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common skin infections Flashcards

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1
Q

what is tinea capitis

A

An infection of scalp hair follicles and the surrounding skin, caused by dermatophyte fungi

Tinea capitis is a fungal infection of the scalp, involving both the skin and hair. It is also known as scalp ringworm.

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2
Q

common organisms to cause tinea capitis

A

Microsporum canis

Trichophyton tonsurans.

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3
Q

classification for tinea capitis

A

Ectothrix (dermatophyte infection remains confined to the hair surface) e.g. M. canis

Endothrix (dermatophyte infections of the hair that invade the hair shaft and internalize into the hair cell) e.g. T. tonsurans, most common in the UK

Favus: Honeycomb destruction of hair shaft

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4
Q

tinea capitis seen commonly in who

A

Most commonly seen in healthy preadolescent children and immunocompromised adults

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5
Q

clinical features of tinea capitis

A

Scale, bald patches, regional lymphadenopathy

Kerion (abscess caused by fungal infection)

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6
Q

what Ix one ca do for tinea capitis

A

1) Wood’s lamp
Some dermophyte fungi e.g. ectothrixMicrosporumspecies demonstrate bright green fluorescence of infected hairs
Others don’t (e.g. nonfluorescent Trichophyton infection)

2) Dermoscopy
Black dot hairs, comma shaped hairs, cork-screw hairs

3) Specimens for microscopy + culture (diagnostic)
Scalpel scraping, hair pluck, brush or swab as appropriate to the lesion

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7
Q

risk factors of tinea capitis

A 
animal contact
household crowding
lower socioeconomic status
warm humid environments
contact sport.
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8
Q

complications of tinea capitis

A

alopecia
scarring alopecia - bald patches
erythema nodosum
ID reaction - get after starting the antifungal treatment

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9
Q

what would you see under a dermoscope for tinea capitis

A

Comma hairs

Corkscrew hairs

Zigzag hairs

Barcode-like (Morse code-like) hairs

Bent hairs.

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10
Q

tinea capitis DD

A

Alopecia areata and trichotillomania; cause patchy alopecia but are not scaly

Seborrhoeic dermatitis, atopic dermatitis, and scalp psoriasis; may mimic non-inflammatory tinea capitis, but the scale is usually more diffuse

Discoid lupus erythematosus and lichen planopilaris; cause scarring alopecia

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11
Q

tinea capitis management

A

4 weeks of systemic medication

Prescribe either oral griseofulvin (licensed) or oral terbinafine (off-label) empirically until culture results are available.

If the person lives in an urban area, start treatment with terbinafine for 4 weeks. - trichophyton tonsurans

If the person lives in a rural area, start treatment with griseofulvin for 4–8 weeks - griseofulvin

selenium sulfide or ketoconazole shampoo to be used at least twice weekly for 2–4 weeks, or an imidazole cream (in children less than 5 years of age) to be used daily for one week.

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12
Q

what is tinea corpis

A

Trunk and limbs

Itchy circular/annular rash with a clearly defined raised and scaly edge

Usually treat with topical antifungals; oral antifungals if unsuccessful

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13
Q

what is tinea cruris

A

involvement of groin and natal cleft

See management of Tinea cruris; may also benefit from topical corticosteroids for pruritus

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14
Q

what is tinea pedis and how does it look

A

athlete’s foot

moist scaling and fissuring in toewebs
spreads to sole and dorsal aspect of the foot

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15
Q

what is tinea manuum

A

Infection of the hand

Less common than infection of the foot

Scaling and dryness in the palmar creases

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16
Q

what is tinea unguium

A

ONYCHOMYCOSIS
Infection of the nail

Yellow discolouration, thickened and crumbly nail

Can lead to nail dystrophy

Mild infections can be managed with topical antifungals, oral antifungals often required for cure

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17
Q

What is tinea incognita

A

Inappropriate treatment of tinea infection with topical or systemic corticosteroids
Original infection also extends
Management: Cessation of steroid and standard antifungal treatment

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18
Q

features of cellulitis

A
  • Dimpled skin (peau d’orange)
  • Warmth
  • Blistering
  • Erosionsand ulceration
  • Abscessformation
  • Purpura:petechiae,
    ecchymoses, or haemorrhagicbullae

Systemic features
Fever
Malaise
Lymphangitis

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19
Q

what is cellulitis

A

A common bacterialinfectionthat involves the deep subcutaneous tissue

localisedarea of red, painful, swollen skin, andsystemicsymptoms

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20
Q

causes of cellulitis

A

Streptococcus pyogenes, Staphylococcus aureus

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21
Q

risk factors of cellulitis

A

Breaks in skin barrier: Wounds, ulcers, athlete’s foot, insect bites, IVDU, pressure sores

Poor venous flow / lymphatic drainage

Immunosuppression

Diabetes, chronic kidney disease, chronic liver disease

Obesity, pregnancy, alcoholism

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22
Q

investigations for cellulitis

A

Bloods: Inflammatory markers, Anti-streptococcal O titre (ASOT)

increase in CRP, leukocytosis

Skin swab

Imaging if required

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23
Q

management for cellulitis

A

Systemic antibiotics (usually oral); often penicillin-based e.g. Flucloxacillin, benzyl

Potential alternatives if penicillin-allergic: Clindamycin, Doxycycline, Vancomycin

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24
Q

complications of cellulitis

A

Necrotisingfasciitis

Gasgangrene

Severesepsis

Infection of other organs, e.g. osteomyelitis, meningitis, pneumonia

Endocarditis

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25
Q

what is erysipelas

A

Superficial form of cellulitis: Affects the upperdermisand extends into the superficial cutaneouslymphatics

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26
Q

differentials of cellulitis

A

Eczema/dermatitis due to stasis, contact factors

Fungal infection eg tinea corporis, tinea pedis
Drug eruption
Psoriasis
Lipodermatosclerosis
Thrombophlebitis
Insect bites and stings
Radiation damage following radiotherapy
Inflammatory breast cancer (carcinoma erysipeloides).
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27
Q

how to differentiate between erysipelas and cellulitis

A

erysipelas - well defined border

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28
Q

clinical features of erysipelas

A

sharp and raised border

It is bright red, firm and swollen. It may be finely dimpled (like an orange skin).

It may be blistered, and in severe cases may become necrotic.

Bleeding into the skin may cause purpura.

Cellulitis does not usually exhibit such marked swelling but shares other features with erysipelas, such as pain and increased warmth of affected skin.

In infants, it often occurs in the umbilicus or diaper/napkin region.

Bullous erysipelas can be due to streptococcal infection or co-infection with Staphylococcus aureus (including MRSA).

abrupt in onset and often accompanied by fevers, chills and shivering.

Erysipelas predominantly affects the skin of the lower limbs, but when it involves the face, it can have a characteristic butterfly distribution on the cheeks and across the bridge of the nose.

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29
Q

complications of erysipelas

A
  • Persistence of risk factors
  • Lymphatic damage (hence impaired drainage of toxins).

RARE

Abscess
Gangrene
Thrombophlebitis
Chronic leg swelling
Infections distant to the site of erysipelas
Infective endocarditis (heart valves)
Septic arthritis
Bursitis
Tendonitis
Post-streptococcal glomerulonephritis (a kidney condition affecting children)
Cavernous sinus thrombosis (dangerous blood clots that can spread to the brain)
Streptococcal toxic shock syndrome (rare).

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30
Q

skin manifestations of SLE

A

photosensitive ‘butterfly’ rash
discoid lupus
alopecia
livedo reticularis: net-like rash

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31
Q

what is pityriasis versicolor

A

superficial cutaneous fungal infection caused by Malassezia furfur

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32
Q

features of pityriasis versicolour

A
  • most commonly affects trunk
  • patches may be -hypopigmented, pink or brown (hence versicolor). May be more noticeable following a suntan
  • scale is common
  • mild pruritus
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33
Q

predisposing factos of pityriasis versicolor

A
  • occurs in healthy individuals
  • immunosuppression
  • malnutrition
  • Cushing’s
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34
Q

management of pityriasis versicolor

A

topical antifungal =ketoconazole

fail
scrapings + oral itraconazole

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35
Q

when can a child return to daycare if they have impetigo

A

Patients may return to school or work when they are no longer contagious which is when all lesions have crusted over or 48h after treatment starts

36
Q

how long must child wait to return to skl if they had measles or rubella

A

4 days following the onset of the rash

37
Q

what is impetigo

A
  • superficial bacterial skin infection usually caused by either Staphylcoccus aureus or Streptococcus pyogenes.

primary infection or a complication of an existing skin condition such as eczema (in this case), scabies or insect bites.

38
Q

where does impetigo tend to occur

A

anywhere on the body but lesions tend to occur on the face, flexures and limbs not covered by clothing.

39
Q

how is impetigo spread

A

Spread is by direct contact with discharges from the scabs of an infected person.

The bacteria invade the 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.§

40
Q

incubation period for impetigo

A

4-10 days

41
Q

features of impetigo

A

‘golden’, crusted skin lesions typically found around the mouth

very contagious

42
Q

management for impetigo

A

1) hydrogen peroxide 1% cream for ‘people who are not systemically unwell or at a high risk of complications’

2) topical antibiotic creams:
topical fusidic acid
topical mupirocin should be used if fusidic acid resistance is suspected
MRSA is not susceptible to either fusidic acid or retapamulin. Topical mupirocin should, therefore, be used in this situation

Extensive disease
oral flucloxacillin
oral erythromycin if penicillin-allergic

stay off skl 48hrs after AB Mx or til all the lesions are crusted/healed

43
Q

what is erythrasma

A

asymptomatic, flat, slightly scaly, pink or brown rash usually found in the groin or axillae.

44
Q

cause of erythrasma

A

overgrowth of the diphtheroid Corynebacterium minutissimum

45
Q

examination of erythrasma

A

Wood’s light reveals a coral-red fluorescence.

46
Q

management of erythrasma

A

Topical miconazole or antibacterial are usually effective. Oral erythromycin may be used for more extensive infection

47
Q

causes of erythema nodosum

A

NO – idiopathic
D – drugs (penicillin sulphonamides)
O – oral contraceptive/pregnancy
S – sarcoidosis/TB
U – ulcerative colitis/Crohn’s disease/Behçet’s disease
M – microbiology (streptococcus, mycoplasma, EBV and more)

48
Q

pathogen responsible for molluscum contagiosum

A

poxvirus

49
Q

management for tinea pedis

A

Management includes general measures (drying of feet, avoiding occlusive footwear etc), topical antifungals - imidazole, undecenoate - 4 weeks

oral terbinafine and oral antifungals if unsuccessful

50
Q

Ix for pityriasis versicolor

A

Woods light yellow green fluorescence

51
Q

features of iron deficinecy anaemia

A

Pallor

Other signs: koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis

52
Q

polycythaemia features

A

Pruritus particularly after warm bath
‘Ruddy complexion’
Gout
Peptic ulcer disease

53
Q

CKD features

A

Lethargy & pallor
Oedema & weight gain
Hypertension

54
Q

lymphoma features

A

Night sweats
Lymphadenopathy
Splenomegaly, hepatomegaly
Fatigue

55
Q

liver disease features

A

History of alcohol excess
Stigmata of chronic liver disease: spider naevi, bruising, palmar erythema, gynaecomastia etc
Evidence of decompensation: ascites, jaundice, encephalopathy

56
Q

tests for suspecting impetigo

A

swabs for microbiology

57
Q

risk of prolonged use of ABx in impetigo

which bacterial toxin is implicted in impetigo

A

staph aureus has shown to develop AB resistance particularly to fusidic acid if it is used for linger than 2 wekks

staph aureus
Group A strep

58
Q

if impetigo treatment fail intially

A

check swab and see if it sensitive to given AB

59
Q

why may there be recurrent cases of impetigo in family

A

nasal carriage of staph aureus is quite common - not eradicated by oral or topical treatment

eraducated by use of antibacterial nasak ointment and antiseptic skin washes

60
Q

what is erythrasma

A

generally asymptomatic, flat, slightly scaly, pink or brown rash usually found in the groin or axillae. It is caused by an overgrowth of the diphtheroid Corynebacterium minutissimum

61
Q

examination of erythrasma

A

woods light coral red fluorescence

62
Q

Mx for erythrasma

A

Topical miconazole or antibacterial are usually effective. Oral erythromycin may be used for more extensive infection

63
Q

description of staphylococcal scalded skin syndrome

A

● Commonly seen in infancy and early childhood

64
Q

causes of staphylocco

A

● Production of a circulating epidermolytic toxin from phage group
II, benzylpenicillin-resistant (coagulase positive) staphylococci

65
Q

RFs of erysipelas

A
  • previous episode
  • breaks in the skin barrier
    current/prior injury
  • exposure of umbilical cord and vaccination injury
  • nasopharyngeal infection
  • venous disease
  • immune deficiency
    — diabetes
    — alcoholism
    — obesity
    — HIV
  • nephrotic syndrome
  • pregnancy
66
Q

causes of erysipelas

A

Strep pyogenes - group A beta haemolytic streptococci
staph aureus
MRSA

67
Q

Mx of erysipelas

A
  • cold packs and analgesics to relieve local discomfort
  • elevation of an infected limb
  • compression stockings
  • wound care

ABx
- oral/IV pencillin

68
Q

Mx of recurrent cellulitis

A
  • Avoid trauma, wear long sleeves and pants in high-risk activities, such as gardening
  • Keep skin clean and well moisturised, with nails well tended
  • Avoid having blood tests taken from the affected limb
  • Treat fungal infections of hands and feet early
  • Keep swollen limbs elevated during rest periods to aid lymphatic circulation. Those with chronic lymphoedema may benefit from compression garments.
69
Q

what is scabies

A

caused by mite sarcoptes scabiei - spread by prolonged skin contact

70
Q

pathophysiology of scabies

A

mite burrows into the skin, laying its eggs in the stratum corneum

intense pruritis ass w scabies is due to a delayed type IV hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection

71
Q

features of scabies

A
  • widespread pruritus
  • linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist
  • in infants the face, scalp may also be affected
  • 2 Features - scratching: excoriation, infection
72
Q

Mx of scabies and what do u tell the family

A

FIRST LINE - premethrin 5%
SECOND LINE - malathion 0.5%
- pruritus persists up to 4- 6 weeks post eradication

  • avoid close physical contact with others until treatment is complete
  • all household and close physical contacts should be treated at the same time, even if asymptomatic
  • kill off mites with high heat
73
Q

what is crusted scabies (Norwegian)

Mx

A

crusted scabies in pts with suppressed immunity esp HIV

Ivermectin

74
Q

causes of onychomycosis

A
  • dermatophytes - - Trichophyton rubrum
    yeasts - candida
  • non-dermatophyte moulds
75
Q

RFs for fungal nail infections

A

diabetes mellitus

increasing age

76
Q

DD for onychomycosis

A

psoriasis
repeated trauma
lichen planus
yellow nail syndrome

77
Q

Ix of onychomycosis

A

nail clippings

scrapings of the affected nail

78
Q

Mx of onychomycosis

A

Diagnosis should be confirmed before starting treatment

Dermatophyte
- oral terbinafine FIRST LINE
6 weeks to 3 months therapy

Candida
- topical antifungals

really severe ORAL ITRACONAZOLE period of 12 weeks

topical Tx upto 6 months for fingernails and 9-12 months for toenails

79
Q

what is hidradenitis suppurativa

characterisitcs

suspected in who

A

chronic, painful, inflammatory skin disorder.

characterised by the development of inflammatory nodules, pustules, sinus tracts and scars in intertriginous areas.

suspected in pubertal or post-pubertal patients who have a diagnosis of recurrent furnucles or boild

80
Q

epidemiology and pathogenesis of hidradenitis suppurativa

A

epi

  • women are more likely to devleop HS than men
  • under 40

path
- chronic inflam occlusion of folliculopilosebaceous units that obstructs the apocrine glands and prevents keratinocytes from propely shedding from the follicular epithelium

81
Q

RFs of hidradenitis suppurativa

A

FH
smoking
obesity, diabetes, PCOS
mechanical stretching of skin

82
Q

clinical features of hidradenitis suppurativa

A
  • > Initial manifestation involves recurrent, painful, and inflamed nodules.
  • > HS occurs most commonly on intertriginous skin. However, non-intertriginous skin involvement also can occur. The axilla is the most common site
  • > Other areas include inguinal, inner thighs, perineal and perianal, inframammary skin.
  • > The nodules may rupture, discharging purulent, malodorous material.
  • > Coalescence of nodules can result in plaques, sinus tracts and ‘rope-like’ scarring.
83
Q

Mx of hidradenitis supparativa

A
  • Encourage good hygiene and loose-fitting clothing
  • Smoking cessation
  • Weight loss in obese
  • Acute flares can be treated with steroids (intra-lesional or oral) or flucloxacillin. Surgical incision and drainage may be needed in some cases.
  • Long-term disease can be treated with topical (clindamycin) or oral (lymecycline or clindamycin and rifampicin) antibiotics.
  • Lumps that persist despite prolonged medical treatment are excised surgically.
84
Q

complications of hidradenitis supparativa

A
  • Sinus tracts, fistulas
  • Comedones
  • Scarring - severe scarring can lead to dense, rope-like bands in the skin with strictures and lymphedema
  • Contractures
  • Lymphatic obstruction
85
Q

DDx of hidradenitis supparativa

A
  • Acne vulgaris - It primarily occurs on the face, upper chest, and back, whereas HS primarily involves intertriginous areas.
  • Follicular pyodermas (folliculitis, furuncles, carbuncles) - Unlike HS, follicular pyodermas are transient and respond rapidly to antibiotics
  • Granuloma inguinale (donovanosis) - It is a sexually transmitted infection caused by Klebsiella granulomatis. Suspect donovanosis if there is an enlarging ulcer that bleeds in the inguinal area.
86
Q

features of seborrhoeic dermatitis

ass

A

nflammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur

eczematous lesions on the sebum-rich areas: scalp (may cause dandruff), periorbital, auricular and nasolabial folds
otitis externa and blepharitis may develop

HIV
parkinson

scalp - T-gel - zinc pyrithione
ketoconazole
selenium sulphide and topical corticosteroid may also be useful

Face and body management
topical antifungals: e.g. ketoconazole
topical steroids: best used for short periods
difficult to treat - recurrences are common

87
Q

mosaic warts

A

It is a cluster of viral warts sometimes several cm in diameter

Topical salicyclic preparations after soaking and rubbing away hard skin (may work better if covered by tape overnight). Treatment takes a long time and perseverance is essential. Repeated liquid nitrogen application may be required and will be difficult on an extensive area. Formalin soaks several times per week can be used. Other specialist treatment can include bleomycin intralesional injections. It is reasonable to do nothing as most warts eventually disappear spontaneously

DERMATOLOGY (21 decks)

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