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Neurology and special senses (Y4) > 6- Dermatology (Skin infections: Viral and infestations) > Flashcards

6- Dermatology (Skin infections: Viral and infestations) Flashcards

1
Q

chicken pox background

A
  • Highly infectious disease
  • Mostly mild to moderate and self-limiting
    o Milder in younger children
    o Infection severe in pregnancy- high risk of pneumonia and risk to fetus
  • Can be dangerous for immunocompromised or older adults
  • Endemic in most countries
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2
Q

shingles

A

Reactivation of dormant virus after bout of chickenpox leads to herpes zoster (Shingles)
o Like chickenpox but confided to just one dermatome

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3
Q

causes of chicken pox

A

Varicella-Zoster virus (DNA)

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4
Q

Risk factors for chicken pox

A
  • Immunocompromised missed e.g. HIV, children
  • Older age
  • Steroid use
  • Malignancy
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5
Q

transmission of chicken pox

A
  • Transmission- virus enters through upper respiratory tract
  • Viraemia occurs 4-6 days later
  • Skin lesions last 10-14 days
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6
Q

chicken pox infectivity

A

Infectivity is from a few days before onset of lesions until the crust falls off

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7
Q

Presentation of chicken pox

A
  • Prodrome- pyrexia, headache and malaise
  • Crops of vesicles , mostly on head , neck and trunk, sparse on limbs (new lesions stop after 4 days)
  • Papules -> vesicles -> pustules -> crust
  • When crust falls off they may leave a mark which will be present for a few weeks (higher risk of scarring in older children )
  • Redness around lesion could be bacterial superinfection
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8
Q

management of chickenpox

A
  • Simple advice: fluid intake, minimising scratching, avoid contact with pregnant women and neonates
  • Symptomatic treatment – paracetamol (analgeisa and antipyretic), give antihistamine and emollients to help with pruritus
  • Do not give NSAIDS (risk of necrotising soft tissue infections)!!!
  • Acyclovir not recommended in children
  • Encephalitis – admission to hospital
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9
Q

Advice to give parents whos children have chicken pox

A
  • Incubation period of 14-16 days
  • Keep child home from school for 5 days
  • Infective 24h before and until rash crusts
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10
Q

herpes zoster

A

shingles

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11
Q

shingles background

A
  • Viral infections, almost always affect the skin of a single dermatome

- Occurs wh›en the host is immunosuppressed- VZV (varicella zoster virus) reactivates and travels through peripheral nerve to skin of single dermatome

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12
Q

pathophysiology of shingles

A

Virus travels through a cutaneous nerve and remains dormant in dorsal root ganglion after chickenpox

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13
Q

presentation of shingles

A
  • Rash along nerve root
  • Painful blisters that scab over
  • Itchy, tingly, burning pain
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14
Q

shingles management

A

Severe e.g. **Hutchinson’s sign **or visual symptoms or serious complication, immunocompromised
- Admit to hospital
- May require aciclovir

Mild
- Analgesia

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15
Q

Prevention of shingles

A

zoster vaccine (>70-79)

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16
Q

Molluscum contagiosum
Background

A
  • Viral skin infection caused by molluscum contagiosum virus, which is a type of poxvirus
  • Spread through direct contact or by sharing towels or bedsheets
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17
Q

presentation of molluscum contagiosum

A

Presentation
- Small flesh colours papules (raised individual bumps on the skin) that characteristically have a central dimple
- Appear in crops of multiple lesions in a local area

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18
Q

manageemnt of molluscum

A

Papules resolve by themselves, although this can take up to 18 months.
- Can continue all their normal activities
- Should avoid towel sharing
- Bacterial superinfection may require topical fusidic acid or oral flucloxacillin

Advice
Scratching or picking should be avoided as it can lead to spreading, scarring and infection

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19
Q

management of molluscum if immunocompromised or very extensive lesions

A

If immunocompromised or very extensive lesions or lesions in genital or eyelids:
- Topical potassium hydroxide, benzoyl peroxide, podophyllotoxin, imiquimod, tretinoin
- Surgical removal and cryotherapy – can lead to scarring

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20
Q

Pityriasis rosea background

A

Background
- acute, self-limiting rash which tends to affect young adults.

Causes/ risk factors
- The aetiology is not fully understood but is thought that herpes hominis virus 7 (HHV-7) may play a role.

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21
Q

presentation of pityriasis rosea

A
  • in the majority of patients there is no prodrome, but a minority may give a history of a recent viral infection
  • herald patch (usually on trunk)
  • followed by erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer.
  • This may produce a ‘fir-tree’ appearance
22
Q

management of pityriaisis rosea

A

Self limiting- disappears in 6-12 weeks

23
Q

differentiating guttate psoriasis and pityriasis rosea

A
24
Q

Herpes simplex virus (HSV)
Background

A
  • Worldwide herpes virus is estimated to infect 66% of the population; more low- and middle-income.
  • Responsible for both cold sores (herpes labialis) and genital herpes
  • Many people have no symptoms
  • Transmitted by contact of herpetic lesions, saliva or skin containing HSV-1/2 virus
  • Clinical manifestation depends on site of disease and whether primary or latent infection.
25
Q

Pathophysiology of HSV

A
  • After an initial infection, the virus becomes latent in the associated sensory nerve ganglia.
  • Typically this is the trigeminal nerve ganglion with cold sores and the sacral nerve ganglia with genital herpes.
26
Q

HSV-1

A
  • Cold sores
  • It is often contracted initially in childhood (before five years), remains dormant in the trigeminal nerve ganglion and reactivates as cold sores, particularly in times of stress.
  • Can cause herpes in genitalia through oral sex
27
Q

HSV-2

A
  • Spreads by sexual contact and causes genital herpe
  • Genital herpes caused by HSV-1 is usually contracted through oro-genital sex, where the virus spreads from a person with an oral infection to the person that develops a genital infection.
28
Q

presentation of herpes simplex infection

A
  • Incubation- 2 weeks
  • Asymptomatic
  • Initial presentation most severe
  • Ulcers or blistering lesions affecting the genital area
  • Neuropathic type pain (tingling, burning or shooting)
  • Flu-like symptoms (e.g. Fatigue and headaches)
  • Dysuria (painful urination)
  • Inguinal lymphadenopathy
     Symptoms can last for 3 weeks in primary infection
29
Q

investigations for HSV

A

Investigations
- The diagnosis can be made clinically based on the history and examination findings.
- A viral PCR swab from a lesion can confirm the diagnosis and causative organism.

30
Q

management of genital herpes (usually HSV2)

A

Antiviral: aciclovir

Additional measures
- Paracetamol
- Topical lidocaine 2% gel (instillagel)
- cleaning with warm salt water- key prevents secondary bacterial infection and dries up lesion
- topical vaseline
- additional oral fluid
- loose clothing
- avoid intercourse with symptoms

31
Q

management of cold sore (HSV1)

A
  • most resolve after 5 days without treatment
  • topical antivirals applied prodromally can reduce duration by 12 to 18 hours
  • if frequent, severe, and predictable triggers:
  • consider oral prophylaxis: aciclovir 400mg, twice daily, for 5 to 7 days
32
Q

Warts/ HPV Background

A
  • Common benign lesion caused by infection with human papilloma virus
  • Can be classified by site as being:
    o Cutaneous e.g. Verrucas
    o Mucosal e.g. Sexually acquired anogenital warts
33
Q

Pathophysiology of warts

A

HPV
- Double stranded DNA virus
- Infection begins in the basal layer of the epidermis, cuasing proliferation of the keratinocytes (skin cells) and hyperkeratosis, and production of infectious virus particles- the wart
- Virus subtypes which infect the skin: 1,2,3,4,10,27,29,57
- Spread via direct skin to skin contact or autoinoculation
o E.g. if a wart is scratched or picked may devlop under the fingernail
- Incubation period as long twelve months

34
Q

risk factors for warts

A

Risk factors
- School aged children
- People with immunosuppression

35
Q

presentation of warts

A
  • Cutaneous viral wards are hard due to their keratinous surface
  • Tiny red or black dots can be visible in the wart are papillary capillaries
36
Q

Management of warts

A
  • Most warts resolve spontaneously especially in children

Indication for active treatment
- Immunosuppression
- Presence of complications
- Patient preference

37
Q

treatments for warts

A

Topical treatment
- Paints or patches containing salicylic acid or podophyllin which remove the surface skin cells
- Applied once daily

Cryotherapy
- Liquid nitrogen – 3-4 months of regular freezing

Electrosurgery
- Curettage and cautery for large and resistant warts

Others
- Imiquimod cream
- Bleomycin injections

38
Q

prevention of warts

A
  • Wash hands regularly don’t touch warts
  • Vaccines for anogenital warts
39
Q

Differential diagnoses for a cutaneous viral wart can include:

A
  • Seborrhoeic keratosis
  • Squamous cell carcinoma
  • Plantar corn and callus.
40
Q

Head lice
Background

A
  • Pediculus humanus capitis parasite
  • Causes infestations of the scalp
  • Spread by close contact with someone that has head lice
  • Transmission is by head to head contact or by sharing equipment
  • Lice cannot jump between hair
41
Q

which parasite causes head lice

A

Pediculus humanus capitis parasite

42
Q

presentation of head lice

A
  • Itchy scalp
  • Feel movement
  • Often visible
43
Q

risk factors of headlice

A

Risk factors
- School aged children

44
Q

management of head lice

A

Management
- Dimeticone 4% lotion can be applied to the hair and left to dry. This is left on for 8 hours (i.e. overnight), then washed off. This process is repeated 7 days later to kill any head lice that have hatched since treatment.
- Special fine combs can be used to systematically comb the nits and lice out of the hair. They can be used for detection combing to check the success of treatment. NICE clinical knowledge summaries recommend The Bug Buster kit.

45
Q

scbaies is causes by which parasitic mite

A

Sarcoptes scabiei

46
Q

causes of scabies

A
  • Spread through prolonged skin contact
  • Typically affects children and young adults
  • The scabies mite burrows into the skin, laying its eggs in the stratum corneum. The intense pruritus associated with scabies is due to a delayed-type IV hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection.
47
Q

Risk factors
for scabies

A
  • Overcrowding
  • Poverty
  • Poor nutritional status
  • Poor hygiene
  • Sexual contact
  • Immune suppression e.g HIV
  • Most common in children
  • Secondary to eczema and impetigo
48
Q

Presentation of scabies

A

Presentation
- Severe pruritus worse at night
- Close contact with people with similar symptoms
- White lines – linear burrows indicative of mite burrowing
- Lesion may be
o Papules
o Vesicles
o Pustules
o Nodules
o erythematous

49
Q

investigations for scabiee

A

Investigations
- Skin scrape
- Extraction of mite
- View under microscope

50
Q

investigations for scabiee

A

Investigations
- Skin scrape
- Extraction of mite
- View under microscope

51
Q

manageemnt of scabies (which treatment is first line vs second line)

A

Management (everyone in household treated)
- Permethrin 5% is first-line
- Malathion 0.5% is second-line
- Antihistamines
- Pruritus persists for up to 4-6 weeks post eradication

Neurology and special senses (Y4) (52 decks)

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