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BRS - Year 2 > 👍🏻Dermatology👍🏻- Infections & Infestations of Skin > Flashcards

👍🏻Dermatology👍🏻- Infections & Infestations of Skin Flashcards

(60 cards)

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1
Q

What is folliculitis?

A

Follicular erythema; sometimes pustular
May be infectious or non-infectious

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2
Q

What types of non-infectious folliculitis are there?

A

Eosinophilic (non-infectious) folliculitis is associated with HIV

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3
Q

What can cause recurrent folliculitis?

A

Recurrent cases may arise from nasal carriage of Staphylococcus aureus, particularly strains expressing Panton-Valentine leukocidin (PVL)

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4
Q

What is the treatment for folliculitis?

A

Antibiotics (usually flucloxacillin or erythromycin)
Incision and drainage is required for furunculosis

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5
Q

What is furunculosis?

A

Skin condition that causes painful boils, or furuncles, to develop on the body

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6
Q

What is the difference between a furuncle and a carbuncle?

A

A furuncle is a deep follicular abscess
Involvement with adjacent connected follicles = Carbuncle

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7
Q

Why are carbuncles more serious than furuncles?

A

Carbuncle more likely to lead to complications such as cellulitis and septicaemia

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8
Q

What can lead to infection by staph. aureus?

A

Establishment as a part of the resident microbial flora - abundant in nasal flora
Immune deficiency
- Hypogammaglobulinaemia
- Hyper-IgE syndrome – deficiency - Chronic granulomatous disease
- AIDS
- Diabetes Mellitus

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9
Q

What is Panton Valentine Leukocidin ?

A

Toxin produced by some strains of Staphylococcus aureus (S. aureus)

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10
Q

What effect panton valentine leukocidin produce?

A

β-pore-forming exotoxin
Leukocyte destruction and tissue necrosis
Higher morbidity, mortality and transmissibility
Skin
- Recurrent and painful abscesses
- Folliculitis
- Cellulitis
- Often painful, more than 1 site, recurrent, present in contacts

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11
Q

What are the extracutaneous effects of panton valentine leukocidin?

A

Necrotising pneumonia
Necrotising fasciitis
Purpura fulminans

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12
Q

What are the “risk of acquiring” 5 C’s?

A

Close Contact – e.g. hugging, contact sports
Contaminated items , e.g. gym equipment, towels or razors.
Crowding – crowded living conditions such as e.g. military accommodation, prisons and boarding schools.
Cleanliness (of environment)
Cuts and grazes – having a cut or graze will allow the bacteria to enter the body

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13
Q

How is a staph. aureus infection producing PVL treated?

A

Consult local microbiologist / guidelines
Antibiotics (often tetracycline)
Decolonisation – often:
- Chlorhexidine body wash for 7 days
- Nasal application of mupirocin ointment 5 days)
Treatment of close contacts

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14
Q

What is cellulitis?

A

Infection of lower dermis and subcutaneous tissue
Tender swelling with ill-defined, blanching erythema or oedema

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15
Q

What is the treatment for cellulitis?

A

Systemic Abx

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16
Q

What is a predisposing factor for cellulitis?

A

Oedema

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17
Q

What is impetigo?

A

Superficial bacterial infection, stuck-on, honey-coloured crusts overlying an erosion
Often affects face (perioral, ears, nares)

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18
Q

What causes impetigo?

A

Caused by:
- Streptococci (non-bullous)
or
- Staphylococci (bullous)

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19
Q

What is meant by bullous or non-bullous impetigo?

A

Bullous has boils, non-bullous is more common with a golden crust

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20
Q

What is the treatment for impetigo?

A

Topical +/- systemic antibiotics

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21
Q

What is impetiginisation?

A

Occurs in atopic dermatitis
- Gold crust
- Staphylococcus aureus

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22
Q

What is Borreliosis?

A

Lyme disease
Annular erythema develops at site of the bite of a Borrelia-infected tick
Initial cutaneous manifestation: Erythema migrans (only in 75%)
- Erythematous papule at the bite site
- Progression to annular erythema of >20cm

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23
Q

What is the progression of Borreliosis/Lyme disease?

A

1-30 days after infection, fever, headache
Multiple secondary lesions develop - similar but smaller to initial lesion
Neuroborreliosis
- Facial palsy / other CN palsies
- Aseptic meningitis
- Polyradiculitis
Arthritis – painful and swollen large joints (knee is the most affected join)
Carditis

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24
Q

What is the treatment for Lyme disease?

A

Doxycycline
Amoxicillin
Azithromycin

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25
Why is Lyme disease/borreliosis quite difficult to treat?
Serology not sensitive Histopathology - non-specific High index of suspicion required for diagnosis
26
What is syphilis?
An STI
27
What occurs upon primary infection with syphilis?
Chancre -painless ulcer with a firm indurated border Painless regional lymphadenopathy one week after the primary chancre Chancre appears within 10-90 days
28
What is secondary syphilis?
Begins ~50 days after chancre Malaise, fever, headache, pruritus, loss of appetite, iritis
29
Why is syphilis (particularly in later stages) quite difficult to diagnose?
Great mimicker’ – low threshold for testing - imitates many other conditions, has non-specific and systemic features - Rash (88-100%) -Pityriasis rosea-like rash - Alopecia (‘moth-eaten’) - Mucous patches - Lymphadenopathy - Residual primary chancre - Condylomata lata - wart like lesions - Hepatosplenomegaly
30
What are common signs of syphilis?
Orogenital lesions Can be misdiagnosed as HPV infection
31
What are Lues maligna?
Rare manifestation of secondary syphilis Pleomorphic skin lesions with pustules, nodules and ulcers with necrotising vasculitis More frequent in HIV manifestation
32
What is tertiary syphilis?
Serious and potentially fatal stage of syphilis Can occur years or even decades after initial infection
33
What is seen in tertiary syphillis?
Gumma skin lesions - nodules and plaques Extend peripherally while central areas heal with scarring and atrophy Mucosal lesions extend to and destroy the nasal cartilage Cardiovascular disease Neurosyphilis (general paresis or tabes dorsalis)
34
What is the treatment for syphilis?
IM benzylpenicillin or oral tetracycline
35
Outline HSV
Herpes simplex virus HSV-1 – direct contact with contaminated saliva / other infected secretions HSV-2 - sexual contact Replicates at mucocutaneous site of infection
36
How does HSV cause neurological symptoms and meningitis?
Travels by retrograde axonal flow to dorsal root ganglia
37
What are the characteristic features of HSV?
Primary and recurrent vesicular eruptions Favour orolabial and genital regions Transmission can occur even during asymptomatic periods of viral shedding
38
How long do the symptoms take to arise in HSV?
Symptoms with 3-7 days of exposure Preceded by tender lymphadenopathy, malaise, anorexia ± Burning, tingling
39
What are the systemic manifestations of HSV?
Aseptic meningitis in up to 10% of men
40
Outline the orogenital manifestations of HSV
Painful rouped vesicles on erythematous base → ulceration / pustules / erosions with scalloped border Crusting and resolution within 2-6 weeks Orolabial lesions – often asymptomatic Genital involvement – often excruciatingly painful→ urinary retention
41
What is an emergency dermatological manifestation of HSV?
Eczema herpeticum Monomorphic, punched out erosions (excoriated vesicles) Typically background of poorly-controlled eczema
42
What is the treatment for Eczema herpeticum?
IV acyclovir and treatment of eczema
43
What is herpetic whitlow?
HSV (1>2) infection of digits – pain, swelling and vesicles (vesicles may appear later) Misdiagnosed as paronychia or dactylitis Often in children
44
How does neonatal HSV infection arise?
Exposure to HSV during vaginal delivery – risk higher when HSV acquired near time of delivery HSV 1 or 2 Onset from birth to 2 weeks
45
How doe neonatal HSV present?
Vesicles → bullae erosions Encephalitis → mortality >50% without treatment, 15% with treatment → neurological deficits Requires IV antivirals
46
Outline sever or chronic HSV
47
How is HSV diagnosed?
Swab of Polymerase chain reaction
48
How is HSV treated?
Don't delay Oral valacyclovir or acyclovir 200mg five times daily in immunocompetent localised infection Intravenous 10mg/kg TDS X 7-19 days
49
What is pityriasis versicolor?
Superficial fungal infection Hypopigmented, hyperpigmented or erythematous macules +/- fine scale Begins during adolescence (when sebaceous glands become active) Flares when temperatures and humidity are high – e.g. in summer months Topical azole
50
What are dermatophytes?
Fungi that live on keratin
51
What fungus causes the most infections?
Trichophyton rubrum
52
What is kerion?
an inflammatory fungal infection that may mimic a bacterial folliculitis or an abscess of the scalp; scalp is tender and patient usually has posterior cervical lymphadenopathy
53
What is candidiasis?
Commonly known as a yeast infection *Candida albicans* Most sites show erythema oedema, thin purulent discharge Usually an intertriginous infection (skin folds) or of oral mucosa A common cause of vulvovaginitis Can become systemic (immunocompromise)
54
What can predispose candidiasis?
occlusion moisture warm temperature diabetes mellitus
55
What is mucormycosis?
Opportunistic fungal infection Oedema, then pain, then eschar Can lead to - fever, headache proptosis, facial pain, orbital cellulitis +/- cranial nerve dysfunction
56
What are the associations of mucormycosis?
Diabetes mellitus (1/3 of patients - DKA very high risk Malnutrition Uraemia Neutropaenia Medications: Steroids / antibiotics / desferoxamine Burns HIV
57
What is the treatment for mucomycosis?
Aggressive debridement & antifungal therapy amphoteracin
58
What is scabies?
Contagious infestation caused by Sarcoptes species Female mates, burrows into upper epidermis, lays her eggs and dies after one month
59
How does scabies appear?
Insidious onset of red to flesh-coloured pruritic papules Affects interdigital areas of digits, volar wrists, axillary areas, genitalia **A diagnostic burrow consisting of fine white scale** Crusted or ‘Norwegian’ scabies - hyperkeratosis - Often asymptomatic; immunocompromised individuals
60
What is the treatment of scabies?
Permethrin, oral ivermectin - Two cycles of treatment are required

BRS - Year 2 (75 decks)

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