Dermatology Flashcards

1
Q

Briefly summarise the management of eczema

A

Management is based on maintenance and management of flares:

  • Lifestyle: avoid triggers (foods, stress, washing powders, soaps etc..)
  • Emollients
  • Use emollients or soap substitutes instead of soap
  • Topical steroids
  • Wet wraps during flares
  • Other specialist management in severe eczema: zinc impregnated bandages, topical tacrolimus, phototherapy, oral corticosteroids, other immunosuppressants (e.g. azathioprine, methotrexate)
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2
Q

State some examples of:

  • Thin emollient creams
  • Thick, greasy emollient creams
A

Thin creams:

  • E45
  • Diprobase cream
  • Oilatum cream
  • Aveeno cream
  • Cetraben cream
  • Epaderm cream

Thick, greasy emollients:

  • 50:50 ointment (50% liquid paraffin)
  • Hydromol ointment
  • Diprobase ointment
  • Cetraben ointment
  • Epaderm ointment
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3
Q

In eczema, the thicker the skin the weaker the steroid required; true or false?

A

FALSE; thicker the skin the stronger the steroid required

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4
Q

State an example of a:

  • Mild
  • Moderate
  • Potent
  • Very potent

… topical steroid used in eczema

A

The steroid ladder from weakest to most potent:

  • Mild: Hydrocortisone 0.5%, 1% and 2.5%
  • Moderate: Eumovate (clobetasone butyrate 0.05%)
  • Potent: Betnovate (betamethasone 0.1%)
  • Very potent: Dermovate (clobetasol propionate 0.05%)
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5
Q

Discuss which areas of body are commonly affected by eczema in:

  • Infants
  • Children
A
  • In infants, primarily involves the face, the scalp, and the extensor surfaces of the limbs
  • In children and adults often localized to the flexure of the limbs
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6
Q

What is the most common organism causing bacterial skin infections in patients with eczema?

Discuss the management

A
  • Staphylococcus aureus
  • Management:
    • Oral abx (e.g. flucloxacillin)
    • If severe may require admission & IV abx
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7
Q

What is eczema herpeticum?

A
  • Viral skin infection caused by HSV or VZV
  • HSV-1 is most common causative organism
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8
Q

Are investigations typically done prior to starting treatment for eczema herpeticum?

A

Treatment usually started based on clinical appearance but can do viral swabs of vesicles to confirm diagnosis

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9
Q

What is eczema herpeticum?

A
  • Viral skin infection caused by HSV or VZV
  • HSV-1 is most common causative organism
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10
Q

Discuss the presentation of eczema herpeticum

A
  • Hx of skin condition (e.g. eczema)
  • Widespread, painful, vesicular rash
  • WITH systemic features:
    • Fever
    • Lethargy
    • Irritability
    • Lymphadenopathy
    • Reduced oral intake
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11
Q

Discuss management of seborrhoeic dermatitis in infants

A
  • Reassure parents (not serious, often resolves spontaneously by 8months)
  • Use olive oil to loosen scales, brush gently with baby brush then wash off with shampoo
  • Bath in emollients as oppose to soap if other areas affected
  • If not effective, next step is a topical antifungal cream (e.g. clotrimazole or miconazole) for up to 4 weeks
  • If severe, mild topical steroids (e.g.1% hydrocortisone) may be used
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12
Q

Discuss the management of seborrheic dermatitis of scalp (commonly occurs in adolescents & adults)

A
  • First line= ketoconazole shampoo (leave for 5 mins before washing)
  • If severe itching= topical steroids
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13
Q

Discuss the management of seborrhoeic dermatitis of face & body

A
  • First line= antifungal cream (e.g. clotrimazole or miconazole)
  • Second line= topical steroid (e.g. 1% hydrocortisone)/
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14
Q

Which of the two types of psoriasis are medical emergencies?

A
  • Pustular psoriasis
  • Erythrodermic psoriasis
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15
Q

Discuss the management of eczema herpeticum

A
  • Aciclovir
    • Mild-moderate: PO
    • Severe: IV
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16
Q

State some potential complications of eczema herpeticum

A
  • Can be life-threatening if immunocompromised
  • Bacterial superinfection (leading to more severe illness)
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17
Q

. Briefly describe two types of contact dermatitis

A

Irritant Contact Dermatitis

  • Common
  • Non-allergic
  • Only areas exposed are affected
  • Common on hands
  • Stinging, burning, tightness are common symptoms
  • Erythema, crusting (vesicles less common in irritant)

Allergic Contact Dermatitis

  • Uncommon
  • Type IV hypersensitivity reaction
  • Areas that are not directly exposed may also be affected
  • Often seen on head following hair dye use
  • Itching is common symptom
  • Erythema, vesicles, weeping eczema (if more severe)

Management

  • Avoiding contact with irritant/allergen
  • Emollients
  • Consider of topical corticosteroids
  • Treat any secondary skin infection
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18
Q

What proportion of pts with psoriasis had symptoms that started in childhood?

A

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19
Q

Remind yourself of the different types of psoriasis; briefly describing the presentation of each

A
  • Chronic plaque psoriasis (most common in adults): plaques that are thickened, erythematous, silver scaled, extensor surfaces & scalp
  • Guttate psoriasis (2nd most common in adults, commonly occurs in children): small raised papules across trunk & limbs, papules are erythematous and may be scaley. Over time papules can turn to plaques. Triggers: streptococcal throat infection, stress, medications.
  • Inverse psoriasis: flexor areas affected, erythema, lacks scales, smooth
  • Pustular psoriasis (rare): pustules form under erythematous skin- the pus is not infectious. May be systemically unwell.
  • Erythrodermic psoriasis (rare): extensive erythematous areas covering most of skin. Get exfoliation of large areas of skin leaving raw exposed areas.
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20
Q

Presentation of psoriasis in children may be different to that in adults however there are some specific signs that are suggestive of psoriasis; state these

A
  • Auspitz sign: areas of bleeing when plaques are scraped off
  • Koebner phenomenon: lesion develops in area of skin trauma
  • Residual pigmentation: alterations to pigmentation after lesion resolved (darker)
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21
Q

Briefly describe the management of psoriasis (more in special senses block)

A
  • Regular emollients
  • First line:
    • Potent topical corticosteroids
    • Topical vitamin D analogues
  • Second line: increase Vit D to BD & stop steroid
  • Third line increase steroid to BD & stop vit D
  • Others: coal tar preparations, topical dithranol, phototherapy with narrow band UV B light
  • Psychosocial support

If topical treatments fail may be started on unlicensed systemic treatments e.g. methotrexate, retinoids, biologics etc..

NOTE: dovobet & enstilar contain both potent steroid & vit D analogue. Not licensed in children but may be prescribed by specailist.

*****Topical calcineurin inhibitors (e.g. tacrolismus) usually only used in adults

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22
Q

Describe the pathophysiology of acne vulgaris

A

Acne is caused by chronic inflammation +/- infection in the pilosebaceous units. Acne occurs due to:

  • Increased production sebum (androgens increase it)
  • Trapping of keratin (dead skin cells)
  • Blockage of pilosebaceous unit

… leading to swelling and inflammation of the pilosebaceous unit.

Also thought that excessive growth of Propionibacterium acnes bacteria worsens acne (hence many treatments aim to reduce these bacteria)

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23
Q

State some conditions associated with psoriasis

A
  • Nail psoriasis
  • Psoriatic arthritis
  • Psychosocial (depression, anxiety)
  • Obesity
  • Hypertension
  • Hyperlipidaemia
  • T2DM
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24
Q

Describe the presentation of acne vulgaris

A

Usually presents as erythematous, inflamed, sore spots typically on face, back & upper chest. Specific skin changes/signs include:

  • Macules
  • Papules
  • Pustules
  • Closed comedones
  • Open comedones (blackheads)
  • Ice prick scars (small indentation in skin where acne lesion was)
  • Hypertrophic scars (small lumps in skin after acne lesion healed)
  • Rolling scars (irregular wave-like irregularities of skin that remain after acne healed)
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25
Q

What are aims of acne management?

A
  • Reduce symptoms
  • Reduce risk of scarring
  • Minimise psychosocial impact
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26
Q

Briefly discuss the management of acne vulgaris (more in special senses block- including mechanisms of action, ADRs etc)

A
  • First line:
    • Topical retinoid (e.g. adapalene) + topical benzoyl peroxide
    • Topical retinoid (e.g. tretinoin) + topical clindamycin
    • Topical benzoyl peroxide + topical clindamycin
    • IF PERSON DOES NOT WANT retinoid or abx can try topical benzoyl peroxide monotherapy
  • Second line: add oral tetracycline abx (e.g. lymecycline, doxycycline) *DO NOT use topical & oral abx in combination. Always prescribe topical benzoyl peroxide to reduce risk antibiotic resistance
  • Third line: add COCP (co-cyprindiol is most effective due to anti-androgen effect)
  • Fourth line: add oral isotretinoin (specialist)
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27
Q

What is urticaria?

Describe pathophysiology

A
  • “Hives”- small itchy lumps on skin which may have associated patchy erythematous rash, angioedema & flushing. Can be acute or chronic.
  • Due to release of histamine and other inflammatory mediators by mast cells in skin. Can be due to allergic reaction (most commonly) or autoimmune reaction (as in chronic idiopathic urticaria)
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28
Q

State some potential causes of acute urticaria

A
  • Allergies to food, medications or animals
  • Contact with chemicals, latex or stinging nettles
  • Medications
  • Viral infections
  • Insect bites
  • Dermatographism (rubbing of the skin)
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29
Q

Chronic urticaria is when rash persists or comes and goes for more than 6 weeks. There are 3 sub classifications; state & describe each

A
  • Chronic idiopathic urticaria (most likely autoimmune): unknown cause or trigger
  • Chronic inducible urticaria: induced by certain triggers e.g. sunlight, temp change, exercise, dermatographism, strong emotions
  • Autoimmune urticaria: associated with underlying autoimmune condition
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30
Q

Discuss the management of urticaria

A
  • Identify trigger & avoid
  • Non-sedating antihistamine e.g. loratadine, cetirizine, fexofenadine (first choice in chronic urticaria) for up to 6 weeks
  • If severe, consider oral steroids (e.g. prednisolone for up to 7 days)
  • May refer to specialist for: LTRAs (e.g. montelukast), omalizumab (targets IgE), ciclosporin
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31
Q

At what age is nappy rash most common?

A

9-12 months

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32
Q

Remind yourself of risk factors for nappy rash

A
  • Delayed changing of nappies
  • Irritant soap products and vigorous cleaning
  • Certain types of nappies (poorly absorbent ones)
  • Diarrhoea
  • Oral antibiotics predispose to candida infection
  • Pre-term infants
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33
Q

Infants with nappy rash may also get added infections with fungus (candida) or bacteria (staphylococcus or streptococcus); state some features that would suggest a candida infection

A
  • Satellite lesions (small similar patches or rash or pustules near to main rash)
  • Oral thrush
  • Rash extending into skin folds
  • Larger red macules
  • Well demarcated scaley border
34
Q

Discuss the management of nappy rash

Discuss the extra management required if infant has candida infection

A

Management Nappy Rash

  • Change nappy regularly
  • Clean with cotton wool and water
  • Ensure nappy area dry before putting new one on
  • Maximise time without a nappy
  • Switch to highly absorbent nappy
  • Use nappy rash barrier cream (e.g. zinc & caster oil, sudocrem, metanium)

If have candida infection or bacterial infection

  • Candida: topical antifungal cream (clotrimazole or miconazole) & cease use of barrier cream until candida infection settled
  • Bacterial: oral flucloxacillin
35
Q

Discuss the management of head lice

A

Range of treatments available:

  • Wet combing (NICE recommend Bug Buster kit. Regimen is four sessions spaced over 2 weeks (on days 1, 5, 9, and 13).
  • Physical insecticides e.g. dimeticone 4% (leave on for ~8hrs- some require less- then wash off. Repeat 7 days later)
  • Chemical insecticide e.g. Malathion
36
Q

What is erythema nodosum?

A

Raised erythematous nodules on shins due to inflammation of subcutaneous fat (panniculitis) caused by hypersensitivity reaction

37
Q

There isn’t always an identifiable cause of erythema nodosum; however, state some possible causes & associations

A
  • Streptococcal throat infections
  • Gastroenteritis
  • Mycoplasma pneumoniae
  • Tuberculosis
  • Pregnancy
  • Medications, such as the oral contraceptive pill and NSAIDs
  • Inflammatory bowel disease
  • Sarcoidosis
  • Lymphoma
  • Leukaemia
38
Q

What investigations may you consider in someone with erythema nodosum & why?

A
  • Inflammatory markers (CRP and ESR): infection, IBD
  • Throat swab for streptococcal infection
  • Chest xray can help identify mycoplasma, tuberculosis, sarcoidosis and lymphoma
  • Stool microscopy and culture for gastroenteritis campylobacter and salmonella
  • Faecal calprotectin for inflammatory bowel disease
39
Q

Discuss the management of erythema nodosum

A
  • Treat underlying cause (if identified)
  • Supportive/conservative:
    • Rest
    • Analgesia
    • Steroids may used

Usually resolves within 6 weeks

40
Q

For pityriasis rosea, discuss:

  • Who it occurs in
  • Cause
A
  • Adolescents & young adults
  • No definitive organism identified but thought that HHV-6 or HHV-7 involved
41
Q

Describe presentation of pityriasis rosea

A
  • Prodrome before rash: headache, lethargy, lack of appetite, flu-like symptoms
  • Rash starts with herald patch ~2 days before rash (faint red/pink, scaly, oval shaped usually on torso)
  • Widespread faint red or pink, slightly scaly, oval lesions in characteristic Christmas tree pattern
  • May have generalised itching
42
Q

Discuss the management of pityriasis rosea

A
  • No treatment as it resolves spontaneously within 3 months
  • Educate & reassure pt
    • Not contagious
    • Can use emollients and antihistamines to help with itching
43
Q

For impetigo, discuss:

  • Cause
  • Whether it is contagious
  • Two different types
A
  • Superficial skin infection most commonly caused by Staphylococcus aureus bacteria and less commonly by Streptococcus pyogenes. NOTE: bullous impetigo ALWAYS caused by S.aureus
  • Contagious so keep off school
  • Non-bullous and bullous
44
Q

For non-bullous impetigo, discuss:

  • Presentation
  • Management
A

Presentation

  • Typically around nose or mouth
  • Exudate gives ‘golden crust’

Management

  • If localised and pt not at risk of complications or systemically unwell: antiseptic cream (e.g. hydrogen peroxide 1%)
  • Alternatively, topical fusidic acid
  • If suspect fusidic acid resistance, topical mupirocin
  • Extensive disease: oral flucloxacillin or erythromycin if penicillin allergic

Exclude from school until lesions crusted and healed (as spread is via discharge from lesions) or 48hrs after commencing abx treatment

45
Q

For bullous impetigo, discuss:

  • Pathophysiology
  • Presentation
  • Who more common in
  • Treatment
A
  • Staphylococcus aureus bacteria produce epidermolytic toxins that break down protein holding skin cells together resulting in formation of fluid filled vesicles. These grow then burst to form golden crust. Lesions may be painful & itchy.
  • Presentation: see above, common to have systemic symptoms e.g. fever
  • More common in neonates & children <2yrs
  • Management:
    • Antibiotics- flucloxacillin PO or IV dependent on how well/unwell and risk of complications
    • Advise that must stay off school until all lesions crusted over and healed or had 48hrs abx
46
Q

What do we call it if someone has bullous impetigo that is widespread and severe?

Other than usual bullous impetigo symptoms & signs, what other specific sign is present in SSS?

What is the management?

A
  • Staphylococcus scalded skin syndrome
  • Presentation:
    • Same as for bullous impetigo: starts with erythema, skin looks thin & wrinkled, then get bullae formation which leave skin sore & erythematous when they burst. Can have systemic symptoms (fever, lethargy, irritability)
    • Nikolsky sign: gentle rubbing of skin causes it to peel away
  • Management:
    • Admission for IV abx
    • Monitoring and correction of fluid & electrolyte imbalances as prone to dehydration

*Most make full recovery without scarring if adequately treated

47
Q

State some potential complications of impetigo

A

Complications are rare but may include:

  • Cellulitis (if infection gets deeper into skin)
  • Sepsis
  • Scarring
  • Post-streptococcal glomerulnephritis
  • Staphylococcus scalded skin syndrome
  • Scarlet fever
48
Q

For scabies,

  • Causative organism
  • Presentation
  • Management
A
  • Mites called Sarcoptes scabei that burrow under skin and lay eggs leading to further infection
  • Presentation:
    • Itchy
    • Small red spots
    • Track marks/linear burrows
    • Commonly in finger webs but may affect face & scalp in infants
  • Management:
    • First line= permethrin 5% cream (apply to whole body when skin is cool and leave on for 8-12hrs then wash off. Repeat 1 week later. Everyone in household needs to be treated and anyone had sexual contact with in last 8 weeks also needs treating)
    • Alternative= malathion cream (wait 24hrs before wash off)
    • Can give crotamiton cream & sedating antihistamines at night to help sleep
    • Wash all clothes, bedding etc on high temp
    • Hoovering of carpets & furniture
    • If have crusted scabies (more common in immunosupressed) then PO ivermeticin

*NOTE: itching can last for a few weeks even after scabies been treated

49
Q

For crusted/Norwegian scabies, discuss:

  • Presentation
  • Who common in
  • Management
A
  • Patches of red skin that turn into scaly plaques
  • Immunocompromised (e.g. HIV)
  • Require admission for oral ivermectin and isolation
50
Q

For erythema multiforme, discuss:

  • Common causes
  • Presentation
  • Management
A
  • Hypersensitivity reaction caused most commonly by viral infections (e.g. HSV), medications and bacteria such as mycoplasma
  • Presentation:
    • Widespread, erythematous rash
    • Itchy
    • Target lesions
    • Sore mouth/stomatitis
    • Associated symptoms: fever, lethargy, arthrlagia, flu-like symptoms
  • Management:
    • Often resolves spontaneously in 1-4 weeks without treatment
    • Severe cases- particularly if affects oral mucosa- may require admission for IV fluids, analgesia, steroids (systemic or topical)
51
Q

For molluscum contagiosum, discuss:

  • Causative organism
  • Presentation
  • Management
A
  • Viral skin infection caused by molluscum contagiosum virus
  • Presentation:
    • Small, flesh coloured papules with central dimple
    • Typically occur in crops in a local area
  • Contagious (direct contact or sharing items e.g. towels)
  • Management:
    • Reassurance and education regarding transmission. Usually resolves without treatment but can take up to 18 months
    • If extensive lesions or lesions in problematic areas (e.g. eyelids, anogenital) refer to specialist for further treatments e.g. topical KOH, benzoyl peroxide, cyrotherapy
52
Q

For hand, foot & mouth disease, discuss:

  • Causative organism
  • Contagious?
  • Presentation
  • Management
  • Complications
A
  • Caused by intestinal viruses of Picornaviridae family most commonly Coxsackie A16 virus and enterovirus 71.
  • Very contagious
  • Presentation:
    • URTI symptoms (fever, sore throat, lethargy)
    • After 1-2 days get mouth ulcers- can be painful
    • Then get vesicles on body most notable on hands, feet & around mouth
    • Rash may be itchy
  • Management:
    • Supportive: fluids, analgesia
    • Education: contagious hence avoid sharing e.g. towels, should resolve in a week to 10 days, do not need to exclude child from school unless child unwell
  • Potential complications (rare):
    • Dehydration
    • Bacterial superinfection
    • Encephalitis
53
Q

For chickenpox, discuss:

  • Causative organism
  • Presentation
  • Incubation period
  • When people are contagious
  • Management
  • Complications
A
  • Varicella zoster virus
  • Presentation:
    • First symptom often fever
    • Widespread, erythematous, vesicular rash that starts on trunk or face and moves outwards affecting whole body over 2-5 days
    • Itching
    • Generalised fatigue & malaise
    • Lesions eventually crust over
  • Incubation period 10-21 days
  • Infective 4 days before rash until all have crusted over (usually about 5 days after rash appeared)
  • Management:
    • Supportive: keep cool, trim nails to stop scratching, calamine lotion for itch
    • Keep off school until all lesions crusted over
    • Avoid pregnant women & immunocompromised pts
    • Consider varicella zoster immunoglobulins in immunocompromised pts who have been exposed, non-immune pregnant women and newborns with peripartum exposure. If develop chickenpox should give IV Aciclovir (zero to finals says give Aciclovir to Newborns aswell as immunoglobulins)
  • Complications:
    • Bacterial superinfection
    • Dehydration
    • Pneumonia
    • Encephalitis
    • Shingles or Ramsey Hunt syndrome later in life
54
Q

State the 6 viral exanthems

A
  • First disease: Measles
  • Second disease: Scarlet Fever
  • Third disease: Rubella (German Measles)
  • Fourth disease: Dukes’ Disease
  • Fifth disease: Parvovirus B19
  • Sixth disease: Roseola Infantum

**Remember xanthem is eruptive widespread rash

55
Q

For measles, discuss:

  • Causative organism
  • Spread
  • Incubation
  • Presentation
A
  • Measles virus
  • Highly contagious spread via respiratory droplets
  • 10-12 days
  • Presentation:
    • Prodrome of fever, coryzal symptoms & conjunctivitis
    • Koplik spots 2 days after fever (pathognomonic)
    • Erythematous macular rash that starts on face- usually behind ears- then spreads to rest of body
56
Q

Discuss the management of measles

A

Usually self-limiting although 30% can develop a complication. Management includes:

  • Supportive
  • Notify public health
  • Isolating until 4 days after symptoms resolved
  • Admission if immunocompromised or pregnant
  • Contacts who are not immunized should be offered vaccine within 72hrs
57
Q

State some potential complications of measles- highlighting most common

A
  • Otitis media
  • Pneumonia (most common cause death)
  • Encephalitis
  • Diarrhoea
  • Dehydration
  • Febrile convulsions
  • Myocarditis
  • Subacute sclerosing panenecephalitis (very rare. 5-10yrs after)
  • Death
58
Q

For scarlet fever, discuss:

  • Causative organism
  • Spread
  • Presentation
  • Management
  • Complications- highlight most common
A
  • Group A Streptococcus/Streptococcus pyogenes- produces exotoxin (usually associated with tonsillitis)
  • Spread via respiratory droplets
  • Presentation:
    • Rash: red-pink, macular rash with rough ‘sandpaper’ skin that starts on trunk and spread outwards
    • Desquamination may occur later
    • May have red/flushed cheeks
    • Strawberry tongue
    • Sore throat
    • Lymphadenopathy
    • Fever
    • Lethargy
  • Management:
    • Abx: phenoxymethylpenicillin for 10 days
    • Notify public health
    • Keep children off school until 24hrs after abx
  • Complications/associations:
    • Otitis media
    • Post-streptococcal glomerulonephritis
    • Acute rheumatic fever
59
Q

For rubella, discuss:

  • Causative organism
  • Spread
  • Presentation
  • Management
  • Complications
A
  • Rubella virus
  • Respiratory droplets- very contagious- 14 day incubation
  • Presentation:
    • Erythematous macular rash that starts on face & spread to rest of body (milder than measles) - lasts about 3/7
    • Cervical lymphadenopathy (suboccipital & post-auricular)
    • Mild fever
    • Arthralgia
    • Sore throat
  • Management:
    • Supportive
    • Notify public health
    • Stay off school for at least 5 days after rash has disappeared
    • Avoid pregnant women
  • Complications (rare):
    • Thrombocytopenia
    • Encephalitis
    • Congenital rubella syndrome in fetus of pregnant women (deafness, blindness & congenital heart disease)
60
Q

For fifth disease/slapped cheek syndrome/erythema infectiosum, discuss:

  • Causative organism
  • Infectious period
  • Presentation
  • Management
  • Complications
    *
A
  • Parvovirus B19
  • Infectious 3-4 days before rash; once rash has emerged no longer infectious so don’t need to keep of school
  • Presentation:
    • Mild prodrome: muscle, aches, lethargy
    • Rash: starts on cheeks then spreads to become reticular mildly erythematous rash on trunk & limbs that can be raised & itchy
    • Rash fades after ~1 week but may find that for months after things can trigger the rash e.g. hot bath
  • Management:
    • Supportive (fluids, analgesia)
    • See separate FC for management of those at risk of complications
  • Complications:
    • Aplastic anaemia (if have chronic anaemia/haematological abnormality)
    • Pancytopenia (if immuncompromised)
    • Encephalitis
    • Meningitis
    • Pregnancy complications including fetal death
61
Q

Certain groups are at risk of complications from fifth disease/slapped cheek syndrome/erythema infectiosum; state some of these groups

What investigations do these groups need?

A
  • Immunocompromised
  • Pregnant
  • Haematological conditions:
    • Sickle cell anaemia
    • Thalassaemia
    • Hereditary spherocytosis
    • Haemolytic anaemia

These pts need:

  • Serology for parvovirus B19 to confirm infection
  • FBC & reticulocytes (to check for aplastic anaemia in those with haematological conditions & pancytopenia that can occur in immunosuppressed)
62
Q

For roseola infantum, discuss:

  • Causative organisms
  • Infectivity
  • Presentation
  • Management
  • Main complication
A
  • HHV-6 (or less commonly HHV-7)
  • Incubation of 5-15 days. Don’t need excluding from school once fever resolved
  • Presentation:
    • High fever lasting few days; may have coryzal symptoms, diarrhoea
    • Fever resolves then get maculopapular rash across arms, legs, trunk & face. NOT ITCHY. Lasts for 1-2 days.
    • Nagayamas spots (red papules on uvula & soft palate)
  • Management:
    • Supportive (fluids, analgesia)
  • Complications:
    • Febrile convulsions
    • Hepatitis
    • Immunocompromised may be at risk of myocarditis, thrombocytopenia, Guillain-Barre syndrome
63
Q

What is ringworm?

What’s most common type of fungus to cause ringworm?

A
  • Ringworm/tinea/dermatophytosis is a fungal infection of the skin
  • Most common type of fungus= trichophyton (spread via infected individuals, animals or soil)
64
Q

We call ringworm different things based on where it is; state some examples

A
  • Tinea capitis refers to ringworm affecting the scalp
  • Tinea pedis refers to ringworm affecting the feet, also known as athletes foot
  • Tinea cruris refers to ringworm of the groin
  • Tinea corporis refers to ringworm on the body
  • Onychomycosis refers to a fungal nail infection
65
Q

Describe the appearance of the classical ringworm rash

A
  • Erythematous
  • Scaly
  • Well demarcated
  • Ring shaped
  • Edge is darker/more red and centre is more pale
  • Itchy
66
Q

For tinea capitis (which is mainly seen in children) discuss the presentation and management

A
  • Presentation:
    • Well demarcated hair loss
    • Itching
    • Dryness
    • Erythema
    • Kerion may form (raised, pustular, spongey mass)
  • Management:
    • Measures to prevent infection (e.g. don’t share towels, wash hats etc, avoid scratching… check & treat other family members)
    • Self-care: can soften crusts then tease away
    • PO antifungals e.g. terbinafine or griseofulvin
    • Consider also prescribing ketoconazole shampoo twice weekly for at least 2 weeks
67
Q

For tinea pedis (which is common in adolescents) discuss the presentation & management

A
  • Presentation:
    • Interdigital (most common): White, red or flaky patches between toes, skin may be split (which can lead to bleeding)
    • Moccasin/dry: Scaling & hyperkeratosis affecting heel and side of foot
    • Vesicobullous: multiple small vesicles and blisters mainly on the arches and soles of the feet
  • Management:
    • Self-care: keep cool feet & dry, change shoes regularly, cotton absorbant socks
    • Advice to prevent transmission (e.g. footwear in public spaces, avoid scratching)
    • Topical antifungal e.g. terbinafine, clotrimazole, miconazole etc…
    • Consider prescribing mildly-potent corticosteroid
    • Consider oral antifungals (e.g. terbinafine)
68
Q

Discuss the management of tinea corporis

A
  • Self care: loose fitting clothing, good hygiene, dry area thouroughly
  • Advice to prevent transmission (e.g. don’t share towels)
  • Topical antifungal (e.g. terbinafine)
  • Consider mildly potent topical corticosteroid
  • Consider PO antifungal (e.g. terbinafine)
69
Q

What is tinea incognito?

A
  • Extensive fungal skin infection that is less well recognised/doesn’t present in typical way that results from use of steroids
  • Often occurs when initial presentation is misdiagnosed as dermatitis hence topical steroids prescribed
  • Steroids improve symptoms but accelerate growth of fungus by dampening immune response in local area
  • When steroid stops, rash becomes symptomatic again and is much worse than it was previously
  • Rash is less well-demarcated and has fewer scales
70
Q

For mongolian blue spots, discuss:

  • Appearance
  • Pathophysiology
  • Management
A
  • Blue-grey marking of skin with poorly defined edges, usually in lower back & buttock region, in newborn babies
  • Due to functional melanocytes in the dermis
  • Benign hence just reassure parents; most fade in early childhood but bigger ones may persist but becomes less noticeable
71
Q

For erythema toxicum, discuss:

  • Appearance
  • When it occurs
  • Management
A
  • Erythematous maculopapular rash that often begins on face and spreads to trunk and limbs
  • Generally occurs in first 3-14 days of life. Rash can come & go- doesn’t usually last for more than 24hrs
  • Reassurance is all that is needed
72
Q

For milia, discuss:

  • Appearance
  • Pathophysiology
  • Managment
A
  • Small white bumps commonly on nose, cheeks and chin
  • Due to occlusion of pilosebaceous glands and sometimes developing sweat glands
  • Reassurance as most resolve in first few weeks of life
73
Q

For baby acne, discuss:

  • ‘Proper’ name
  • Appearance
  • Management
A
  • Erythema toxicum neonatorum
  • Erythematous or white papules and some puss-filled spots
  • Reassurance and advice to not pick the spots and treat baby’s skin as normal
74
Q

For stork bites/salmon patches, discuss:

  • Appearance
  • Pathophysiology
  • Management
A
  • Kind of vascular birthmark which are pink, blotchy an commonly found at nape of neck, eyelids & forehead
  • Blood vessels underneath skin becomes stretched or dilated; may notice it’s more prominent when baby upset
  • Reassurance as usually fade in few months
75
Q

For strawberry naevus (capillary haemangioma), discuss:

  • Appearance
  • Potential complications
  • Management
A
  • Erythematous, raised and multilobed tumours (rapidly growing, benign proliferations of endothelial cells”) appearing shortly after birth that increase in size until around 6-9 months. Commonly affect face, scalp and back.
  • Potential complications: mechanical such as obstruction visual fields or airway, bleeding, ulceration, thrombocytopenia
  • Management:
    • 95% resolve before 10yrs so no treatment needed (1st sign it’s resolving is it going pale in centre)
    • If treatment is needed, topical beta blockers e.g. timolol are used (work by reducing vascular endothelial growth factor)
76
Q

For port wine stains, discuss:

  • Appearance
  • Management
A
  • Vascular birth marks that are deep red or purple in colour, flat and present at birth. Often on unilateral face, neck & trunk. They don’t spontaneously resolve; they actually darken over time and can thicken.
  • Management:
    • Cosmetic camouflage
    • Laser therapy
77
Q

What are sucking blisters?

What causes them?

A

Sucking blisters are caused by vigorous sucking by the infant whilst still in the womb. Intact blisters or erosions may be found on the forearm, wrist, hands or fingers. They resolve within a few days.

78
Q

State some differential diagnoses for non-blanching rashes

A
  • Meningococcal septicaemia
  • HSP
  • Idiopathic thrombocytopenic purpura
  • HUS
  • Acute leukaemia’s
  • Traumatic
  • Viral illness (e.g. influenza & enterovirus)
79
Q

What investigations would you consider in a child with a non-blanching rash & why?

A
  • Full blood count: Anaemia can suggest HUS or leukaemia. Low white cells can suggest neutropenic sepsis or leukaemia. Low platelets can suggest ITP or HUS.
  • Urea and electrolytes: High urea and creatinine can indicate HUS or HSP with renal involvement.
  • C-reactive protein (CRP): This is a non-specific indication of inflammation or infection and can be useful but not definitive in excluding sepsis.
  • Erythrocyte sedimentation rate (ESR): This is a non-specific indication of inflammatory illness such as a vasculitis (HSP) or infection.
  • Coagulation screen, including PT, APTT, INR and fibrinogen can diagnose clotting abnormalities.
  • Blood culture: This can be useful but not definitive in diagnosing or excluding sepsis.
  • Meningococcal PCR: This can confirm meningococcal disease, although this should not delay treatment.
  • Lumbar puncture: To diagnose meningitis or encephalitis.
  • Blood pressure: Hypertension can occur in HSP and HUS. Hypotension can occur in septic shock.
  • Urine dipstick: Proteinuria and haematuria can suggest HSP with renal involvement, or HUS.
80
Q

Discuss the management of pt’s with non-blanching rashes

A
  • Urgent referral/A&E for investigations (unless there is clear or unconcerning cause)
  • If doubt, pts usually treated as meningococcal sepsis without waiting for investigations
  • Definitive management based on underlying cause