Dermatology - Skin Infection Flashcards
(99 cards)
1
Q
What is tinea capitis?
A
Infection of scalp hair follicles and the surrounding skin, caused by dermatophyte fungi.
2
Q
Presentation of tinea capitis.
A
Prepubertal children:
- patchy hair loss
- scaling
- erythema
- regional lymphadenopathy
3
Q
Examining tinea capitis.
A
- Wood’s lamp
- clinical pattern
- dermoscopy
4
Q
Investigating tinea capitis.
A
Laboratory investigations advised to isolate the causative organism and direct management:
- scalp scrapings
- plucked hairs
Process for microscopy and culture.
5
Q
Medical management of tinea capitis.
A
Oral antifungal treatment guided by microscopy and culture.
6
Q
Social management of tinea capitis.
A
- children CAN attend school
- family screening and treatment of those +ve
- cleansing of hairbrushes / combs
7
Q
What is tinea pedis?
A
Foot infection due to dermatophyte fungus.
8
Q
Risk factors for tinea pedis.
A
- male
- young adult
- excessive sweating
- occlusive footwear
- systemic corticosteroids
- walking barefoot in public
9
Q
Presentation of tinea pedis.
A
- itchy erosions between the toes
- scales covering the sole of feet
- blisters on inner foot
10
Q
Management of tinea pedis.
A
Topical antifungal therapy daily.
11
Q
How can recurrence of tinea pedis be prevented?
A
- dry feet after bathing
- avoid occlusive footwear
- dry shoes and boots
- clean the shower and bathroom floors with bleach
- treat shoes with antifungal powder
12
Q
What is the causative organism or vulvovaginal candidiasis?
A
Candida albicans
13
Q
Risk factors for vulvovaginal candidiasis.
A
- menstruation
- pregnancy
- COCP
- empirical abx
- obesity
- diabetes mellitus
14
Q
Presentation of vulvovaginal candidiasis.
A
- itching / soreness
- dysuria
- vulval oedema
- cottage-cheese discharge
15
Q
Investigating vulvovaginal candidiasis.
A
- pH derangement
- vaginal swab
16
Q
Treatment of vulvovaginal candidiasis.
A
Topical antifungal pessaries, tablets or cream.
Oral antifungals if severe or recurrent infection.
17
Q
Conservative measures to manage vulvovaginal candidiasis.
A
- loose fitting clothing
- soak in salt bath
- antifungal creams before menstruation
18
Q
The following measures have not been shown to help with vulvovaginal candidiasis.
A
- Treatment of sexual partner
- Special low-sugar, low-yeast or high-yoghurt diets
- Putting yoghurt into the vagina
- Probiotics (oral or intravaginal lactobacillus species)
- Natural remedies and supplements (except boric acid)
19
Q
Risk factors for oral candidiasis.
A
- infancy / old age
- immunosuppression
- dentures
- smoking
- broad spectrum abx
- inhaled corticosteroids
20
Q
Presentation of oral candidiasis.
A
- white patches in mouth
- angular cheilitis
- geographic tongue
NB: severe infections may extend to the oesophagus causing difficulty with swallowing.
21
Q
Conservative measures to treat oral candidiasis.
A
- good oral hygiene (brish teeth regularly, warm saline water mouth wash)
- clean dentures
- remove dentures overnight
22
Q
Medical management of oral candidiasis.
A
First line: Topical antifungal products (e.g. oral nystatin)
Systemic antifungal treatment may be considered in severe infection.
23
Q
Causative organism of impetigo.
A
Staphylococcus aureus - causes honey-yellow crusting.
24
Q
Risk factors for impetigo.
A
- skin trauma
- skin conditions (e.g. dermatitis, scabies)
- immunosuppression
- warm climate
- poor hygiene
- crowded environment
25
Clinical features of non-bullous impetigo.
- honey-coloured crusts
- rapid spreading
- itching
- regional lymphadenopathy
NB: usually systemically well.
26
Clinical features of bullous impetigo.
Quickly appearing:
- bullae
- spontaneous rupture
- systemic symptoms (e.g. fever, malaise)
27
Complications of impetigo.
- staphylococcal scaled skin syndrome
- ecthyma
- cellulitis
28
Investigating impetigo.
Usually a clinical diagnosis, unless it is severe or recurrent.
If severe / recurrent, consider skin swab.
29
General management of impetigo.
- regular gentle cleansing to remove honey-coloured crusts
- practice good hand hygiene
- cover affected areas with watertight dressing to prevent spread
30
Medical management of non-bullous impetigo.
Topical antiseptic (e.g. hydrogen peroxide 1% cream).
31
Medical management of bullous impetigo.
First line: Flucloxacillin
32
Preventative measures of impetigo.
- avoid touching affected areas
- good hand hygiene
- clean cloth when drying
- do not share towels
- clothing and bedding changed daily
- avoid close contact with others
33
How long to stay off school with impetigo.
Treatment for 24 hours or until lesions crust over.
34
What is folliculitis?
An inflammed hair follice, causing a tender red spot with a surface pustule.
35
Causes of folliculitis.
- infection
- blockage
- irritation
- skin diseases
36
Infective causes of folliculitis.
Bacterial - Staphylococcus aureus
Fungi - tinea capitis
Parasitic infection - scabies
37
How to prevent folliculitis from regrowing hairs.
- electric razor
- apply shaving gel if using a blade shaver
38
How to avoid folliculitis due to occlusion.
Choose oil free moisturisers, as less likely to cause occlusion.
39
What is cellulitis.
A bacterial skin infection resulting in a local area of red, painful and swollen skin.
40
Risk factors for cellulitis.
- venous disease
- injury
- immunodeficiency
- CKD
- CLD
- obesity
- pregnancy
- alcoholism
41
Most common causes of cellulitis.
1. Streptococcus pyogenes
2. Staphylococcus aureus
42
Presentation of cellulitis.
Unilateral skin changes:
- painful
- red
- swollen
Systemic symptoms (e.g. fever, rigor) also present.
43
Complications of cellulitis.
- necrotising fasciitis
- gas gangrene
- severe sepsis
- endocarditis
44
Investigations for cellulitis.
Bloods:
- FBC (raised WCC)
- CRP (raised)
- blood culture
- D-dimer
Imaging may be performed:
- doppler ultrasound (exclude DVT)
45
Treatment of uncomplicated cellulitis.
Oral antibiotics at home, plus:
- analgesia
- adequate water/fluid intake
46
Treatment of cellulitis with systemic illness.
Admit to hospital:
- fluids
- IV antibiotics (penicillin based)
- oxygen
Can switch to oral antibiotics once fever has settled, cellulitis has regressed and CRP is reducing.
47
Associations of herpes simplex virus:
a) HSV-1
b) HSV-2
a) cold sores
b) genital herpes (STI)
48
Presentation of genital herpes.
- ulcers or blistering lesions
- neuropathic pain
- flu-like symptoms
- dysuria
- inguinal lymphadenopathy
49
Diagnosis of genital herpes.
Clinical diagnosis based upon history and examination.
Viral PCR from a lesion to confirm the diagnosis.
50
Management of genital herpes.
Referral to GYM specialist.
First line: aciclovir.
51
Conservative measures in genital herpes.
- paracetamol
- topical lidocaine
- cleaning with warm salt water
- additional oral fluids
- wear loose clothing
- avoid intercourse with symptoms
52
Aetiology of chickenpox.
Varicella-Zoster virus (VZV)
53
Transmission of chickenpox.
Highly contagious - spread by:
- droplet transmission
- direct contact with fluid
54
Clinical features of chickenpox.
Itchy red papules progressing to vesicles on the stomach, back and face.
Systemic features include fever, headache, coryzal symptoms.
55
Diagnosis of chickenpox.
Clinical diagnosis - often history elicits exposure to infected contact within the last 3 weeks.
Laboratory tests include:
- skin swab for viral PCR
- serology in pregnant women
56
Complications of chickenpox.
- secondary bacterial infection
- dehydration (N+V)
- exacerbation of asthma
- viral pneumonia
- thrombocytopenia
- shingles
- scarring
57
Treatment of chickenpox in children.
Symptomatic therapy:
- trim fingernails to minimise scratching
- warm bath and moisturising cream
- paracetamol for fever and pain
- calamine lotion
58
Prevention of the spread of chickenpox.
Children should stay away from school until the blisters have formed scabs (up to 10 days).
Pregnant women should avoid visiting friends or family when there is a known case of chickenpox.
59
Complications of chickenpox during pregnancy.
Maternal complications:
- pneumonia
- hepatitis
- encaphalitis
- death
Fetal complications:
- congenital abnormality
- severe infection after birth
60
Management of chickenpox exposure in pregnancy:
a) immune to chickenpox
b) not immune to chickenpox
a) no management; return if chickenpox rash
b) Varicella-Zoster immunoglobulin (VZIG) within 10 days of contact
61
Treatment of chickenpox in pregnancy.
Oral aciclovir.
NB: VZIG not useful after chickenpox rash appears.
62
What is shingles?
After primary VZV infection (ie. chickenpox), the virus remains dormat in the dorsal root ganglia of a spinal nerve.
It can reactivate and migrate down sensory nerves, causing shingles.
63
Triggers for shingles.
- pressure on nerve roots
- radiotherapy
- spinal surgery
- infection
- injury
64
Presentation of shingles.
Single dermatome:
- neuropathic pain
- red papules / pustules
65
Complications of shingles.
- eye complications
- scarring
- Ramsay Hunt syndrome
- systemic infection
66
What is post-herpetic neuralgia?
Persistence of recurrence of pain in the same dermatomal distribution of shingles.
It causes extreme sensitivity to the skin and itchiness.
67
Treatment of shingles.
Conservative measures:
- rest and pain relief
- protective ointment to the rash
Medical management:
- antiviral treatment (e.g. aciclovir)
68
When is immunisation against shingles recommended in the UK?
National shingles vaccination programme vaccinates those aged 70-79, due to high risk of complications.
69
Management of post-herpetic neuralgia.
- early use of antiviral medication
- amitriptyline
- local anaesthetic applications
NB: NSAIDs and opioids are generally unhelpful.
70
Aetiology of cutaneous warts.
Human papilloma virus
71
Risk factors for viral warts.
- school-aged children
- dermatitis (defective skin barrier)
- immunosuppression
72
Features of warts.
Hard, keratinous surface.
Small red or black dot in the wart (papillary capillaries)
73
Complications of cutaneous viral warts.
- psychosocial effect
- nail dystrophy / destruction
- squamous cell carcinoma
74
Examining viral warts.
Usually a clinical diagnosis +/- dermoscopy.
May use excisional biopsy if considering SCC.
75
When is active treatment recommended for viral warts?
- immunosuppression
- presence of complications
- patient preference
76
Active treatment of warts.
- topic treatment (e.g. salicylic acid)
- cryotherapy
- electrosurgery
77
What causes molluscum contagiosum?
Poxvirus - there are at least 4 viral subtypes.
78
Transmission of molluscum contagiosum.
- direct skin-to-skin contact
- direct contact (e.g. shared towels)
- auto-inoculation by scratching or shaving
- sexual transmission
79
Presentation of molluscum contagiosum.
Skin infection of childhood:
- clusters of papules
- arise in warm, moist places (e.g. armpit, groin)
80
Complications of molluscum contagiosum.
- secondary bacterial infection
- conjunctivitis
- disseminated secondary eczema
- scarring
81
How is molluscum contagiousum diagnosed?
Recognised by characteristic clinical appearance or on dermatoscopy.
82
What is the treatment of molluscum contagiosum?
Unable to kill the virus:
- topical antiseptics
- wart paints (e.g. salicylic acid)
Physical treatments (e.g. cryotherapy, laser ablation) can cause scarring and are avoided where possible.
83
Prevention of molluscum contagiosum.
- keep hands clean
- avoid scratching / shaving
- cover visible lesions with clothing
- do not share towels or clothing
- practice safe sex / abstain
84
Prognosis of molluscum contagiosum.
Usually harmless - but can take up to 2 years to clear.
85
Risk factors for scabies.
- crowded conditions
- poor hygiene
- poverty
- malnutrition
- homelessness
- immunodeficiency
86
Transmission of scabies.
Scabies infection is usually transmitted through close bodily skin-to-skin contact.
Spread via fomites (e.g. towels, clothing) is uncommon as the mite perishes within hours of leaving the host.
87
Scabies cycle.
1) Male mite fertilises the female on the surface of skin, then dies.
2) Female mite burrows into the stratum corneum, laying eggs.
3) Eggs hatch into larvae after approximately 5 days.
4) Hatched larvae mature into adult mites, and migrate to the skin surface.
88
Signs of scabies.
- generalised itch
- erythematous rash
- crusting
- burrows (web spaces, palms, soles)
- nodules
89
What is crusted scabies?
An altered host immune response results in uncontrolled proliferation of mites (thousands of mites, compared to 10-15 in classical scabies).
90
How is scabies diagnosed?
Clinical diagnosis with dermoscopy confirmation.
91
Medical management of scabies.
Topical 5% permethrin cream or lotion at night-time.
Repeat after 7-10 days.
92
Practical advice to patients regarding scabies.
Close contacts should complete eradication therapy, regardless of symptoms.
Air sheets, towels, clothes, duvets, blankets for 72 hours.
93
A patient applies topical 5% permethrin as eradication therapy for scabies. Their itching continues for several weeks.
Has the therapy worked?
Yes - post-scabetic itch is common and may persist for weeks. This does not represent persistent infection or treatment failure.
Antihistamines, emollients and soap avoidance should be advised.
94
Risk factors for headlice infestation.
- female sex
- children in family
- sharing beds
- sharing hair brushes
95
Features of head lice.
Scalp:
- visibly see nits
- itch
- irritation
- red-brown spots (excreted digested blood)
- crusting
- scaling
96
Complications of headlice.
- dermatitis
- impetigo
- lymphadenopathy
97
How are head lice diagnosed?
Identify the nits to make a diagnosis.
Can use dermoscopy of the scalp and hair.
98
Management of head lice.
- wet combing
- physical insecticide (topical dimeticone)
99
General advise on head lice.
- can attend school
- no need to treat clothing or bedding
- cannot prevent
- BAD leaflet on head lice
