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3 - Y5 Paeds > Skin disease > Flashcards

Skin disease Flashcards

1
Q

What is a Macule

A
  • small flat area of altered colour or texture
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2
Q

What is a patch

A

larger flat area of altered colour or texture

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3
Q

What is a papule?

A
  • small raised lesion
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4
Q

What does maculopapular mean?

A

Maculopapular

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5
Q

What is a Plaque?

A
  • larger raised lesion, wider than it is high
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6
Q

What is a Nodule?

A

larger raised lesion with a deeper component

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7
Q

What is a Vesicle?

A
  • small clear fluid-filled lesion
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8
Q

What is a Bulla?

A

large clear fluid-filled lesion

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9
Q

What is a wheal?

A

transient raised lesion due to dermal oedema

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10
Q

What is a Pustule?

A
  • pus-containing blister
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11
Q

What is Purpura?

A
  • bleeding into the skin or mucosa; small areas are petechiae, large areas are ecchymoses; do not blanch on pressure
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12
Q

What is Excoriation?

A

scratch mark; loss of epidermis following trauma

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13
Q

What is Lichenification?

A

roughening of skin with accentuation of skin markings

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14
Q

What are scales?

A
  • flakes of dead skin
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15
Q

What is a Crust?

A

dry mass of exudates consisting of serum, dried blood, scales, pus

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16
Q

What is a Scar?

A

formation of new fibrous tissue post-wound healing

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17
Q

What is an Erosion?

A
  • loss of epidermis
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18
Q

What is an Ulcer?

A

loss of epidermis and dermis

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19
Q

What is a mongolian blue spot?

A

Blue/black macular discolouration at the base of the spine and on the buttocks

Aka dermal melanocytosis

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20
Q

Aetiology of mongolian blue spot?

A

Caused by entrapment of melanocytes in the dermis during their migration from the neural crest into the epidermis in foetal development

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21
Q

epidemiology of mongolian blue spot?

A

Most common in Afro-Caribbean or Asian infants

  • Seen in 90-100% of Asians and Africans; 10% in Caucasians
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22
Q

Signs and symptoms of mongolian blue spot?

A
  • Can occur anywhere on the body, but most commonly base of spine and buttocks
  • Present at birth
  • No tenderness
  • No change in colour over succeeding days
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23
Q

Ix for mongolian blue spot?

A
  • Clinical diagnosis
    • Important to note its presence at birth (at newborn check) so it is not mistaken for bruises
  • If bruising is suspected, monitor over a few days to confirm that it is not changing (bruises would change)
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24
Q

Mx for mongolian blue spot?

A

Reassurance

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25
Q

Complications and prognosis of mongolian blue spot?

A

Fade slowly over the first few years

They are of no significance unless misdiagnosed as bruises

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26
Q

What are milia?

A

Benign, keratin-filled epidermoid cysts

Aka milk spots

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27
Q

Aetiology of milia?

A

Due to retention of keratin and sebaceous material in the pilosebaceous follicles (gland and hair follicles)

Arise spontaneously

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28
Q

Epidemiology of milia?

A

Common in all ages

Affect 50% infants

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29
Q

Signs and symptoms of milia?

A
  • Superficial, uniform, white to yellowish, domed lesions
    • 1-2mm in diameter
    • Most common on face (esp cheeks, nose and around the eyes)

Usually asymptomatic; occasionally itchy

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30
Q

Ix for milia?

A
  • Clinical diagnosis
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31
Q

Mx for milia?

A

Reassurance

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32
Q

Complications and prognosis of milia?

A

Harmless and benign

Usually clear within a few weeks; can persist for a few months

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33
Q

What is a haemangioma?

A
  • Infantile haemangiomas: benign vascular lesions that appear during the first few weeks of life as blue/pink macules or patches, and subsequently regress → aka strawberry naevi
  • Congenital haemangiomas: fully-formed at birth and do not involute
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34
Q

Aetiology of haemangioma?

A

Thought originate from angiogenesis, maybe in response to hypoxia, local growth factors, cytokines and oestrogens

RFs: prematurity, low BW, advanced maternal age, multiple gestation, pre-eclampsia

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35
Q

Epidemiology of haemangioma?

A

Reasonably common à 1-3% of all newborns; 14% of infants whose BW is 1000-1500g

1/3 are evident at birth

36
Q

Signs and symptoms of haemangioma?

A
  • Usually present in the first few weeks of life
    • Occasionally present at birth
    • Initial signs are subtle pink patches or telangiectasias
  • Grow rapidly during the first 3-15 months of life (proliferative phase), then gradually regress (involution)
  • Soft
  • May be flat macules or patches, or nodules
  • May be multiple
37
Q

Ix for haemangioma?

A
  • Clinical diagnosis
  • Consider:
    • Doppler USS
      • To differentiate haemangioma from vascular/lymphatic malformations if necessary

Biopsy

38
Q

Mx for haemangioma?

A

Education and reassurance

If large or interfere with function:

  • Topical/oral propranolol +/- corticosteroid
  • Surgical excision if particularly large/obvious/may interfere with function
39
Q

Complications and prognosis of haemangioma?

A

Complications:

  • Cosmetic disfigurement
  • Ulceration and bleeding (esp in areas of friction)
  • Interference with sight, hearing, breathing, swallowing, speaking (if large on face)
  • Propranolol and corticosteroid SEs
  • Residual skin changes: scarring, atrophy, discolouration, telangiectasia

Growth is almost always complete by 9mo; regression occurs over 1-8yrs

Residual changes persist in 50%

40
Q

What is a nappy rash?

A

Inflammation of the skin in the area of the body covered by a nappy

41
Q

Causes of nappy rash?

A
  • Irritant (contact) dermatitis
    • Most common cause
    • Main irritants are moisture from urine and faeces, and faecal enzymes (ureases, proteases, lipases)
      • Other potential irritants are nappy components, friction from nappy, repeated wiping of the area or application of baby care products
    • May occur if nappies are not changed frequently enough or baby has diarrhoea
      • But can occur even if nappy area is cleaned regularly
  • Infection
    • May cause or exacerbate nappy rash
    • Candida is most common; also S. aureus, coxsackie virus, HSV
  • Underlying dermatological disorders are associated with nappy rash development:
    • Infantile seborrhoeic dermatitis
    • Atopic eczema
42
Q

RFs of nappy rash?

A
  • age <2yo,
  • diarrhoea,
  • underlying dermatological disorder,
  • infrequent nappy changes,
  • excess use of baby care products,
  • excess wiping,
  • no nappy-free time,
  • recent antibiotic use
43
Q

epidemiology of nappy rash?

A

Very common à 50%

Majority of newborns have some skin breakdown in the nappy area by 1wk of age, with increasing severity by 3wks

Most common in first 2yrs of life (when wearing nappies) but can occur in anyone who routinely wears nappies

44
Q

Signs and symptoms of nappy rash?

A
  • Irritant:
    • Acute onset
    • Affects convex surfaces of the buttocks, perineal region, lower abdomen and top of thighs
      • Flexures are spared → differentiates from other causes of nappy rash
    • Erythematous, may have a scalded appearance
    • Erosions and ulcers if severe
  • Candida:
    • Shiny erythematous patches
    • Includes skin flexures
    • May be satellite lesions (folds of groin, neck, axilla, oral candidiasis)
    • Nappy rash persisting for >3d is frequently associated with C. albicans
45
Q

Ix for nappy rash?

A
  • Clinical diagnosis
  • Consider if diagnostic doubt/treatment failure:
    • KOH test of skin scraping for Candida
    • Bacterial and fungal cultures of skin
  • Serum zinc level (zinc deficiency can cause rash)
46
Q

Mx for nappy rash?

A

Advise good nappy practice:

  • Change/inspect for soiling every 2hrs (more frequent in newborns/diarrhoea)
  • Remove potential irritants (wipe the area)
  • Use products with minimal additives
  • Allow nappy-free time whenever practical

Irritant:

  • Mild: protective emollient
  • Severe: low potency topical corticosteroids, e.g. hydrocortisone BD for 3-14d
    • Used if suspected pain
    • Protective emollient applied after steroid

Candida:

  • Topical antifungal, e.g. nystatin
  • Used if rash persists for >3d; continue use for 3d after rash clears
  • Protective emollient applied after the antifungal

If secondary bacterial infection is suspected:

  • Topical antibacterial therapy, e.g. mupirocin

Refer to dermatologist for patch testing/biopsy if persists for >14d

47
Q

Complications and prognosis of nappy rash?

A

Complications:

  • Secondary bacterial infection

Acute irritant contact nappy dermatitis typically resolves within 1wk

Nappy rash infected with candida may take 10d-3wks to resolve

48
Q

What is sebhoarreic dermatitis?

A

Common inflammatory skin disorder of the scalp that, in infants, manifests as scaling of the scalp (aka cradle cap)

49
Q

Aetiology of sebhoarreic dermatitis?

A

Aetiology is unknown

  • May be hormonally-dependent à explains why it arises in infancy, disappears spontaneously in childhood and re-emerges after puberty
  • Probably due to proliferation of the resident Malassezia furfur fungus
    • This fungus metabolises triglycerides to form oleic acid à oleic acid causes inflammation when it filters through the epidermis
50
Q

Epidemiology of sebhoarreic dermatitis?

A

Most common in first 3 months of life; prevalence decreases rapidly by 1yo; incidence increases again in adults

Cradle cap occurs in 42%

51
Q

Signs and symptoms of sebhoarreic dermatitis?

A
  • Starts on the scalp as an erythematous scaly eruption
    • The scales form a thick yellow adherent layer à cradle cap
  • The scaly rash may spread to the face, behind the ears, and then extend to the flexures and nappy area
    • May be more erythematous in other areas and less yellow/scaly
  • Not itchy and child is not bothered by it
    • In contrast to atopic eczema
  • In adults: presents with erythema, pruritis and scaling of scalp, glabella and nasolabial folds

Rare in children

52
Q

Ix for sebhoarreic dermatitis?

A
  • Clinical diagnosis
53
Q

Mx for sebhoarreic dermatitis?

A

Cradle cap in infants:

  • Emollients, e.g. topical olive oil
  • Topical corticosteroids, e.g. hydrocortisone
    • If severe and hasn’t responded to emollients
  • Ointment containing low-concentration sulphur and salicylic acid
    • To clear the scales on the scalp
    • Applied daily for a few hrs then washed off

Scalp seborrhoeic dermatitis in children:

  • Topical shampoos (e.g. coal tar)
  • +/- topical hydrocortisone

Widespread eruptions:

  • Topical corticosteroid (hydrocortisone)
  • +/- antibacterial/antifungal agent
  • Dermatology referral
54
Q

Complications and prognosis of sebhoarreic dermatitis?

A

Complications:

  • Secondary bacterial infection (impetigo)
  • Increased risk of developing atopic eczema

Self-limiting and generally declines from 4 months after birth

NB in adults it has a fluctuating course and tends to flare (esp in response to stress)

55
Q

What is atopic eczema?

A

Inflammatory skin condition characterised by dry, pruritic skin with a chronic relapsing course

Aka atopic dermatitis

56
Q

Aetiology of atopic eczema?

A

Aetiology is multifactorial à combination of genetic susceptibility and environmental factors

  • There is thought to be deficiency of skin barrier function (due to loss of function mutations in filaggrin protein)
    • Impairment of the skin’s barrier leads to increased immune sensitisation to cutaneous antigens à associations with food allergy, asthma and atopic rhinitis
  • Predominantly mediated by Th2 cells

Can be described as acute of chronic

  • Acute eczema: flare-up of symptoms (exacerbation)
    • Intracellular epidermal oedema (spongiosis) and leukocyte infiltration
  • Chronic eczema: the condition when the patient develops signs of chronic inflammation (e.g. lichenification)
    • Thickening of epidermis and striatum corneum, and dysfunction of keratinisation
57
Q

RFs of atopic eczema?

A
  • FHx of atopy (eczema, asthma, allergic rhinitis),
  • exclusive breastfeeding delays onset but doesn’t impact prevalence in later childhood
  • 1/3 children with atopic eczema will develop asthma
58
Q

Epidemiology of atopic eczema?

A

Prevalence 20% in children

Onset is usually in first year of life

  • Uncommon in first 2 months (unlike infantile seborrhoeic dermatitis)
59
Q

Signs and symptoms of atopic eczema?

A
  • Pruritis (main symptom)
    • Results in scratching and exacerbation of the rash à excoriation
    • May disturb sleep
  • Excoriated areas become erythematous, weeping and crusted
  • Dry skin
  • Hypopigmentation
  • Lichenification
    • Accentuation of normal skin markings
    • With prolonged scratching and rubbing
  • Distribution varies with age:
    • Infant (>2mo): mostly face, also trunk; spares nappy area
    • Older child: mostly flexor and friction surfaces (elbows and knees, neck, ankles)
60
Q

Ix for atopic eczema?

A
  • Clinical diagnosis
  • Skin prick testing
    • If allergy is suspected
    • Dietary elimination of food allergens may be needed for 4-6wks to detect improvement
61
Q

Mx of atopic eczema?

A

Avoid irritants and precipitants

  • Avoid soap and biological detergents
  • Clothing next to the skin should be pure cotton where possible (avoid nylon and pure wool)
  • Cut nails short to reduce damage from scratching; mittens at night may help young children
  • Avoid allergens if they are the trigger (e.g. cows milk)

Emollients:

  • Mainstay of management
  • Apply liberally 2-3x/d and after a bath
  • Baths using emollient oil and soap substitute can be used

Topical corticosteroids:

  • Mild steroids, e.g. hydrocortisone: apply 1-2x/d
  • Moderately potent steroids, e.g. fluticasone
    • Used for acute exacerbations; keep use to a minimum
    • Apply thinly and avoid face

Immunomodulators (calcineurin inhibitors):

  • E.g. tacrolimus ointment
  • In children >2yo with eczema not controlled by topical steroids and where there is risk of important SEs from further topical steroid use

Bandages/wet wraps:

  • Used over the limbs where scratching and lichenification is a problem
  • May be impregnated in zinc or tar paste
  • Worn overnight for 2-3d at a time until the skin has improved
  • Wet stockinette wraps:
    • Used short-term in young children with widespread itching
    • Diluted topical steroids mixed with emollients are applied to the skin, overlied with damp wraps and then dry wraps

Oral antihistamines:

  • For itch suppression
  • 2nd generations are not sedative

Antibiotics:

  • Antibiotics with hydrocortisone can be applied topically for mildly infected eczema
  • Systemic (oral) antibiotics for more widespread bacterial infection
  • Should cover S. aureus, e.g. flucloxacillin

Dietary elimination:

  • Food allergy may be suspected if the child reacts consistently to food, or in infants and young children with moderate-severe atopic eczema, esp if associated with GI symptoms
  • Trial of extensively hydrolysed or amino acid formula for formula-fed infants <6mo
  • Dietician input (to ensure whole food groups are not being avoided)
  • Food challenge is required to be fully objective

Psychosocial support:

  • Can disrupt child and whole family
  • National Eczema Society gives support and education
62
Q

Complications and prognosis of atopic eczema?

A

Complications:

  • Exacerbations
  • Psychological stress
  • Complications of steroids à skin thinning, systemic SEs
  • Regional lymphadenopathy
  • Impetigo
    • Localised, highly-contagious infection, (S. aureus or Group A Strep)
    • Most commonly occurs in eczema (as destruction of the epidermal barrier allows the bacteria easy access), but also occurs in other skin disease
      • Other RFs are poor hygiene, overcrowding, chronic colonisation with S. aureus and increased humidity
    • Classic honey-coloured crust
      • Also erythema, vesicles, pustules, sometimes bullae
    • Treatment:
      • Topical antibiotics (e.g. mupirocin) for mild cases
      • Oral antibiotics (e.g. flucloxacillin, erythromycin) for more severe cases
      • Do not go to school until lesions dry
  • Eczema herpeticum (see images)
    • Infection with HSV à spreads rapidly on atopic skin à extensive vesicular reaction
    • Grouped vesicles or pustules, may later progress to ‘punched out’ ulcerations
      • Often extensive skin involvement but areas of active eczema seem to be most severely affected
    • Emergency
    • IV acyclovir
      • In primary care give oral (then transfer to hospital for IV)

Mainly a disease of childhood à most severe in 1st year of life, resolves in 50% by 12yo and 75% by 16yo

63
Q

What is molluscum contagiosum?

A

Inflammatory skin condition characterised by dry, pruritic skin with a chronic relapsing course

Aka atopic dermatitis

64
Q

Aetiology of molluscum contagiosum?

A

Aetiology is multifactorial à combination of genetic susceptibility and environmental factors

  • There is thought to be deficiency of skin barrier function (due to loss of function mutations in filaggrin protein)
    • Impairment of the skin’s barrier leads to increased immune sensitisation to cutaneous antigens à associations with food allergy, asthma and atopic rhinitis
  • Predominantly mediated by Th2 cells

Can be described as acute of chronic

  • Acute eczema: flare-up of symptoms (exacerbation)
    • Intracellular epidermal oedema (spongiosis) and leukocyte infiltration
  • Chronic eczema: the condition when the patient develops signs of chronic inflammation (e.g. lichenification)
    • Thickening of epidermis and striatum corneum, and dysfunction of keratinisation

RFs: FHx of atopy (eczema, asthma, allergic rhinitis), exclusive breastfeeding delays onset but doesn’t impact prevalence in later childhood

  • 1/3 children with atopic eczema will develop asthma

Causes of exacerbations of eczema:

  • Bacterial infection (e.g. S. aureus), viral infection (e.g. HSV), irritants (e.g. soap), allergens (e.g. egg, cow’s milk protein), heat/humidity, drugs, psychological stress
65
Q

Epidemiology of molluscum contagiosum?

A

Prevalence 20% in children

Onset is usually in first year of life

  • Uncommon in first 2 months (unlike infantile seborrhoeic dermatitis)
66
Q

Signs and symptoms of molluscum contagiosum?

A
  • Pruritis (main symptom)
    • Results in scratching and exacerbation of the rash à excoriation
    • May disturb sleep
  • Excoriated areas become erythematous, weeping and crusted
  • Dry skin
  • Hypopigmentation
  • Lichenification
    • Accentuation of normal skin markings
    • With prolonged scratching and rubbing
  • Distribution varies with age:
    • Infant (>2mo): mostly face, also trunk; spares nappy area
    • Older child: mostly flexor and friction surfaces (elbows and knees, neck, ankles)
67
Q

Ix for molluscum contagiosum?

A
  • Clinical diagnosis
  • Skin prick testing
    • If allergy is suspected
    • Dietary elimination of food allergens may be needed for 4-6wks to detect improvement
68
Q

Mx for molluscum contagiosum?

A

Avoid irritants and precipitants

  • Avoid soap and biological detergents
  • Clothing next to the skin should be pure cotton where possible (avoid nylon and pure wool)
  • Cut nails short to reduce damage from scratching; mittens at night may help young children
  • Avoid allergens if they are the trigger (e.g. cows milk)

Emollients:

  • Mainstay of management
  • Apply liberally 2-3x/d and after a bath
  • Baths using emollient oil and soap substitute can be used

Topical corticosteroids:

  • Mild steroids, e.g. hydrocortisone: apply 1-2x/d
  • Moderately potent steroids, e.g. fluticasone
    • Used for acute exacerbations; keep use to a minimum
    • Apply thinly and avoid face

Immunomodulators (calcineurin inhibitors):

  • E.g. tacrolimus ointment
  • In children >2yo with eczema not controlled by topical steroids and where there is risk of important SEs from further topical steroid use

Bandages/wet wraps:

  • Used over the limbs where scratching and lichenification is a problem
  • May be impregnated in zinc or tar paste
  • Worn overnight for 2-3d at a time until the skin has improved
  • Wet stockinette wraps:
    • Used short-term in young children with widespread itching
    • Diluted topical steroids mixed with emollients are applied to the skin, overlied with damp wraps and then dry wraps

Oral antihistamines:

  • For itch suppression
  • 2nd generations are not sedative

Antibiotics:

  • Antibiotics with hydrocortisone can be applied topically for mildly infected eczema
  • Systemic (oral) antibiotics for more widespread bacterial infection
  • Should cover S. aureus, e.g. flucloxacillin

Dietary elimination:

  • Food allergy may be suspected if the child reacts consistently to food, or in infants and young children with moderate-severe atopic eczema, esp if associated with GI symptoms
  • Trial of extensively hydrolysed or amino acid formula for formula-fed infants <6mo
  • Dietician input (to ensure whole food groups are not being avoided)
  • Food challenge is required to be fully objective

Psychosocial support:

  • Can disrupt child and whole family
  • National Eczema Society gives support and education
69
Q

Complications and prognosis of molluscum contagiosum?

A

Complications:

  • Exacerbations
  • Psychological stress
  • Complications of steroids à skin thinning, systemic SEs
  • Regional lymphadenopathy
  • Impetigo
    • Localised, highly-contagious infection, (S. aureus or Group A Strep)
    • Most commonly occurs in eczema (as destruction of the epidermal barrier allows the bacteria easy access), but also occurs in other skin disease
      • Other RFs are poor hygiene, overcrowding, chronic colonisation with S. aureus and increased humidity
    • Classic honey-coloured crust
      • Also erythema, vesicles, pustules, sometimes bullae
    • Treatment:
      • Topical antibiotics (e.g. mupirocin) for mild cases AI
      • Oral antibiotics (e.g. flucloxacillin, erythromycin) for more severe cases
      • Do not go to school until lesions dry
  • Eczema herpeticum
    • Infection with HSV à spreads rapidly on atopic skin à extensive vesicular reaction
    • Grouped vesicles or pustules, may later progress to ‘punched out’ ulcerations
      • Often extensive skin involvement but areas of active eczema seem to be most severely affected
    • Emergency
    • IV acyclovir
      • In primary care give oral (then transfer to hospital for IV)

Mainly a disease of childhood à most severe in 1st year of life, resolves in 50% by 12yo and 75% by 16yo

70
Q

What is tinea?

A

A viral skin infection that causes benign, raised lumps

71
Q

Aetiology of tinea?

A

Caused by the molluscum contagiosum virus (a ubiquitous poxvirus)

  • In children it is caused by the MCV 1 and 1v subtypes
    • NB MCV2 causes sexually-transmitted disease in the groin in adults
  • The virus infects keratinocytes and mucosa à abnormal keratinocyte growth

Lesions appear within a few days to up to 6wks after viral infection

72
Q

What are the classifications of tinea?

A

Infection is classified according to site:

  • Scalp: tinea capitis
  • Feet: tinea pedis
  • Hands: tinea manuum
  • Nail: tinea unguium/onychomycosis
  • Body (incl trunk and arms): tinea corporis
73
Q

RFs for tinea?

A
  • exposure to infected people/animals/soil/fomites,
  • atopic dermatitis,
  • immunosuppression,
  • humid weather
74
Q

Epidemiology of tinea?

A
  • Tinea capitis (image):
    • Can cause hair loss with broken hairs at the surface
    • There may be circumscribed areas of scaling and inflammation
  • Tinea corporis (image):
    • Skin lesions have annular scaly plaques with raised edges
    • May be vesicles and pustules
    • Characteristic pattern of inflammation à active border
      • Greater degree of redness and scaling at the edge of the lesion
      • Central clearing is often present (distinguishes from psoriasis, lichen planus)
  • Tinea pedis:
    • Affects web of toe à skin may be erythematous
  • Tinea unguium:
    • Onycholysis
    • Nail dystrophy with separation of the nail from the nail bed
75
Q

Signs and symptoms of tinea?

A
  • Tinea capitis (image):
    • Can cause hair loss with broken hairs at the surface
    • There may be circumscribed areas of scaling and inflammation
  • Tinea corporis (image):
    • Skin lesions have annular scaly plaques with raised edges
    • May be vesicles and pustules
    • Characteristic pattern of inflammation à active border
      • Greater degree of redness and scaling at the edge of the lesion
      • Central clearing is often present (distinguishes from psoriasis, lichen planus)
  • Tinea pedis:
    • Affects web of toe à skin may be erythematous
  • Tinea unguium:
    • Onycholysis
  • Nail dystrophy with separation of the nail from the nail bed
76
Q

Ix for tinea?

A
  • Clinical diagnosis
  • Potassium hydroxide (KOH) microscopy of skin scrapings and nail clippings
    • To confirm diagnosis when unclear clinically (and always before starting treatment in nail infection)
    • Fungal spores and hyphae can be seen
  • Fungal culture
    • For definitive identification of fungus
  • Examination of tinea capita under filtered UV (Wood’s) light
    • May show bright green/yellow fluorescence of the infected hairs with some fungal species
77
Q

Mx of tinea?

A

Tinea capitis:

  • Systemic antifungal therapy
    • Griseofulvin (children >2yo) or itraconazole
    • Can just treat with topical antifungals (shampoo) if mild
  • Topical antifungal shampoo
    • E.g. selenium sulphide 1-2.5%

Tinea corporis, tinea pedis:

  • Topical antifungal therapy
    • E.g. miconazole, ketoconazole
    • Applied for 2-4wks

Animal sources of infection also need to be treated

78
Q

Complications and prognosis of tinea?

A

Complications:

  • Kerion: inflammatory, painful scalp patch associated with untreated tinea capitis
    • Can cause scarring alopecia
    • Treat with prednisolone
  • Secondary bacterial infection in tinea pedis

Prognosis is excellent with treatment

79
Q

What acne vulgaris?

A

Inflammatory skin condition characterised by red pimples on the skin, esp on the face, due to inflamed or infected sebaceous glands (pilosebaceous units)

80
Q

Aetiology of acne vulgaris?

A

Usually begins around puberty following adrenergic stimulation of the sebaceous glands and an increased sebum excretion rate

  • Obstruction to the flow of sebum in the sebaceous follicle (by hyperkeratosis) à distension of sebaceous follicle à neutrophil infiltration (inflammation)
  • External factors occasionally contribute, e.g. cosmetics, corticosteroids
  • Exacerbations may be associated with menstruation and emotional stress
81
Q

RFs of acne vulgaris?

A
  • 12-24yo,
  • genetic predisposition,
  • greasy skin type,
  • precipitating drugs (androgens, corticosteroids)

Infantile acne:

  • appears in <3mo;
  • transient and due to maternal androgens
82
Q

Epidemiology of acne vulgaris?

A

Very common (esp in adolescents – 75%)

More common in boys during adolescence, but in women during adulthood

83
Q

Signs and symptoms of acne vulgaris?

A
  • Variety of lesions:
    • Initially closed comedones (whiteheads – contain serous fluid) or open comedones (blackheads – due to oxidation of melanin)
    • Progress to:
      • Papules
      • Pustules
      • Nodules
      • Cysts
    • Skin lesions can be described as inflammatory or non-inflammatory
      • Non-inflammatory are open and closed comedones inflammatory are papules/pustules/nodules/cysts
  • Mainly on the face, back, chest and shoulders
  • Leads to scarring if severe
84
Q

ix for acne vulgaris?

A
  • Clinical diagnosis
  • May investigate underlying cause if indicated (e.g. PCOS, Cushing’s)
85
Q

Mx of acne vulgaris?

A

Advice:

  • Non-greasy cosmetics, daily face wash
  • Sunlight (in moderation) can help (phototherapy can help)
  • Dietary restriction is not beneficial

Mild-moderate non-inflammatory acne:

  • Topical retinoid (e.g. tretinoin) or salicylic acid
    • In children >12yo
    • Topical retinoids (vit A) encourage skin to peel and reduce obstruction within follicle
    • Salicylic acid is keratolytic and encourages skin peeling
    • Apply to affected area every evening

Mild inflammatory acne:

  • Topical retinoid (tretinoin)
    • topical antibiotic
      • E.g. clindamycin, erythromycin
      • Retinoid and antibiotic are available separately or in combination à synergistic
  • +/- topical benzoyl peroxide
    • Keratolytic agent to encourage skin to peel

Moderate-severe inflammatory acne:

  • Topical retinoid
    • oral antibiotic
      • E.g. tetracyclines (only if >12yo as may discolour teeth in younger children), erythromycin
  • +/- topical benzoyl peroxide

Severe/resistant acne:

  • Oral retinoid (e.g. isotretinoin)
    • For severe acne in teenagers unresponsive to other treatments
    • SEs: depression and suicidal ideation, teratogenicity (must counsel women), myalgia, headaches
    • Effective contraception must be used in oral and topical retinoid use

If hormone-related in females:

  • COCP
  • Consider anti-androgens (spironolactone)
86
Q

Complications and prognosis of acne vulgaris?

A

Complications:

  • Psychological morbidity → depression, social isolation, anxiety
  • Scarring
  • Secondary infection
  • Dyspigmentation

Usually resolves in late teens, but may persist

  • Persist at 25yo in 12% women and 5% men

3 - Y5 Paeds (13 decks)

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