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0.1 Paediatrics - RB > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is Roseola Infantum also known as, and what is it caused by?

A

Exanthem subitum, sixth disease, caused by HHV6

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2
Q

In what age of patients does Roseola Infantum present?

A

6 months to 2 years old

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3
Q

What is the incubation period of Roseola Infantum?

A

1-2 weeks

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4
Q

After the incubation period of Roseola Infantum, what is the presentation?

A
  • High grade fever lasting 3-5 days → Febrile convulsions in 10%
  • Maculopapular rash (AFTER FEVER)
  • Bulging fontanelle
  • NAGAYAMA SPOTS (Uvulopalatal spots)
  • Periorbital oedema
  • Cervical, occipital, postauricular lymphadenopathy
  • Acute otitis media
  • Rhinorrhoea, cough
  • Diarrhoea and vomiting
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5
Q

How long does the Maculopapular rash last for in Roseola Infantum?

A

Can last for 1-2 days, but can disappear within 2-4 hours

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6
Q

How is Roseola Infantum diagnosed?

A
  • Clinical diagnosis based on history

- May be aided with PCR to test for HHV6

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7
Q

How is Roseola Infantum treated?

A

Supportive management i.e. fluids, antipyretics

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8
Q

What is the consensus of school exclusion for Roseola Infantum?

A
  • School exclusion is not necessary
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9
Q

What is the main complication of Roseola Infantum?

A

Febrile seizures

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10
Q

What is Slapped Cheek Syndrome also known as, and what is it caused by?

A

Erythema infectiosum, fifth disease, caused by Parvovirus B19

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11
Q

What is the incubation period of Slapped Cheek Syndrome?

A

4-14 days

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12
Q

After the incubation period of Slapped Cheek Syndrome, what is the presentation?

A
  • Mild flu-like symptoms
  • AFTER viraemia: Slapped cheek rash sparing mouth (circumoral pallor), palms and soles and reticular rash on body, plus arthralgia and arthritis
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13
Q

How might the presentation of Slapped Cheek Syndrome differ to those with underlying comorbidities?

A
  • Immunosuppressed patients → Pancytopenia
  • SCD / HS / Thalassemia patients → Aplastic crises
  • In foetus’ → Hydrops fetalis, foetal loss in early pregnancy
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14
Q

How long does the rash last for in Slapped Cheek Syndrome?

A

Usually peaks for a week, however can re-appear on triggers such as a warm bath, sunlight, heat or fever in next few months

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15
Q

How is Slapped Cheek Syndrome diagnosed?

A
  • Clinical diagnosis based on history
  • Test IgG and IgM levels against Parvovirus B19 (especially in pregnant women)
  • PCR for Parvovirus B19 (especially immunocompromised patients with low Ig levels)
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16
Q

If a pregnant woman has been exposed to Slapped Cheek Syndrome, what is recommended?

A
  • Check IgM and IgG levels against Parvovirus B19
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17
Q

What is the management of Slapped Cheek Syndrome?

A
  • Majority of cases are mild and resolve on their own
  • Treat aplastic crises with blood products / IV Ig
  • Treat polyarthralgia / arthritis with NSAIDs
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18
Q

What is the consensus of regarding time off school for Slapped Cheek Syndrome?

A

School exclusion is NOT necessary

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19
Q

What is fourth disease known as?

A

Duke’s disease

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20
Q

What is Duke’s disease known as?

A

Fourth disease

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21
Q

What is Rubella also known as? What is it?

A

German measles, it is a viral infection caused by Rubella virus

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22
Q

What is the incubation period of Rubella?

When are outbreaks more common?

A

14-21 days

Winter and spring

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23
Q

What is the presentation of Rubella?

A
  • Prodrome → Low-grade fever
  • Mild erythematous rash (compared to measles), starts on face → rest of the body
  • SUBOCCIPITAL AND POSTAURICULAR LYMPHADENOPATHY
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24
Q

What is the risk of damage to a foetus if the mother has been infected with Rubella?

A

As high as 90% in the first 8-10 weeks, and damage is rare after 16 weeks

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25
Q

What is the management of a pregnant women with suspected cases of Rubella?

A
  • Suspected cases should be discussed immediately with the local Health Protection Unit (HPU)
  • IgM antibodies are raised in women recently exposed to the virus
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26
Q
  • Congenital Rubella syndrome is a triad of?
A
  • Deafness, blindness, congenital heart disease
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27
Q

Is the Rubella vaccine safe to take in pregnancy?

A
  • NO, it is live attenuated vaccine. Must give postnatally
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28
Q

What are complications of Rubella?

A
  • Thrombocytopenia
  • Encephalitis
  • Myocarditis
  • Arthritis
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29
Q

What is Scarlet Fever?

A

A reaction to toxins produced by Group A haemolytic streptococci (usually Streptococcus pyogenes)

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30
Q

How is Scarlet Fever spread?

A

Via respiratory route by droplets or by direct contact with nose and throat discharges

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31
Q

What is the age of onset of Scarlet Fever?

A

2-6 years, with a peak at 4 years old

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32
Q

What is the incubation period of Scarlet Fever?

A

2-4 days

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33
Q

What is the presentation of Scarlet Fever?

A
  • RASH:
  • Fine punctate erythema (‘pinhead’) which appears first on the torso and spares palms and soles
  • Children have a flushed appearance plus circumoral pallor. The rash is often more obvious in the flexures
  • Rough ‘sandpaper’ texture
  • Desquamation later in the course of illness, particularly around the fingers and toes
  • Fever: typically lasts 24 to 48 hours
  • Malaise, headache, nausea/vomiting
  • Sore throat
  • ‘Strawberry’ Tongue
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34
Q

How do you investigate suspected Scarlet Fever?

A

A throat swab normally taken, but antibiotic treatment should be commenced immediately rather than waiting for results

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35
Q

How is Scarlet Fever managed?

A
  • Oral Penicillin V for 10 days
  • If Pencillin allergy → Azithromycin
  • Notify Public Health England
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36
Q

What is the consensus of regarding time off school for Scarlet Fever?

A

Children can return to school 24 hours after commencing antibiotics

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37
Q

What are the complications of Scarlet Fever?

A
  • Otitis media (MOST COMMON)
  • Rheumatic fever → 20 days after infection
  • Acute glomerulonephritis →10 days after infection
  • RARE → Meningitis, necrotising fasciitis
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38
Q

What is Measles?

A

A viral disease caused by RNA Paramyxovirus

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39
Q

What is the incubation period of Measles?

A

10-14 days

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40
Q

How is Measles spread?

A

By droplet infection

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41
Q

What are the features of Measles?

A
  • Prodrome: irritable, conjunctivitis, fever (Fever + 4 C’s: cough, conjunctiva, coryzal symptoms, Koplick spots)
  • Koplik spots (before rash): white spots on buccal mucosa
  • Rash: starts behind ears 3-5 days after fever → whole body, discrete maculopapular rash becoming blotchy & confluent (cephalocaudal progression)
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42
Q

What are the investigations to diagnose Measles?

A

IgM antibdies

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43
Q

What is the management of Measles?

A

Supportive management

Notify Public Health England

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44
Q

What are the complications of Measles?

A
  • Otitis media: the most common complication
  • Pneumonia: the most common cause of death
  • Encephalitis: typically occurs 1-2 weeks following the onset of the illness)
  • Subacute sclerosing panencephalitis: very rare, may present 5-10 years following the illness
  • Febrile convulsions
  • Keratoconjunctivitis, corneal ulceration
  • Diarrhoea
  • Increased incidence of appendicitis
  • Myocarditis
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45
Q

How should the contacts of a Measles patient be managed?

A
  • If a child not immunized against measles comes into contact with measles then MMR should be offered
  • This should be given within 72 hours
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46
Q

What are the six Viral Exanthemas?

A
  1. First disease → Measles
  2. Second disease → Scarlet Fever
  3. Third disease → German Measles / Rubella
  4. Fourth disease → Dukes Disease
  5. Fifth disease → Slapped Cheek / Erythema Infectiosum / Parvovirus B19
  6. Sixth disease → Roseola Infantum / Exanthem Subitum / HHV6
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47
Q

What is Eczema? Describe a brief pathophysiology

A
  • A chronic atopic condition caused by defects in the continuity of the skin barrier. These defects allow irritants, microbes and allergens to create an immune response, leading to inflammation of the skin
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48
Q

Where is Eczema commonly seen in infants, younger children and older children?

A
  • In infants the face and trunk are often affected
  • In younger children eczema often occurs on the extensor surfaces
  • In older children a more typical distribution is seen, with flexor surfaces affected and the creases of the face and neck
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49
Q

What are poor prognostic factors of Eczema?

A
  • Onset at age 3-6 months
  • Severe disease in childhood
  • Associated asthma or hay fever
  • Small family size
  • High IgE serum levels
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50
Q

What is the maintenance therapy for Eczema?

A
  • Emollients, as thick and greasy are possible particularly after washing and before bed
  • Avoid activities which break down the skin barrier such as bathing in hot water, scratching, rubbing. Avoid soaps which strip the skin of oils. Use soap substitutes
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51
Q

How is Eczema flare-up managed?

A
  • Thick Emollients & Topical Steroids: large quantities should be prescribed (e.g. 250g / week), roughly in a ratio of with topical steroids of 10:1
  • If a topical steroid is also being used the emollient should be applied first followed by waiting at least 30 minutes before applying the topical steroids
  • Wet wraps may be used
  • Specialist treatments in severe eczema → zinc impregnated bandages, topical tacrolimus, phototherapy and systemic immunosuppressants, such as oral corticosteroids, methotrexate and azathioprine
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52
Q

Give examples of thin emollient creams?

A
  • Aveeno cream
  • Cetraben
  • Diprobase
  • E45
  • Epaderm
  • Oilatum cream
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53
Q

Give examples of thick of emollient creams?

A
  • 50% Liquid paraffin
  • Cetraben
  • Diprobase
  • Epaderm
  • Hydromol
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54
Q

Discuss the Steroid Ladder?

A
  • Mild: Hydrocortisone 0.5%-2.5%
  • Moderate: Eumovate and Betnovate RD
  • Potent: Betnovate and Cutivate
  • Very potent: Dermovate
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55
Q

What is the “finger-tip” rule?

A
  • 1 finger tip unit (FTU) = 0.5 g, skin area about twice that of the flat of an adult hand
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56
Q
  • What is the most common opportunistic bacterial infection microbe for eczema?
A
  • Staphylococcus aureus
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57
Q

What is the management for a Bacterial infection of Eczema?

A
  • Flucloxacillin
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58
Q

What is Eczema Herpeticum

A
  • A severe primary infection of the skin by HSV1, HSV2 or VZV
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59
Q

What is the presentation of Eczema Herpeticum?
What is seen on examination of Eczema Herpeticum?
- What is the management of Eczema Herpeticum?

A
  • Presents as a rapidly progressive, widespread, vesicular, painful rash
  • Systemic symptoms of fever, irritability, lethargy, reduced oral intake, lymphadenopathy
  • O/E → Monomorphic punched-out erosions (circular, depressed, ulcerated lesions) usually 1–3 mm in diameter are typically seen
  • Mild-Moderate → Oral Acyclovir
  • Severe → IV Acyclovir
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60
Q

What is Psoriasis? What is the pathophysiology?

A
  • Psoriasis is a chronic autoimmune condition which causes psoriatic skin lesions. It is caused by rapid turnover of new cells, causing abnormal build-up and skin thickening
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61
Q

Describe what Psoriatic skin may appear like?

Where can they be found?

A
  • Dry, flaky, scaly, faintly erythematous skin lesions which appear in raised, roughened plaques

Commonly over the extensor surfaces of elbows, knees, scalp

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62
Q

State the subtypes / associations of Psoriasis?

Painful Pink Psoriasis -> Germy Itch Episodes

A
  1. Plaque Psoriasis
  2. Pustular Psoriasis
  3. Psoriatic Arthritis
  4. Guttural Psoriasis
  5. Inverse / Flexural Psoriasis
  6. Erythrodermic Psoriasis
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63
Q

What may exacerbate a Psoriasis flare-up?

A
  • Trauma
  • EtOH
  • Medications: BBs, lithium, Chloroquine and Hydroxychloroquine), NSAIDs, ACEIs, Infliximab
  • Systemic steroid withdrawal
64
Q

What are the nail associations of Psoriasis?

A

Nail pitting, thickening, discoloration, ridging, onycholysis

65
Q

What are complications of Psoriasis?

A
  • Psoriatic arthropathy (around 10%)
  • Increased incidence of metabolic syndrome, CVD, VTE
  • Psychological distress i.e. depression, anxiety
66
Q

IMPORTANT POINTS for Vitamin D analogues used in Psoriasis

A
  • Examples: Calcipotriol, Calcitriol, Tacalcitol
  • ↓ Cell division and differentiation
  • Adverse effects uncommon
  • Unlike corticosteroids, can be used long-term
  • Unlike coal tar and dithranol they do not smell / stain
  • ↓ Scale and thickness of plaques, not the erythema
  • Should be avoided in pregnancy
  • Maximum weekly amount for adults → 100g
67
Q

IMPORTANT POINTS for Corticosteroids used in Psoriasis

A
  • Patients should have 4 week breaks between topical steroid courses
  • Very potent steroids → 4 weeks at a time maximum
  • Potent steroids → 8 weeks at a time maximum
  • Scalp, face and flexures → Prone to steroid atrophy → Topical steroids not be used for more than 1-2 weeks/month
68
Q

What is the recommended management for Scalp Psoriasis?

A

Potent topical steroid OD for 4 weeks

69
Q

What is the recommended management for Face, flexural, genital Psoriasis?

A

Mild or moderate potency corticosteroid applied OD / BD for a maximum of 2 weeks

70
Q

What is the most common type of Psoriasis? Describe it?

A

Plaque Psoriasis

Flattened areas of elevation, white silvery scales, commonly seen on extensor surfaces and scalp. Plaques are between 1-10cm in diameter

71
Q

How is Plaque Psoriasis managed? First, second, third line?

A
  • Regular emollients to reduce scale loss and pruritis
  • First-line: NICE recommendation of potent corticosteroid OD + Vitamin D analogue OD → Apply separately i.e. morning and night → 4 weeks
  • Second line: NICE recommendation of Vitamin D analogue BD if no improvement after 8 weeks
  • Third line: NICE recommendation of potent corticosteroid BD for up to 4 weeks or a coal tar preparation applied OD/BD if no improvement after 8-12 weeks
72
Q

Describe what Pustular Psoriasis appears like?

What is the management?

A
  • Appears as small erythematous elevations of cloudy pus, usually tender, can form on the hands and feet
  • Patients can be SYSTEMICALLY UNWELL → admit to hospital, treat as medical emergency
73
Q
  • What are the different types of Psoriatic Arthritis?
A
  1. Rheumatoid-like polyarthritis (30-40%, most common type)
  2. Asymmetrical oligoarthritis: typically affects hands and feet (20-30%)
  3. DIP joint disease(10%)
  4. Sacroiliitis
  5. Arthritis mutilans
74
Q

What is the second most common type of Psoriasis?
In what patients is it common?
Describe it?
What causes it?

A

Guttate (commonly occurs in children)

  • Small, raised TEAR-DROP SHAPED papules on the trunk and limbs. Are mildly erythematous and can be scaly. Over time Guttate Psoriasis → Plaque Psoriasis
  • Guttate Psoriasis is often triggered by a Streptococcal Throat Infection, stress or medications
75
Q

Describe Inverse Psoriasis?

A
  • Appears as smooth and shiny red lesions, lack scales, typically form within skin folds i.e. genital region, axilla, under breasts
76
Q

Describe Erythrodermic Psoriasis?

A
  • Fire-red scales, extremely itchy and painful. Skin sheds away in large patches i.e. exfoliation resulting in raw, exposed areas
77
Q

What is the least common form of Psoriasis?

A

Erythrodermic

78
Q

From outer to inner, what are the three layers of skin?

A
  • Epidermis, Dermis, Hypodermis
79
Q

From outer to inner, what are the five layers of Epidermis? (Come Let’s Get Some Beer)

A
  • Stratum corneum
  • Stratum lucidum
  • Stratum granulosum
  • Stratum spinosum
  • Stratum basale
80
Q

In short and simple terms, what is Acne Vulgaris?

A
  • Acne vulgaris is a common skin disorder affecting people during puberty and adolescence. It is characterised by chronic inflammation of the Pilosebaceous Unit with or without infection
81
Q

What is the pathophysiology of Acne Vulgaris?

A
  • Chronic inflammation of the Pilosebaceous Unit, with or without localised infection
  • The pathophysiology can be explained by 1) Sebum production, 2) Keratin Plugs 3) Bacterial overgrowth
  1. The pilosebaceous unit produces sebum, which increases during puberty due to a rise in Androgens. This blocks the unit
  2. This also traps Keratin within the follicle, and patients may also have increased keratin production (Hyperkeratosis) which blocks the unit further. This forms both open (blackhead) comedone
  3. Propionibacterium can also colonise the follicle, which forms a closed (whitehead) comedone
82
Q

What is a comedone?

A
  • A dilated sebaceous follicle
83
Q

Why are open comedones black?

A
  • Melanin within the keratin plugs oxidise, turning black
84
Q

What is a macule, papule, pustule?

A
  • Macule → Flat mark on the skin
  • Papule → Raised lump on the skin
  • Pustule → Raised lump on the skin containing pus
85
Q

What two scars are associated with Acne Vulgaris?

A
  • Ice-pick scars

- Hypertrophic scars

86
Q

How can acne vulgaris be classified?

A
  • Mild → Open and closed comedones -/+ sparse inflammatory lesions
  • Moderate → Papules and pustules + widespread non-inflammatory lesions
  • Severe → Nodules, pitting, scarring + extensive inflammatory lesions
87
Q

What is the management of Acne Vulgaris?

A
  • No treatment in MILD cases
    1. Single topical therapy (Topical Benzoyl peroxide OR Topical retinoid)
    2. Topical combo therapy (Topical Benzoyl peroxide AND Topical retinoid AND Topical Antibiotic)
    3. Oral antibiotic → Tetracyclines such as Lymecycline, Oxytetracycline, Doxycycline
    • Can use COCP in lieu of Oral antibiotic in women
      1. Isotretinoin → Under specialist supervision
88
Q

What is the safety profile of Oral antibiotics for Acne Vulgaris?

A
  • Avoid tetracyclines in pregnant and breastfeeding women → Use erythromycin instead
  • Avoid use >3 months if only using Oral antibiotics
  • Avoid in children under the age of 12
  • Avoid Minocycline → causes irreversible pigmentation
  • Co-prescribe with Topical retinoid or Benzoyl Peroxide to reduce risk of ABX resistance
89
Q

What is the safety profile of COCP for Acne Vulgaris?

A
  • Should be used in combination with topical agents
90
Q

What is the safety profile of Isotretinoin for Acne Vulgaris?

A
  • Must be prescribed by a dermatologist
  • Must be on contraception → Teratogenic to foetus
  • Must stop Isotretinoin for 1 month before trying to get pregnant
91
Q

Side-effects of Isoretinoin?

A
  • Dry skin and lips (most common)
  • Photosensitivity to skin and sunlight
  • Depression, anxiety, suicidal ideation
  • Stevens-Johnson syndrome (rare)
  • Toxic Epidermal Necrolysis (rare)
92
Q

What medications contribute to drug-induced acne?

Describe the appearance of drug-induced acne?

A
  • Corticosteroids
  • Anabolic steroids
  • Lithium
  • Thyroid hormones

Monomorphic and pustular

93
Q

What is acne fulminans?

How is it managed?

A
  • Very severe acne associated with systemic upset i.e. fever

- Hospital admission required, condition responds to oral steroids

94
Q

What is Erythema Multiforme?

A

An erythematous rash caused by a hypersensitivity reaction

95
Q

What are causes of Erythema Multiforme?

A
  • Viruses: HSV, Orf
  • Bacteria: Mycoplasma pneumoniae, Streptococcus pneumoniae
  • Drugs: Penicillin, Sulphonamides, Carbamazepine, Allopurinol, NSAIDs, Oral contraceptive pill
  • Connective tissue disease e.g. Systemic lupus erythematosus
  • Sarcoidosis
  • Malignancy
  • Idiopathic
96
Q

What are the features of Erythema Multiforme?

A
  • Target lesions → red rings within larger red rings, with the darkest in the centre
  • Initially seen on dorsal aspect of hands and feet → → Torso
  • Upper limbs > more affected that lower limbs
  • Pruritus is seen HOWEVER MILD
  • Stomatitis may be seen also (Erythema Multiforme major)
97
Q

How is Erythema Multiforme diagnosed?

How is Erythema Multiforme managed?

A
  • Clinical diagnosis, on appearance of rash
  • If clear, underlying cause → Manage supportively
  • If no clear cause → CXR to search for underlying cause i.e. Mycoplasma pneumoniae
  • Usually resolves spontaneously within 1-4 weeks
  • May have to admit if oral mucosa is involved (stomatitis) → IV fluids, analgesia, steroids
98
Q

What is Chickenpox? What is Shingles?

A
  • Chickenpox is the primary infection caused by the Varicella Zoster Virus (VZV)
  • Shingles is the reactivation of the dormant VZV in the dorsal root ganglion
99
Q

How contagious is Chickenpox?

How is it spread?

A
  • Highly contagious, and is spread via the respiratory route or direct contact
100
Q

What is the incubation period of Chickenpox?

When are you infective in Chickenpox?

A
  • Incubation period: 10-21 days

- Infectivity: 4 days prior rash → 5 days after rash appeared

101
Q

When do patients stop being Infective with Chickenpox?

A
  • Once all lesions have crusted over, usually 5 days after rash appears
102
Q

What are the clinical features of Chickenpox?

A
  • Fever initially
  • Facial and truncal rash → spreads to whole body within 2-5 days. Initially Macular → Papular → Vesicular
  • General fatigue and malaise
103
Q

What is the management of Chickenpox?

A
  • Supportive management, will resolve on its own
  • Keep patient cool, trim nails to reduce scratching
  • Calamine lotion and Chlorphenamine (antihistamine) → reduces itchiness
  • Acyclovir → Immunocompromised patients
104
Q

What are the complications of Chickenpox?

A
  • Bacterial superinfection
  • Conjunctival lesions
  • Dehydration
  • Disseminated haemorrhagic chickenpox
  • Encephalitis
  • Pneumonia
  • Shingles
  • Ramsay Hunt Syndrome
105
Q

How do you manage a pregnant woman who has been exposed to someone with chickenpox?

A
  • If any doubt about the mother previously having chickenpox→ Checked for varicella antibodies
  • if the pregnant woman is not immune to varicella she should be given varicella-zoster immunoglobulin (VZIG) as soon as possible
  • VZIG is however only effective up to 10 days post exposure
  • Oral aciclovir should be given if pregnant women with chickenpox present within 24 hours of onset of the rash
106
Q

How do you manage a newborn with peripartum exposure or an immunocompromised patient to VZV?

A
  • Should have varicella-zoster immunoglobulin (VZIG)

- If they develop chickenpox, give IV acyclovir

107
Q

What is Hand, Foot and Mouth Disease commonly caused by?

A
  • Coxsackie A16 virus

- Enterovirus 71

108
Q
  • How contagious is Hand, Foot and Mouth? What is the incubation period?
A
  • Highly contagious, and the incubation period is 3-5 days
109
Q
  • What is the presentation of Hand, Foot and Mouth disease?
A
  • First → Tiredness, sore throat, dry cough, fever
  • Second → Small mouth ulcers appear
  • Third → Blistering vesicles over body, but commonly over hands and feet
110
Q

How is Hand, Foot and Mouth diagnosed?

A

Clinically, based on history and examination

111
Q

How is Hand, Foot and Mouth managed?

A
  • Supportive management → Fluids, analgesia
  • Reassurance of no link to disease of cattle
  • Advice on avoiding towel and bedding sharing, washing hands and careful handling of nappies
112
Q

What is the prognosis of Hand, Foot and Mouth?

A
  • Will resolve without treatment within 10 days
113
Q

What are the complications of Hand, Foot and Mouth?

A

Bacterial Superinfection
Dehydration
Encephalitis

114
Q

What is Molluscum Contagiosum?

A
  • A viral skin infection caused by the Molluscum Contangiosum virus, a type of Poxvirus
115
Q

How is Molluscum Contagiosum transmitted?

A
  • Via close personal contact and contaminated surfaces (i.e. towels, clothing)
116
Q

Which set of patients is Molluscum Contagiosum particularly prone in?

A
  • Children with atopic eczema
117
Q

What are the features of Molluscum Contagiosum?

A
  • Small, flesh coloured papules with a central dimple
  • They largely appear in clusters or “crops”
  • Can occur anywhere but SPARING of palms and soles
118
Q

How is Molluscum Contagiosum managed?

A
  • Encourage people not to scratch the lesions
  • Lesions are contagious → avoid sharing towels, clothing, and baths with others
  • Will resolve on its own, but can take upto 18 months
119
Q

If the papules in Molluscum Contagiosum are particularly troublesome, what can be offered?

What about if it is itching? Or is infected?

A
  • Can use simple trauma or cryotherapy
  • If itching → Prescribe emollient + topical hydrocortisone
  • If infected → Topical fusidic acid
120
Q
  • Is exclusion from school, swimming or gym necessary for Molluscum Contagiosum?
A

No

121
Q

When may referral to secondary care be appropriate for some patients with Molluscum Contagiosum?

A
  • HIV+ patients with extensive lesionsurgent referral to a HIV specialist
  • If eyelid-margin / ocular lesions and associated red eye urgent referral to an ophthalmologist
  • If anogenital lesions should be referred to genito-urinary medicine, for screening for other STIs
122
Q

What is Pityriasis Rosea?

A
  • A generalised, acute, self-limiting rash which affects young adults and has an unknown cause
123
Q

What is thought to cause Pityriasis Rosea?

A
  • Thought to be caused by HHV7 or HHV6, but no definitive organism has been found
124
Q

What are the features of Pityriasis Rosea?

A
  • In the majority of patients, NO prodrome, however some may present with a history of viral infection (headache, tiredness, loss of appetite, flu-like symptoms)
  • Rash begins as a HERALD patch, usually on the trunk, will be faint red or pink, scaly, oval shaped and at least 2cm in size
  • The rash will follow the distribution of the body along the “Lines of Langer” in a “christmas / fir tree” pattern
  • In dark skinned patients → lesions may be grey, lighter or darker
  • Other symptoms: generalised itch, low-grade pyrexia, headache lethargy
125
Q

What is the management of Pityriasis Rosea?

A
  • Supportive management if bothered by itching → Emollients, topical steroids, antihistamines
  • Otherwise, no management required
126
Q

What is the prognosis of Pityriasis Rosea?

A
  • Will resolve within 3 months

- Rash may leave discolorations however this will fade

127
Q

What is Seborrhoeic Dermatitis?

A
  • An inflammatory condition affecting the sebaceous glands relating to proliferation of a normal skin fungus Melassezia Furfur
128
Q

Where does Seborrheoic Dermatitis occur commonly in adults?

What are any associated conditions?

A
  • Where there is a high proportion of sebaceous glands i.e. Scalp → dandruff, periorbital, auricular and nasolabial folds
  • Otitis externa and blepharitis may develop
129
Q

Where does Seborrheoic Dermatitis occur commonly in children?

A
  • Scalp → cradle cap, nappy area, face, limb flexures
130
Q
  • What is the presentation of Seborrhoeic Dermatitis?
A
  • Erythematous, crusted, dry skin in sebum rich areas
131
Q

How can you describe cradle cap specifically?

A
  • Erythematous rash, with course yellow scales
132
Q

What is the management of Cradle crap?

What is the prognosis?

A
  • Depends on the severity of Cradle cap
  • If mild-moderate → Baby shampoo and baby oils
  • If severe → Mild topical corticosteroids i.e. 1% hydrocortisone
  • WILL RESOLVE SPONTANEOUSLY BY 8 MONTHS OF AGE
133
Q

What is the management of scalp Seborrhoeic Dermatitis in adults?

A
  • First-line → Zinc Pyrithione (Head & Shoulders) and tar (Neutrogena / T-Gel) are first-line
  • Second-line → Ketoconazole
134
Q

How do you manage face and body seborrhoeic Dermatitis in adults?

A
  • Topical antifungals i.e. ketoconazole, clotrimazole or miconazole
  • Topical steroids (for short-term periods)
135
Q
  1. What is Head lice?
  2. How is Head lice transmitted?
  3. What is the presentation of Head lice?
  4. How is Head lice diagnosed?
  5. How is Head lice managed?
  6. What is the consensus regarding school exclusion for Head lice?
A
  1. A common infection children caused by Pediculus capitis
  2. Close contact with other children, and sharing combs, towels
  3. Itchy scalp, may have visible lice
  4. Diagnosed with fine tooth comb
  5. Wet combing, Malathion, dimeticone 4%, isopropyl myristate and cyclomethicone
  6. Not necessary
136
Q
  1. What is Ring worm?
  2. What is it also known as?
  3. What is the presentation of Ring worm?
  4. What are the different types of Ring worm?
A
  1. Ring worm is a fungal skin infection
  2. It is also known as Tinea and Dermatophytosis
  3. It presents as an itchy rash, erythematous, scaly and well demarcated. One or several rings or circular shaped areas that spread outwards, with well demarcated edge. The edge is prominent and red, area in centre is more faint in colour
  4. Several different types:
    - Tinea capitis → Ringworm of the scalp
    - Tinea pedis → Ringworm of the feet, aka athlete’s foot
    - Tinea cruris → Ringworm of the groin
    - Tinea corporis → Ringworm of the body
    - Onychomycosis → Fungal nail infection
137
Q
  1. What are the different types of nappy rash?

2. Which is the most common?

A
  • Irritant Dermatitis (most common)
  • Candida Dermatitis
  • Seborrhoeic Dermatitis
  • Psoriasis
  • Atopic Eczema
138
Q

When is nappy rash commonly seen?

A

In babies aged between 9-12 months

139
Q

What are risk factors to babies developing nappy rash?

A
  • Delayed changing of nappies
  • Irritant soap products and vigorous cleaning
  • Certain types of nappies (poorly absorbent ones)
  • Oral antibiotics → predisposition to candida infection
  • Premature infants
  • Diarrhoea
140
Q

What are the features of Nappy Rash caused by Candida?

A
  • Rash extending into the skin folds
  • Larger, red macules
  • Well demarcated scaly border
  • Circular pattern to the rash spreading outwards, similar to ringworm
  • Satellite lesions, which are small similar patches of rash or pustules near the main rash
  • Babies MAY also have oral thrush with a white coating on the tongue (check!) this is likely to indicate a fungal infection in the nappy area
141
Q

What are the features of Nappy Rash caused by Irritant Dermatitis?

A
  • Sore, red, inflamed skin in the nappy area
  • Appears in individual patches on exposure areas of the skin that come in contact with the nappy
  • It tends to spare the skin creases → groin creases are healthy
  • There may be a few red papules beside the affected areas of skin
  • Can lead to erosions and ulceration
142
Q

What is the management of Nappy Rash?

A
  • Disposable nappies > towel nappies
  • Expose napkin area to air when possible
  • Apply barrier cream (e.g. Zinc and castor oil)
  • Mild steroid cream (e.g. 1% hydrocortisone) in severe cases
  • Management of suspected candidal nappy rash is with a topical imidazole. Cease the use of a barrier cream until the candida has settled
143
Q
  1. What is Scabies, in simple terms?
  2. What type of Hypersensitivity reaction is Scabies?
    Why?
  3. How long can it take for symptoms to present in Scabies?
  4. What is the presentation of Scabies?
A
  1. Scabies are tiny mites called Sarcoptes scabiei which burrow into the stratum corneum of the skin and cause infection
2. Type IV Hypersentivity
Delayed response (can take 30 days) for reaction to occur to mites / eggs after initial infection
  1. Upto 8 weeks
    • Itchy, small red spots, with possibly track marks where the mites have burrowed
      - Classic location of the rash is in between the finger webs → spreads to the whole body
      - Can also occur in flexor aspects of wrist and
144
Q

What is first and second line management of Scabies?

A
  • First line → Permethrin 5%

- Second line → Malathion 0.5%

145
Q

What are the directions of how to apply the management of Scabies?

A
  • Apply the insecticide on cool, dry skin
  • Allow to dry, leave on skin for 8-12 hours for permethrin, or for 24 hours for malathion, before washing off
  • Repeat treatment 7 days later
146
Q
  1. What is Norweigen Scabies?
  2. What patients is it commonly seen in?
  3. How is the presentation different to normal Scabies?
  4. What is the management?
A
  1. A form of crusted scabies
  2. Seen in HIV patients
  3. These patients may not have an itch because of no immune response → will be misdiagnosed for psoriasis
  4. WILL NEED ADMISSION, managed by Ivermectin and isolation
147
Q

Why do non-blanching rashes occur?

What is petechiae and purpura?

A
  • Non-blanching rashes are caused by bleeding under the skin, for example petechiae or purpura
  • Petechiae = Small <3mm spots
  • Purpura = Larger 3-10mm spots
148
Q

What is the most concerning differential in a child with a non-blanching rash which is important to rule out?

A

Meningococcal sepsis

149
Q

Aside from Meningococcal Sepsis, what are other differentials to consider in children with a non-blanching rash? (7 in total)

What would be the associated features of them?

A
  • Henoch-Schonlein Pupura (HSP) → Pupuric rash on buttocks + haematuria + arthralgia + abdo pain
  • Idiopathic Thrombocytopenia Pupura (ITP) → Will develop over several days in a well child
  • Acute leukaemias → Will develop gradually + anaemia + lymphadenopathy + hepatosplenomegaly
  • Haemolytic Uraemic Syndrome (HUS) → recent diarrhoea + oligouria + anaemia
  • Mechanical i.e. Superior Vena Cava Distribution → petechiae around head, neck, eyes
  • Traumatic i.e. Non-accidental injury → petechiae around the site of trauma
  • Viral illness → diagnosis of exclusion
150
Q

What investigations might you want to perform to rule non-blanching rash differentials in children?

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.

151
Q
  1. What is Erythema Nodosum?
  2. What is the presentation of Erythema Nodosum?
  3. What medications are associated with development of Erythema Nodosum?
  4. What conditions are associated with development of Erythema Nodosum?
A
  • Inflammation of subcutaneous fat
  • Tender, nodular, erythematous lesions usually over the shins
  • COCP, Penicillins, Sulfonamides
  • Inflammatory bowel disease, Sarcoidosis, Lymphoma, Leukaemias, Pregnancy, Infections: Strep throat, Gastroenteritis, TB
152
Q
  1. What is Impetigo?
  2. Is Impetigo a primary or secondary infection?
  3. In what patients is Impetigo common? What time of year?
  4. How is Impetigo transmitted?
  5. What are the features of Impetigo?
  6. What is the management of limited Impetigo?
  7. What is the management of extensive Impetigo?
  8. What is the consensus regarding time off school?
A
  1. Impetigo is a superficial bacterial skin infection caused by Staphylococcus aureus and Streptococcus pyogenes
  2. Can be a primary infection. Can be secondary to existing skin condition such as eczema, scabies, insect bites
  3. Common in children, and occurs during the summer time
  4. Spread is by direct contact with discharges from the scabs of an infected person. The bacteria invade skin through minor abrasions and then spread to other sites by scratching. Infection is spread mainly by the hands, but indirect spread via toys, clothing, equipment and the environment may occur
  5. “Golden” crusted lesions
  6. Topical fusidic acid
  7. Flucoxacillin
  8. Children should be excluded from school until lesions are crusted and healed or 48 hours after commencing antibiotic treatment
153
Q

What is Steven Johnson’s and Toxic Epidermal Necrolysis?

A
  • SJS and TEN are a spectrum of the same pathology, where a disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of skin
  • SJS → affects less than 10% of body surface area
  • TEN → affects greater than 30% if body surface area
154
Q

What are the features of Steven Johnson’s and Toxic Epidermal Necrolysis?

A
  • Systemically unwell i.e. pyrexia, tachycardia

- Positive Nikolsky’s sign → epidermis seperating with lateral pressure

155
Q

What is Nikolsky’s sign?

A

When the epidermis peels off with lateral pressure

156
Q

What medications cause Steven Johnson’s and Toxic Epidermal Necrolysis?

What is the management?

A
  • Never press skin as it can peel
  • NSAIDS
  • Phenytoin
  • Sulfonamides
  • Allopurinol
  • (IV immunoglobulin treatment)
  • Carbamazepine
  • Penicillins

0.1 Paediatrics - RB (16 decks)

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