital abnormalities if acquired during pregnancy
  • Problematic in adults - pneumonitis
115
Q

Describe the normal skin flora

A

Diphtheroids

Corynebacteria

Anaerobes (yeasts)

Staphylococci (S. aureus)

Streptococci (A, B, C, G)

116
Q

How prevalent are squamous cell carcinomas?

A

2nd commonest skin cancer

117
Q

How is dermatitis herpetiformis treated?

A
  • Topical steroids
  • Gluten free diet
  • Oral dapsone
118
Q

What causes bacterial cellulitis?

A

Breach of the normal flora skin barrier allows pathogens to infect, can spread throughout the deeper dermis and fat

Oedema, pain, erythema, warmth (locally at site of breach) - PO antibiotics

Invasive disease - IV antibiotics

119
Q

Which endocrine disorders can features skin changes?

A
  • Thyroid
  • Diabetes
  • Cushing’s/steroid excess
  • Sex hormones
120
Q

List the causative organisms of tinea

A

Trichophyton (most common), microsporum and epidermophytan

121
Q

What are the key government targets for skin cancer treatment?

A

2 week USOC referral to be seen, 31 day commencement of treatment from diagnosis, first treatment within 62 days of referral

122
Q

What are bullae?

A

Large vesicles - fluid filled, blister-like

123
Q

Describe the use of oral isotretinoin in acne treatment?

A
  • Oral retinoid licensed for severe acne vulgaris
  • Concentrated form of vitamin A
  • Reduces sebum, plugging and bacteria
  • Remission of acne in around 80% teenagers
  • Standard course for 16 weeks 1mg/kg
124
Q

Describe the typical appearance of a superficial spreading malignant melanoma

A
  • Irregular, asymmetrical
  • Tumour lump in centre
  • Pigmented
125
Q

Describe the features of PVL producing staph aureus

A
  • PVL is a toxin which destroys white blood cells
  • <2% of UK staph aureus isolates, in the UK most of these are MSSA
  • Community isolates more likely to carry the toxin than hospital
  • Usually associated with necrotising, pyrogenic skin infections but also cause septic arthritis, fulminant pneumonia
  • The role the toxin has in virulence is unclear
  • Suspect in patients with recurrent/multiple boils esp. those in close contact situations
126
Q

How can psoriasis affect the nails?

A
  • Psoriatic nails
    • Lift off nail bed (oncholysis)
    • Pitting of nail - pin-point depressions (can also occur due to trauma)
    • Nails thickened - increased turnover
  • Destructive nail disease raises suspicion of psoriatic arthritis
127
Q

Is there any significance to genetic testing in skin cancer in individuals and families?

A
  • Rarely genetic testing in patients with multiple melanomas or family history 2+ first degree relatives e.g. CDKN2A and CDK4
  • PTCH gene in multiple BCCs seen in Gorlin’s syndrome
128
Q

Give examples of drugs which can cause a photo-toxic drug rash

A

Quinine, bendroflumethazide

129
Q

What signs are associated with a islet cell tumour of the pancreas?

A
  • Necrolytic migratory erythema
  • Hyperglycaemia
  • Diarrhoea
  • Weight loss
  • Glossitis
130
Q

What is Keloid scarring?

A
  • Large scars from small lesions
  • Occurs in genetically predisposed individuals, esp. with dark skin
131
Q

How is toxic epidermal necrolysis managed?

A
  • Stop suspect drugs
  • Dermatological emergency
  • In-patient management dermatology, ITU, burns
  • Analgesia
  • Fluid balance - SCORTEN severity scale
  • Special mattress, sheets
  • Infection control/prophylaxis
  • Non-adherent dressings
  • Urology, gynae, ophthalmology input
  • Some reports >50% mortality rate
132
Q

How prevalent is psoriasis?

A

1.5-3%

133
Q

What are vesicles?

A

Small, fluid filled, blister-like skin lesions

134
Q

When a skin cancer diagnosis is confirmed, what is the most appropriate further management for each type?

A

BCC - full surgical excision with 4mm margin

SCC - full surgical excision with 4-5mm margin, consideration of radiotherapy

Melanoma - wide margin wide local excision (1-2cm), lymph node assessment, BRAF genetic status, targeted anti-BRAF treatment e.g. dabrafenib or immunotherapies e.g. nivolumab

135
Q

How is seborrhoeic dermatitis treated?

A
  • Scalp - medicated anti-yeast shampoo
    • I.e. antifungal ketoconazole - Nizoral, Selsun
  • Face - anti-microbial, mild steroid
    • I.e. Daktacort cream
  • Simple moisturiser
  • Rarely systemic antifungals
  • Often improves with UV/sunlight - reduces abnormal immune reactions
136
Q

What is necrolytic migratory erythema?

A
  • Sometimes called the glucagonoma syndrome
  • Rare disease
  • Erythematous, scaly plaques on acral, intertriginous and periorificial areas
  • Association with an islet cell tumour of the pancreas
137
Q

Describe the management of infected burns

A
  • Cleaning
  • Dressings
  • Topical antimicrobials (gauzes/ointments/creams)
    • E.g. silver sulfadiazine, Bismuth-compounds, chlorhexidine - may impact healing
  • Topical antibiotics e.g. bacitracin
  • Systemic antibiotics (directed by culture results), required in invasive infection
  • Evidence base for comparison of individual agents poor
138
Q

What skin changes are seen in zinc deficiency?

A

Acrodermatitis enteropathica

  • Inherited or acquired condition
  • Pustules, bullae, scaling (acral and perioral in distribution)
  • Inherited - mutation on SLC39A, which encodes an intestinal zinc transporter
  • In infants, deficiency can follow breast-feeding, when breast milk contains low levels of zinc
  • In adults, disease can occur after total parenteral nutrition without zinc supplementation
    • Alcoholism
    • Malabsorption states
    • Inflammatory bowel disease
    • Bowel surgery
139
Q

What systemic conditions can be indicated by changes in the skin?

A
  • Endocrine disease
  • Internal malignancy
  • Nutritional deficiency
  • Systemic infection
  • Systemic inflammatory disease
140
Q

How is tinea diagnosed?

A

Potassium hydroxide preparation from a skin scraping

141
Q

How is erythroderma treated?

A
  • Treat underlying skin disorder, supportive
  • Fluid/temperature balance
142
Q

What skin changes can be seen in diabetes?

A
  • Necrobiosis lipoidica
  • Diabetic dermopathy
  • Scleredema (not scleroderma - connective tissue disorder)
  • Leg ulcers
  • Granuloma annulare
143
Q

Describe the appearance of seborrhoeic dermatitis

A
  • T zone - central face and forehead
  • Finer scaling than atopic eczema
  • Can go all the way down to chest
  • Greasy scales
144
Q

What causes erythema infectiosum (fifth disease)?

A
  • Human parvovirus B19 via respiratory droplets
  • Incubation period of 4-14 days (up to 20 days) and may also be spread through blood or blood products (e.g. maternal-foetal transmission)
    • If mother contracts early in pregnancy can mount immunity against but in 3rd trimester no time for immunity so virus can be passed on to baby - causes aplastic crisis
145
Q

List the subtypes of basal cell carcinomas

A
  1. Nodular
  2. Superficial
  3. Pigmented
  4. Morphoeic/sclerotic
146
Q

Describe the clinical features of infant atopic eczema

A
  • Itchy
  • Occasionally vesicular (small blisters)
  • Often facial component
  • Secondary infection - yellow/golden crust, serous fluid
  • <50% still have eczema by 18 months
  • Occasionally aggravated by food (i.e. milk)
    • Food allergy testing if v severe
147
Q

How are basal cell carcinomas treated?

A
  • BCC on routine waiting list - no urgency to be seen as so slow growing/benign
  • Gold standard - surgical excision 3-4mm margin
  • If older/frail patient who can’t tolerate surgery
    • Curettage and cautery - scrape away and cauterise base (circular scalpel)
    • Cryotherapy - freezing with liquid nitrogen
    • Photodynamic therapy
    • Topical imiquimod/5-fluorouracul cream - stimulate body’s immune system to attack tumour cells
    • Moh’s micrographic surgery
      • Surgical excision with narrow margin - used in aesthetically sensitive areas e.g. face
      • Take out with narrow margin then analyse to see if surgically clear - keep going until margins are clear
148
Q

How is the severity of melanomas graded?

A
  • Breslow depth (mm)
  • Clarks levels 1-5 - skin layer reached (not used as widely)
149
Q

Describe the typical appearance of a squamous cell carcinoma

A
  • Not shiny
  • Keratin crust layer
  • Lump within skin
  • No broken blood vessels
  • History important - quicker onset than basal cell carcinoma
150
Q

Where is diabetic dermopathy often seen?

A

Non-specific, often lower legs but can be generalised

151
Q

List the types of hypersensitivity reactions

A

Type 1 IgE mast cell - anaphylaxis

Type 2 IgG cytotoxic - transfusion reaction

Type 3 IgG immune complex - serum sickness

Type 4 delayed T cell - contact dermatitis

152
Q

Describe the features of pulstular psoriasis

A
  • Acute onset
  • Inflammatory cells in pustules on skin
  • Will also have high temperature and feel unwell
  • Secondary infection risk
  • Micropustules - usually sterile, acute loads of inflammatory cells (usually neutrophils)
153
Q

Describe the development of melanomas

A
  • Most common in skin (but can be bowel, eye, brain)
  • DNA damage - mainly UV, rarely genetic
  • Radial growth phase (across surface of skin), then vertical growth (deep in skin)
  • Spread via lymphatics (+ haematogenous)
  • Pre-malignant form - hard to diagnose (histological diagnosis so biopsy needed)
154
Q

Describe the mechanism of skin allergy

A
  • Skin irritation by nonallergenic and allergenic compounds induces Langerhan’s cell migration and maturation
  • Langerhan’s cells migrate from epidermis to draining lymph
  • Initial sensitization takes 10-14 days from initial exposure to allergen (nickel, dye, rubber etc.)
  • Once an individual is sensitised to a chemical, allergic contact dermatitis can then develop within hours of repeat exposure
155
Q

What are the predisposing factors for cellulitis?

A
  • General
    • Non-modifiable - pregnancy, white Caucasian
    • Modifiable - venous insufficiency, lymphoedema
  • Local - portal of entry for bacteria to enter
    • Non-modifiable - trauma, animal/insect bites, tattoos
    • Modifiable - ulcers, eczema, athletes foot, burns, surgical
156
Q

How are immunobullous disorders treated?

A
  • Reduce autoimmune reaction - topical/oral corticosteroids
  • Steroid sparing agents i.e. azathioprine, anti-inflammatory tetracyclines
  • Burst any blisters
  • Dressings and infection control
  • Check for oral/mucosal involvement
  • Consider screen for underlying malignancy
157
Q

What precautions must be taken when treating acne with oral isotretinoin?

A

Pregnancy prevention program

  • Teratogenic
  • Need to be on two forms of contraception
  • Take a pregnancy test every 4 weeks during treatment, before commencing treatment and a month after finishing
  • If become pregnant during treatment need to discuss with obstetrician whether to continue pregnancy
  • Can be difficult if in young girl, with parents etc.
  • If refuse to follow pregnancy prevention need to sign legal opt out form, doctors take no responsibility
158
Q

List the characteristics of morphoeic/sclerotic basal cell carcinomas

A
  • Indistinct margins
  • Shiny
  • Broken BVs
  • No ulceration, hard to see edge
  • Longer time before patient presents
159
Q

Describe the use of systemic therapy in psoriasis management

A
  • Immunosuppressants - methotrexate, ciclosporin
  • Acitretin (oral retinoid/vitamin A)
  • Dimethyl fumarate
  • Apremilast
  • Biologics - adalimumab (anti TNF), ustekinumab (anti IL 12/23)
  • Most drugs have potent side effects i.e. liver dysfunction, hypertension, risk of infection - so need to be tailored to patient
160
Q

List the main skin cancer types

A
  • Basal cell carcinoma (known colloquially as rodent ulcer) - from basal cells
  • Squamous cell carcnoma - from keratinocytes
  • Malignant melanoma - from melanocytes (also in brain, bowel, eye etc.)
161
Q

Describe the clinical features of atopic eczema

A
  • Itchy, inflammatory skin condition
  • Associated with asthma, allergic rhinitis, conjunctivitis, hayfever (atopy)
  • High Ig-E immunoglobulin antibody levels
  • Genetic and hyperreactive immune aetiology
  • 10-15% infants affected
  • Remission occurs in 75% by 15 y/o
  • 2/3 have a family history of atopy
162
Q

Describe the features of staphylococcal scalded skin syndrome

A
  • Staph aureus strains producing an exfoliative exotoxin
  • Widespread bullae formation and exfoliation
  • In the neonate it is known as Ritter’s disease or Pemphigus neonatorum
  • Epidemics have occurred in nurseries
  • Fever, tenderness and scarlatiniform rash
163
Q

What is erythroderma?

A
  • Descriptive term - intense, widespread reddening of the skin
  • >80-90% involvement, erythema
164
Q

How does vitamin D deficiency develop? What are the consequences?

A
  • During exposure to sunlight, solar UVB photons (290-315nm) are absorbed by 7-dehydrocholesterol in the skin and converted to previtamin D(3)
  • Pre-vitamin D(3) undergoes transformation within the plasma membrane to active vitamin D(3)
  • During our winter there is minimal pre-vitamin D(3) production in the skin, few foods natural contain Vit D
  • Associations of Vitamin D deficiency - increased risk of common cancers, autoimmune diseases, infectious diseases and cardiovascular disease
165
Q

What is a papule?

A

Small (0.5-1cm) raised skin lesion

166
Q

Describe the effect of ultraviolet radiation on the skin

A
  • Damaging effects of ultraviolet on skin - direct cellular damage and alterations in immunologic function. Direct effects include photoaging, DNA damage and carcinogenesis
  • P53 tumour suppressor genes mutated by DNA damage. Implicated in development of melanoma and non-melanoma skin cancers
  • Keratinocytes and melanocytes work together to protect cells from UV DNA damage
  • Chronic UV exposure in human leads eventually to loss of skin elasticity, fragility, abnormal pigmentation and haemorrhage of blood vessels. Wrinkles and premature ageing.
167
Q

What is erythema gyratum repens?

A
  • Rare
  • Very distinctive skin disease
  • Reddened concentric bands whorled woodgrain pattern
  • Severe pruritus and peripheral eosinophilia
  • Strong association with lung cancer
  • Association with breast, cervical, GI cancers less strong
  • Treatment of the underlying malignancy treats skin disease
168
Q

Describe some patterns and distributions of skin lesions which might occur clinically

A
  • Widespread, truncal
  • Urticarial, weals, dermographism
  • Localised drug reactions, fixed drug eruptions
  • Mucosal involvement
  • Sun exposed- photosensitive reactions
  • Contact reactions to creams
169
Q

List the characteristics of nodular basal cell carcinomas

A
  • Commonest basal cell carcinoma
  • Nodule i.e. >0.5cm raised lesion
  • Shiny ‘pearly’
  • Telangiectasia/blood vessels (‘lightning bolt’ BV)
  • Neat edge - rolled edge
  • Often ulcerated centrally
170
Q

What is the risk that a squamous cell carcinom metastasises?

A
  • Risk of metastasis from a high-risk SCC from 10-30% (high risk sites - ears, lips, genital skin, burns/radiotherapy)
  • High-risk features
    • Site - lips, ears, genitals
    • Pathology - poorly differentiated, thicker lesion (invaded deeper)
    • Invasion of lymphatics, vascular spread
    • Immunosuppression
171
Q

What causes psoriasis?

A
  • T cell mediated autoimmune disease
  • Abnormal infiltration of T cells
    • Release of inflammatory cytokines including interferon, interleukins and TNF (tumour necrosis factor)
    • Increased keratinocyte proliferation - skin turnover much faster (thickening)
  • Environmental and genetic factors
    • Linked to - psoriatic arthritis, metabolic syndrome, liver disease/alcohol misuse, depression
172
Q

Describe the prevelance of measles

A
  • Pre-vaccine era - 3-4 million infections/year
    • 500 deaths
    • 48,000 hospitalisations
    • 1000 encephalitis
  • 1996 - first measles vaccine
  • 1988 - MMR
  • 2019 - UK loses its measles-free status - vaccine coverage not high enough
173
Q

List the treatments available for psoriasis

A

In order of increasing effectiveness (and toxicity)

  • Topical creams and ointments
  • Phototherapy light treatment - medical sunbed treatment
  • Systemic drugs/immunosuppressants
  • Biologic therapies
174
Q

How is scarlet fever treated?

A

7-10 day course amoxicillin

175
Q

What causes venous dermatitis?

A
  • Underlying venous disease
  • Affects lower legs
  • Incompetence of deep perforating veins
  • Increased hydrostatic pressure
  • Skin stretched, inflamed and breaks down
  • Skin splits - venous/varicose ulcer
176
Q

List the featues of erysipelas

A
  • Involves the upper dermis and superficial lymphatics
  • Raised lesions with clear line of demarcation
  • Classically butterfly involvement of the face but now accounts for only about 20% of cases, the legs are affected in up to 80% of cases
  • Erysipelas involves the ear, cellulitis does not
  • Infants and elderly
  • Usually group A strep, rarely B, C, G and staph aureus
  • Elevated ASOT 10 days
  • Clinical diagnosis - based on how the skin looks
  • Recurrence in 30% over 3 years
  • Erysipelas involves the ear but cellulitis does not
177
Q

List the characteristics of superficial basal cell carcinomas

A
  • Shiny, rolled edge, nodular, BVs
  • Sun damaged sites - limbs, back, chest (less common on face/head)
178
Q

List the symptoms of HSV

A
  • Primary infection asymptomatic 60%
  • Vesicular, may be painful
  • Recurrent - virus latent in sensory nerve ganglia
179
Q

What is the usual causative organism in typical cellulitis and which antibiotic should be used?

A
  • Organism - S pyrogenes
  • Antibiotic - ampicillin or flucloxacillin
180
Q

What are the treatment options for acne?

A
  • Reduce plugging
    • Topical retinoid, topical benzoyl peroxide
  • Reduce bacteria
    • Topical antibiotics (erythromycin, clindamycin)
    • Oral antibiotics (tetracyclines, erythromycin)
      • Antibiotics reduce bacteria but also anti-inflammatory
    • Benzoyl peroxide reduced bacterial resistance
  • Reduce sebum production
    • Hormones - anti-androgen i.e. Dianette/OCP
  • Dietary modification - controversial
    • Reduced dietary/glycaemic load e.g. milk, chocolate
  • Oral isotretinoin
181
Q

What are the symptoms of measles?

A
  • Fever, cough, coryzal, conjunctivitis
  • 3 days post start symptoms - white Koplik spots appear on tongue
  • 3-5 days post start symptoms - maculopapular red rash
    • Starts on face/hairline as flat spots
    • Spreads downwards involve neck/trunk/arms/lower legs
182
Q

For the three main skin cancers consider the initial diagnostic tests taken

A

Basal Cell Carcinoma – often clinical, sometimes biopsy e.g. punch biopsy or curette or excise whole

Squamous Cell Carcinoma – often clinical, sometimes biopsy e.g. punch biopsy or curette or excise whole, check lymph nodes

Malignant Melanoma – Photography, ideally full excision (except in large lesions, smaller diagnostic incisional), lymph node assessment

183
Q

List the common drugs which cause acute drug rashes

A
  • Antibiotics i.e. penicillins, trimethoprim
  • NSAIDs
  • Chemotherapeutic agents
  • Psychotropic e.g. chlorpromazine
  • Anti-epileptic e.g. lamotrigine, carbamazepine
  • Cardiac drugs e.g. beta blockers, ACE, anticoagulation
184
Q

How is HSV treated?

A

Acyclovir (topical, oral, IV)

185
Q

List immunobullous disorders

A
  • Bullous pemphigoid
  • Mucous membrane pemphigoid
  • Paraneoplastic pemphigoid
  • Pemphigus (e.g. Pemphigus vulgaris)
  • Dermatitis herpetiformis (coeliac disease)
186
Q

Which antibiotic should be used in SSTIs with penicillin allergy?

A

Doxycycline, clindamycin or vancomycin

187
Q

What is tinea?

A
  • Superficial dermatophyte infection characterized by scaly, inflammatory or non-inflammatory patches
  • Generally limited to the epidermis and expands in a centrifugal pattern, transmission is via direct skin-to-skin contact
  • Preferentially inhabit warm, moist areas of the skin and may spread by skin contact, contact with contaminated items or contact with infected animals
188
Q

List the subtypes of melanomas

A
  • Superficial spreading malignant melanoma - commonest, irregular brown patch
  • Nodular melanoma - nodule/lump, pigmented
  • Acral melanoma - hands/feet, nails
  • Amelanotic melanoma - no pigment
  • Precursors - larger, often men on scalp/nose
    • Lentigo maligna
    • Melanoma in situ
189
Q

What investigations should be done in urticaria?

A

Often none, not normally allergy driven (don’t do allergy testing, not patch testing)

190
Q

Describe the appearance of granuloma annulare

A

Circular

Affects back of hands and feet

191
Q

Give examples of benign skin lesions

A
  • Most lesions benign - 75% referral skin cancer benign
  • E.g.
    • Fibro-epithelial polyps - ‘skin tags’
    • Seborrhoeic warts/keratosis (can be misdiagnosed as melanoma)
192
Q

What is the differential diagnosis for amelanotic melanomas?

A
  • Basal cell carcinoma
  • Irritated viral wart
  • Pyrogenic granuloma
193
Q

What is the usual causative organism in necrotising fasciitis and which antibiotic should be used?

A
  • Organism - clostridium perfringes/S. pyrogenes
  • Antibiotic - penicillin + flucloxacillin + clindamycin + gentamicin + metronidazole
194
Q

What skin changes are seen in vitamin C deficiency?

A
  • Punctate purpura/bruising
  • Corkscrew spiral curly hairs
  • Patchy hyperpigmentation
  • Dry skin
  • Dry hair
  • Non-healing wounds
  • Inflamed gums
195
Q

List the causes of acute urticaria

A
  • Unknown
  • Viral infections
  • Medications - NSAIDs, aspirin, ACE
  • Foods and food additives
  • Parasitic infections
  • Physical stimulants - cold, pressure, solar, cholinergic, aquagenic
196
Q

What effect do sex hormone disorders have on the skin?

A
  • Testosterone - acne, hirsutism
    • Polycystic ovarian syndrome
    • Testicular tumours
    • Testosterone drug therapy
  • Progesterone - acne, dermatitis
    • Congenital adrenal hyperplasia
    • Contraceptive treatment
197
Q

What is toxic epidermal necrolysis?

A
  • Dermatological emergency
  • Majority drug induced
  • ? Disease spectrum SJS –> TEN
  • If <10% skin involvement - SJS
  • Most severe mucous membrane involvement
198
Q

List the causes of erythroderma

A
  • Psoriasis
  • Eczema
  • Drug reaction
  • Cutaneous lymphoma
  • Others
199
Q

Define burns

A

Damage to the skin (heat, chemical, radiation) causing protein denaturation

200
Q

What symptoms may a patient with psoriasis complain of?

A
  • Sometimes itch
  • Occasional pain if thick plaques on hands and feet with fissuring
201
Q

What is the pH of skin?

A

Slightly acidic - 5.4

Due to lactic and amino acids

202
Q

Describe the typical distribution of atopic eczema

A
  • Symmetrical distribution
  • Flexural sites - antecubital fossa, popliteal fossa
  • Broken skin due to itch
  • Thickens with damage over time
203
Q

What is acanthosis nigricans?

A

Smooth, velvet-like, hyperkeratotic plaques in intertriginous areas e.g. groin, axillae, neck

204
Q

What are the options for management in SSTIs?

A
  • Surgery
  • ITU/HDU
  • IV immunoglobulins (no good evidence)
  • Antibiotics - IV or oral?
205
Q

Describe the clinical features of scarlet fever

A
  • Diffuse red blush appears on the second day of infection, point of deeper red blanch on pressure
  • Starts on the upper chest and spreads to the trunk, neck and extremities
  • Occlusion of the sweat glands gives the skin a sandpapery touch
  • Palms, soles and face are usually spared
  • Circum-oral pallor
  • White strawberry tongue, then red strawberry tongue
  • Severe cases can be characterised by high fever and systemic toxicity
  • Rash fades over the course of a week and desquamates over several weeks
  • Mild eosinophilia in the early stages
206
Q

Describe the prognosis of melanomas

A
  • Accounts for 75% of deaths from skin cancer
  • Depth of presentation determines prognosis/treatment (use Breslow depth)
  • 5 year survival in nonulcerated tumours is
    • 97% for Breslow thickness of 0-1.0mm
    • 91% for 1.01-2.0mm
    • 79% for 2.01-4.0mm
    • 71% for >4.0mm
207
Q

List the three main skin cancers, diagnostic clinical features and symptoms which can occur with each

A

Basal cell carcinoma - ulceration, telangiectasia, pearly margin, pink/red crusting, bleeding

Squamous cell carcinoma - keratotic, crusting, bleeding, scaly, pain

Melanoma - normally hyperpigmentation, irregular macule sometimes nodule, rarely ulcerated

208
Q

What causes a subungal melanoma?

A
  • Melanocytic lesion at nail matrix
  • Drags pigmentation out as nail grows
  • Presents late, poorer prognosis
  • Surgically hard to resect
209
Q

How is granuloma annulare diagnosed?

A

Histological diagnosis - granuloma seen under microscope

210
Q

What hair/nail changes can be seen in systemic diseases and what causes them?

A
  • Alopecia areata hair loss (autoimmune)
  • Hair thinning
    • B12
    • Iron deficiency
    • Lupus
    • Hypothyroidism
  • Male pattern balding - androgen excess
  • Nail clubbing, nail fold telangiectasia
211
Q

List the features of impetigo

A
  • Staphylococcus infection of epidermis
  • Often peri-oral
  • Honey-coloured crust
  • Affects primarily children or sports person (contact sports - rugby, wrestling)
  • Transmissible
212
Q

How thick is skin? Why is this important?

A

Varies in thickness from 1mm on eyelids to 3mm on palms/soles - thicker skin needs stronger topical treatment

213
Q

When should SSTIs be admitted to hospital?

A
  • Class III or IV
  • Class II (unless have OPAT facilities available)
  • Severe or rapidly deteriorating cellulitis
  • Very young (under 1 year of age) or frail
  • Immunocompromised
  • Facial cellulitis
  • Suspected orbital or periorbital cellulitis (admit under ophthalmology)
214
Q

Define psoriasis

A

Chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin

215
Q

How are skin colour types classified?

A
  1. Very fair - always burns, cannot tan
  2. Fair - usually burns, sometimes tans
  3. Medium - sometimes burns, usually tans
  4. Olive - rarely burns, always tans
  5. Brown - never burns, always tans
  6. Black - never burns, always tans
216
Q

How can necrostising fasciitis be differentiated from cellulitis?

A

Initial PAIN, becoming PAINLESS

RAPID spread

SYSTEMICALLY unwell

DUSKY skin and NECROSIS

MAY have skin crepitus

217
Q

List cutaneous tumour syndromes

A
  • Gorlin’s syndrome
    • Multiple BCCs, jaw cysts, risk of breast cancer
  • Brook spiegler syndrome
    • Multiple BCCs, trichoepitheliomas
  • Gardner syndrome - soft tissue tumours, polyps, bowel cancer
  • Cowden’s syndrome - multiple hamartomas, thyroid, breast cancer
218
Q

At what age does psoriasis commonly present?

A

Age onset often two peaks age 20-30 y/o or 50-60y/o

219
Q

What should be done in a bacterial cellulitis which fails to improve?

A
  • Mark area of inflammation to monitor progress - no progress?
  • Consider
    • Resistant organisms
    • Admission to hospital
    • Underlying condition - bone infection, deep-seated infection, abscess, PVD
    • Alternate diagnosis - DVT, chronic changes
220
Q

Describe the aetiology of acne

A

Accumulation of epithelial cells and keratin

Keratin and thick sebum blockage of sebaceous gland

Androgenic increased production and viscosity

Proprioni bacterium proliferation, mild inflammation - most common

Longer marked inflammation, more trauma - higher chance of permanent scarring

221
Q

How should burns be managed?

A
  • Rapid bacterial colonisation, but infection must be diagnosed clinically
  • Swabs of burns rarely sterile - interpretation of results needs clinical judgement
  • Involves plastic surgeons and microbiology teams early
  • Surgery
222
Q

Describe the receptors responsible for skin sensation

A
  • Encapsulated nerve endings - Meissner, Pacini and Ruffini corpuscles or free nerve endings associated with Merkel cells
  • Merkel cells at the base of the epidermis, respond to sustained gentle and localised pressure, assess shape/edge
  • Meissner corpuscles below epidermis, on the palmar surfaces of the fingers and lips, sensitive to light touch
  • Ruffini’s corpuscles, in the dermis, sensitive to deep pressure and stretching
  • Pacinian corpuscles are mechanoreceptors in the deep dermis, sensitive to deep touch, rapid deformation of skin surface and around joints for position/proprioception
223
Q

Describe a drug induced psoriasiform rash

A
  • Psoriasis-like
  • Well demarcated pink erythema with scale
  • Sudden onset, no FHx
  • Causes e.g. lithium, beta blockers
224
Q

How are management decisions made in SSTIs?

A
  • Assess severity
    • Mark borders - can see progression
  • Anatomical site
    • Facial particularly worrying - can have cranial extention
  • Comorbidities
  • Healthcare associated infection
225
Q

What causes scarlet fever?

A
  • Results from infection with a streptococcal strain that elaborates streptococcal pyrogenic exotoxins or erythrogenic toxins
  • Usually post pharyngeitis but may complicate wound infections and post-partum infections
226
Q

What is the treatment for cutaneous anthrax?

A

5 antibiotics

  • Penicillin
  • Flucloxacillin
  • Clindamycin
  • Ciprofloxacin
  • Metronidazole
227
Q

What causes hand-foot-and-mouth disease?

A
  • Viral illness with oral and distal-extremity lesions
  • Coxsackie virus A16 and typically affects children and infants
  • Highly contagious during the first week of infection
  • May lead to epidemics from direct contact with nasal and oral secretions or faecal material
  • Incubation period typially averages 3-7 days
228
Q

How is hand-foot-and-mouth disease treated?

A

Supportive care

229
Q

What is necrotising fasciitis?

A
  • Rapidly spreading infection of subcutaneous fascia (over hours) - difficult to diagnose and more difficult to manage effectively
  • Medical emergency - mortality 70% untreated
  • Mixed infections - aerobes and anaerobes
  • Toxin mediated - superantigens and cytokines
230
Q

Describe the features of seborrhoeic dermaitis

A
  • Chronic, scaly inflammatory condition
  • Often thought to be ‘dandruff’
    • Not a diagnosis - usually has underlying cause
  • Face, scalp and eyebrows, occasionally upper chest
  • Overgrowth of Pityrosporum Ovale yeast
  • Can be worse in teenagers
  • Occasionally confused with facial psoriasis
  • Can be severe in HIV - recognised diagnostic feature of HIV
231
Q

What is the purpose of a skin cancer MDT? Who is present?

A

Skin cancer MDT - dermatologist, plastic surgeon, maxillo-facial surgeon, oncologist, pathologist, admin cancer tracker, MacMillan skin cancer specialist nurses

Confirm diagnosis, confirm clinical and pathological staging, suggest a treatment plan, discuss difficult scenarios

232
Q

Describe the typical presentation of each types of skin cancer

A
  • Basal cell carcinoma
    • Very slow growing, often many months even years
    • Sun exposed sites, often head and neck, nose, paranasal areas
    • Any age with significant sun exposure late 20’s onwards
    • Starts small, a few MM and expands, can be flat superficial type or start as small elevated papule becoming a nodule
  • Squamous cell
    • Can be mixed onset, sometimes slow insidious onset, occasionally rapidly progressive
    • Any sun exposed site, can be on other areas e.g. chronic ulcers, burns, trauma, radiation treatment zones
    • Rarely anogenital skin
    • Higher risk zones ears, lips
    • Usually middle age – elderly
    • Metastatic LN spread can occur
  • Melanoma
    • Most melanomas don’t originate in pre-existing melanocytic naevi, rather in normal sun damaged skin
    • Men – upper back, females lower posterior legs, but any site, usually sun damaged areas
    • Unusual sites, genitals, acral, nails
    • Relatively slow growing over months area of pigmentation rarely not pigmented
    • Can become nodular or ulcerated
    • Metastatic spread, lymph nodes, organomegaly
233
Q

What causes immunobullous disorders?

A

Autoantibodies to various skin component i.e. basement membrane protein in BP on skin biopsy

234
Q

Describe the clinical features of acne

A
  • For acne diagnosis need
    • Papules
    • Pustules
    • Comedones - closed (whiteheads) and open (blackheads - sebum oxidised), can have either or both
  • Erythema
  • Nodules
  • Cysts
  • Scarring
  • Hyperpigmentation in darker skin types
235
Q

What causes diabetic ulcers to form?

A

Pathogenesis multifactoral - neuropathic, arterial, venous

236
Q

Describe the clinical classification system for SSTIs

A
  • Class I
    • No systemic toxicity
    • No co-morbidities
    • Oral antibiotics
    • Outpatient
  • Class II
    • +/- systemic illness
    • Co-morbidities - PVD, obesity, venous insufficiency
    • IV antibiotics
    • Hospital for at least 48 hours then PO Rx
  • Class III
    • Significant systemic illness
    • Unstable
    • IV antibiotics
    • Hospital
  • Class IV
    • Sepsis syndrome/necrotising fasciitis
    • Unstable
    • IV + surgery
    • Hospital
237
Q

How is atopic eczema management?

A
  • Emollients
  • Topical steroids - encourage protective barrier to reform and reduce abnormal immune response/inflammation
  • Bandages - especially in young children to stop itching
  • Antihistamines - mostly used for sedative effects (not anti-itch, anti-allergy)
  • Antibiotics/antivirals
  • Education for parents/child - National Eczema Society
  • Avoidance of exacerbating factors
    • Rarely dietary avoidance/house dust mite etc.
  • Systemic drugs e.g. ciclosporin, methotrexate (immunosuppressive)
  • Newest biologic agent IL4/13 blocker - Dupilumab

medicine year 3 (15 decks)

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