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Yr 3 - Core Conditions > Dermatology - Skin Infections > Flashcards

Dermatology - Skin Infections Flashcards

1
Q

What virus causes chicken pox?

A

Varicella zoster virus (VZV)

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2
Q

Transmission of VZV?

A

Highly contagious. Droplet spread or direct skin contact with vesicle fluid, with the virus entering the body via the URT.

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3
Q

Incubation period of VZV?

A

10-14 days but can be up to 21 days.

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4
Q

What is the contagious period of VZV?

A

Chickenpox is contagious 1-2 days before rash appears until blisters have scabbed over (5-10 days).

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5
Q

Define a vesicle

A

Small, raised, fluid-filled lesion

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6
Q

Describe the rash first seen in chickenpox

A

Chickenpox is an acute disease characterised by a vesicular rash

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7
Q

Prodromal presentation of chickenpox?

A
  • Vesicular rash
  • High fever (38-39) – often first symptom
  • General malaise
  • Anorexia
  • Headache
  • Nausea
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8
Q

What is a prodrome?

A

an early symptom indicating the onset of a disease or illness

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9
Q

Describe the progression of the rash in chickenpox

A
  • Begins as small erythematous macules on the scalp, face, trunk, and proximal limbs
  • These macules develop into papules, vesicles and pustules which appear in crops
  • Crusting of the vesicles and pustules usually occurs after 5 days, at which point new vesicle formation has ceased (no longer contagious after all lesions have crusted over)
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10
Q

General advice for management of chickenpox?

A
  • Hydration
  • Avoidance of scratching (keep fingernails short) – due to risk of infection and scarring
  • Avoidance of pregnant women, neonates and immunocompromised
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11
Q

What analgesia should be avoided in chickenpox? Why?

A

NSAIDs → increase the risk of necrotising soft tissue infections

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12
Q

Symptomatic management of chickenpox?

A
  • Paracetamol
  • Sedating antihistamines (chlorphenamine)
  • Emollients and calamine lotion for itch
  • Antivirals → Consider oral acyclovir if adolescent or adult presents within 24 hours of rash onset (especially if severe or at high risk of complications)
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13
Q

What antiviral can be considered in the management of chickenpox?

A

Aciclovir

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14
Q

Possible complications of chickenpox?

A
  • Bacterial infections of the skin and soft tissues in children, including Group A streptococcal infections.
  • Infection of the lungs (pneumonia)
  • Infection or swelling of the brain (encephalitis, cerebellar ataxia)
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15
Q

What is Reye’s syndrome?

A

A rare complication seen in children and young adults recovering from viral illness and thought to be related to aspirin use

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16
Q

What is Reye’s syndrome thought to be related to?

A

Aspirin use → AVOID in young children

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17
Q

After chickenpox infection, where can the virus lay dormant?

A

in the sensory dorsal root ganglion cells and cranial nerves

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18
Q

What can chickenpox reactivate later as?

A

Shingles (Herpes Zoster) or Ramsay Hunt syndrome

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19
Q

What is Ramsay Hunt syndrome?

A

Ramsay Hunt syndrome occurs when a shingles outbreak affects the facial nerve near one of your ears. In addition to the painful shingles rash, Ramsay Hunt syndrome can cause facial paralysis and hearing loss in the affected ear.

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20
Q

Who does shingles (herpes zoster reactivation) commonly occur in?

A

Commonly occurs in the elderly and immunosuppressed (shingles in young adults should prompt investigation for an underlying immune condition)

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21
Q

Give some triggers for shingles reactivation

A
  • Nerve pressure
  • Radiotherapy at level of nerve root
  • Spinal surgery
  • Infection
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22
Q

Describe the rash in shingles

A
  • Can manifest first as a tingling sensation severe pain or in a dermatomal distribution
  • Progresses to erythematous papules occurring along one or more dermatomes within a few days → develop into fluid-filled vesicles (blistering rash) which then crust over and heal.
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23
Q

What symptoms can accompany the rash in shingles?

A

May be associated with viral symptoms – fever, headache, malaise, lymphadenopathy in affected area

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24
Q

What is the danger if the trigeminal nerve is affected in shingles?

A

Ophthalmic shingles

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25
Q

Management of uncomplicated shingles?

A
  • Rest and pain relief
  • Protection for rash e.g. Vaseline
  • Isolation – infectious to people who have not had chickenpox
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26
Q

When can oral antivirals (aciclovir) be indicated in shingles?

A
  • Oral antivirals if immunosuppressed or if eye involvement
  • IV antivirals if severe disease
  • Routinely prescribed in people >50
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27
Q

What can ophthalmic shingles lead to?

A

Corneal ulcers, scarring and blindness if eye involved

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28
Q

What nerve is affected in Ramsay Hunt syndrome?

A

Facial nerve (VII)

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29
Q

What nerve is affected in ophthalmic shingles?

A

Trigeminal nerve (V)

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30
Q

What is the most common complication of shingles?

A

Post-herpetic neuralgia - persistence/re-occurrence of pain in the same area more than 1 month after onset of shingles

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31
Q

What can reduce the chance of post-herpetic neuralgia?

A

Aciclovir

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32
Q

What is a risk factor for post-herpetic neuralgia?

A

Age

Facial infections

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33
Q

What are the 2 types of HSV. What infections does each cause?

A
  • Type 1 (HSV1) → oral & facial infections
  • Type 2 (HSV2) → genital & rectal infections, often transmitted sexually

BUT either virus can affect other areas of skin/mucous membranes.

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34
Q

Transmission of HSV?

A

Spread by direct or indirect contact. Virus can be transferred to new skin sites by the patient during an attack.

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35
Q

Is type 1 or type 2 HSV often more symptomatic?

A

Type 2

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36
Q

What does type 1 HSV mostly present as? What age group?

A

Gingivostomatitis (gingivitis is inflammation of gums, stomatitis is inflammation of mouth and lips) in children 1-5 y/o:

  • Fever
  • Restlessness
  • Excessive dribbling and bad breath
  • Gums are swollen/red/bleeding – eating is painful
  • White vesicles → these turn into yellow ulcers on tongue, throat, palate and inside cheeks
  • Lymphadenopathy
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37
Q

What does type 2 HSV mostly present as?

A
  • Genital herpes after onset of sexual activity
  • Painful vesicles, ulcers, swelling, redness for 2-3 weeks
  • In males – glans, foreskin and shaft
    • Anal herpes more common in MSM
  • Females – vulva and vagina
    • Often painful to urinate
    • Cervical infection may lead to severe ulcers
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38
Q

What is diagnostic test for HSV?

A

Swab base of ulcer and send off for nucleic acid amplification tests (NAATs).

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39
Q

Is recurrence of type 1 or 2 HSV more common?

A

Type 2

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40
Q

What are some triggers for HSV recurrence?

A

minor trauma, URTAs, sun exposure, hormones (e.g. prior to menstruation), stress

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41
Q

Complications of HSV infection?

A
  • Eye infection – swollen eyelids and conjunctiva
  • Throat infection – painful and affects swallowing
  • Eczema herpeticum
  • Erythema multiforme
  • Disseminated/widespread infection – serious in immunocompromised
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42
Q

How can HSV lead to eczema herpeticum?

A

Occurs when patient with eczema becomes infected by either HSV or VSV through breaks in skin

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43
Q

How does erythema multiforme present?

A

Targetoid lesions with central blisters

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44
Q

What is the most typical skin manifestation of HIV?

A

Pruritic papular eruption (PPE)

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45
Q

How does pruritic papular eruption present?

A
  • Itchy
  • Discrete scratched red bumps
  • Symmetrical
  • Diffuse
  • Extremities and trunk commonly affected
  • No mucosal. palmar or webbing involvement
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46
Q

What are viral warts? What virus are they caused by?

A

Very common non-cancerous growths.

Human papillomavirus (HPV)

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47
Q

Pathophysiology of warts?

A

Infection occurs in superficial epidermis, causing keratinocyte proliferation and hyperkeratosis.

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48
Q

Describe the presentation of a viral wart

A

Hard surface with black dot in the middle of each scale – this is a thrombosed capillary blood vessel

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49
Q

What are plantar warts?

A

Veruccas - tender, inward growing ‘myrmecia’ with clusters of mosaic warts (less painful)

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50
Q

Topical treatment of warts?

A

Salicylic acid – removes dead surface cells (keratolytic)

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51
Q

Other treatment options for warts?

A
  • Cryotherapy
  • Electrosurgery
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52
Q

What pathogen causes molluscum contagious?

A

Molluscum contagiosum virus - type of poxvirus

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53
Q

Risk factors for molluscum contagiosum?

A
  • Children <10 y/o
  • Warmer climates
  • Wet conditions e.g. swimming pool
  • Overcrowded environments
  • Atopic eczema (deficient skin barrier)
  • Immunocompromised
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54
Q

Transmission of molluscum contagiousum?

A
  • Skin-to-skin
  • Indirect e.g. towels, bedsheets
  • Autoinoculation (shaving or scratching)
  • Sexual transmission
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55
Q

Describe the clinical presentation of molluscum contagiosum

A
  • Clusters of small (1-6mm), round papules (raised bumps) – can be few to 100s in a local area
  • White, pink or brown (fresh coloured)
  • Often shiny with umbilicated pit
  • Papules contain white, cheesy material
  • Arise in warm/moist places e.g. flexures
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56
Q

If bacterial superinfection infection occurs in molluscum contagiosum as a result of scratching, what can you use to treat it?

A

Antibiotics (topical fusidic acid or oral flucloxacillin)

57
Q

What 2ary bacterial infection can you get from molluscum?

A

Impetigo

58
Q

Is impetigo bacterial or viral?

A

Bacterial

59
Q

What is impetigo?

A

Common acute superficial bacterial infection affecting the skin caused by Staphylococcal and Streptococcal bacteria.

60
Q

What 2 pathogens commonly cause impetigo?

A
  1. Staph. aureus - most common
  2. Strep. pyogenes
61
Q

Give some risk factors for impetigo

A
  • Atopic eczema
  • Scabies
  • Skin trauma – bacteria enters skin via break in skin:
    • Chickenpox
    • Insect bite
    • Wound
    • Burn
    • Dermatitis
62
Q

What are the 2 types of impetigo?

A
  1. Bullous (blisters)
  2. Non-bullous (sores)
63
Q

What pathogen ALWAYS causes bullous impetigo?

A

Staph. aureus

64
Q

Where does non-bullous impetigo typically occur?

A

Typically occurs around nose or mouth – staph/strep invade a minor trauma site

65
Q

Describe the lesions in non-bullous impetigo

A
  • exudate from the lesions dries to form a ‘golden crust’:
  • Pink macule → vesicle/pustule → crusted erosion
66
Q

Does non-bullous impetigo or bullous tend to cause systemic symptoms?

A

Bullous

67
Q

Management for non-bullous impetigo?

A
  • Topical fusidic acid, antiseptic cream (hydrogen peroxide 1% cream)
  • Oral flucloxacillin in more widespread/severe impetigo
68
Q

Describe the lesions in bullous impetigo

A
  • Small vesicles → flaccid transparent bullae → burst and form ‘golden crust’
  • Lesions can be painful and itchy
69
Q

Does bullous impetigo scar?

A

no

70
Q

Management for bullous impetigo?

A

Flucloxacillin

71
Q

How long should children with impetigo stay off school?

A
  • Children must avoid school until crust dries OR
  • Avoid school until they have completed 48 hours of antibiotic treatment
72
Q

Potential complications of impetigo?

A
  • Soft tissue infection e.g. cellulitis – risk of subsequent bacteraemia (sepsis)
  • Scarring
  • Staphylococcal scalded skin syndrome
  • Post-streptococcal glomerulonephritis
  • Scarlet fever
73
Q

What is staphylococcal scalded skin syndrome?

A
  • Bullous impetigo can lead to severe infections where the lesions are widespread → this is staphylococcus scalded skin syndrome
  • Dermatological emergency
74
Q

What is cellulitis?

A

A bacterial soft tissue infection of the dermis and subcutaneous tissue.

75
Q

Risk factors for cellulitis?

A
  • Advancing age
  • Immunocompromised e.g. diabetic
  • Predisposing skin condition e.g. ulcers, pressure sores, trauma, lymphoedema (breaches in skin)
76
Q

What pathogens typically cause cellulitis?

A
  • Staphylococcus aureus
  • Group A Streptococcus (S. pyogenes)
  • Group C Streptococcus (S. dysgalactiae)
  • MRSA (less common)
77
Q

Investigations for cellulitis?

A
  • Blood tests including culture
  • Skin swab for culture
78
Q

What is the 1st line Abx in the management of cellulitis?

A

Flucloxacillin (oral or IV depending on severity)

79
Q

Classification of cellulitis:

A
  • Class 1 → No systemic toxicity or comorbidity
  • Class 2 → Systemic toxicity or comorbidity
  • Class 3 → Significant systemic toxicity or significant comorbidity
  • Class 4 → Sepsis or life-threatening
80
Q

Which class of cellulitis requires IV Abx?

A

Class 3 or 4 (also consider admission for frail, very young or immunocompromised patients)

81
Q

Necrotising fasciitis vs cellulitis?

A
  • This can appear similar to cellulitis.
  • It affects the skin, subcutaneous tissue, fascia** and **muscle.
  • Oedema may extend beyond area of erythema (may blister or have bullae)
  • Pain is far more extreme than cellulitis
  • Crepitus on palpation (soft tissue gas)
  • More rapid progression
  • Patient more systemically unwell
82
Q

What is erysipelas?

A

Cellulitis refers to the infection of the dermis and subcutaneous tissue.

Erysipelas refers to the infection of the dermis and the upper subcutaneous tissue (i.e. is an acute, superficial form).

83
Q

What pathogen almost always causes erysipelas?

A

Almost all are caused by group A beta-haemolytic streptococci (unlike cellulitis).

84
Q

Give some risk factors for erysipelas

A
  • Previous erysipelas/cellulitis
  • Venous insufficiency
  • Immune deficiency (e.g. diabetes, HIV, alcoholism)
  • Breaks in skin barrier (bites, ulcers, psoriasis, eczema)
  • Obesity
  • Fissured toes or heels due to athlete’s foot or tinea pedis – cause skin breakage allowing entry of infective organisms
  • Pregnancy
85
Q

Abx management for severe cellulitis?

A

Flucloxacillin + benzylpenicillin

86
Q

What is folliculitis?

A

Group of skin conditions where hair follicles are inflamed (e.g. acne, rosacea)

87
Q

Describe the lesion in folliculitis

A

Tender red spot, often with surface pustule

88
Q

Folliculitis can be bacterial, viral, fungal or infestations. Give some example pathogens for each

A

Bacterial:

  • Staph. aureus
  • Pseudomonal aeruginosa (‘spa pool folliculitis’)

Viral:

  • HSV
  • HZV

Fungal/Yeast:

  • Candida
  • Tinea capitis

Infestations:

  • Hair follicle mas
  • Scabies
89
Q

Management of folliculitis?

A
  • Careful hygiene
  • Antiseptic cleanser
  • Bacterial → topical/oral antibiotics e.g. tetracycline
  • Viral → acyclovir
  • Yeast/fungi → topical/oral antifungal
90
Q

What is intertrigo?

A

Rash in flexures/body folds that may affect one or multiple sites (e.g. behind ears, axillae, groin, buttocks, finger/toe webs)

91
Q

Risk factors for intertrigo?

A
  • Obesity
  • Genetic tendency
  • Hyperhidrosis (excessive sweating)
92
Q

Why does intertrigo occur in body folds?

A
  • Flexural skin has high surface temperature
  • Moisture is stopped from evaporating due to folds
  • Friction from movement of fold skin can cause chafing
  • Bacteria and/or yeast multiply in warm, moist settings
93
Q

Does infectious intertrigo cause unilateral or bilateral lesions?

A

Unilateral

94
Q

Does inflammatory intertrigo cause unilateral or bilateral lesions?

A

Bilateral

95
Q

Management of inflammatory intertrigo?

A
  • Low potency topical steroids e.g. hydrocortisone
  • Calcineurin inhibitors e.g. tacrolimus
96
Q

potential complications of intertrigo?

A
  • Soft tissue infection e.g. cellulitis → risk of subsequent bacteraemia
  • Staphylococcal scalded skin syndrome → dermatological emergency
  • Post-streptococcal glomerulonephritis
97
Q

What is post-streptococcal glomerulonephritis?

A

a rare kidney disease that can develop after group A strep infections.

98
Q

What is staphylococcal Scalded Skin Syndrome (SSSS)? What is it caused by?

A

Severe desquamating rash that affects infants.

Caused by endotoxins released by S. aureus.

99
Q

Clinical features of staphylococcal Scalded Skin Syndrome (SSSS)?

A
  • Superficial fluid-filled blisters
  • Erythroderma (erythema >90% of body surface)
  • Desquamation (peeling of epidermis) and Nikolsky sign is positive
    • Oral mucosa unaffected unlike TEN
  • Fever & irritability – due to infective cause
100
Q

What is desquamation?

A

peeling of epidermis

101
Q

What is Nikolsky sign?

A

superficial epidermis can be dislodged by a slight shearing force – seen in SSSS, TEN and pemphigus vulgaris

102
Q

What is red man syndrome?

A

Red man syndrome is an infusion-related reaction peculiar to vancomycin

103
Q

What are dermatophytes?

A

Fungi that require keratin for growth. These can cause superficial infections of the skin, hair, and nails.

104
Q

What is tinea?

A

Tinea is a dermatophyte (ringworm) fungal infection. Generally more at risk of development if area of skin is warm & moist.

105
Q

What is tinea:

  • capitis
  • corporis
  • cruris
  • pedis
  • unguium
A
  • head
  • body
  • groin
  • foot
  • nail
106
Q

What is athlete’s foot also known as?

A

Tinea pedis

107
Q

Describe the lesions in tinea infections

A

Characterised by a red, scaly patch which classically has an area of central clearing.

108
Q

Diagnosis of tinea infections?

A
  • Skin scrapings
  • Hair/nail clippings
  • If the dermatophyte is Microsporum canis, under a Wood’s lamp affected areas with fluoresce
109
Q

Give 2 systemic antifungal agents that can be used for tinea capitis or onychomycosis (infection of the nail with onycholysis)

A
  1. Terbinafine
  2. Itraconazole
110
Q

Why should topical steroids be avoided in tinea infections?

A

Can cause tinea incognito

111
Q

What is tinea incognito?

A

Tinea incognito is a term used to describe a tinea infection modified by topical steroids. Topical steroids suppress the local immune response and allow the fungus to grow easily.

112
Q

Define pityriasis

A

Used to describe skin conditions in which the scale appears similar to bran.

113
Q

Define versicolor

A

Implies multiple colours

114
Q

What is pityriasis versicolor?

A

Common yeast infection of the skin. Not infectious but may affect more than 1 family member.

115
Q

What pathogen causes pityriasis versicolor?

A

Malassezia Furfur (fungi).

116
Q

Malassezia are part of the normal skin microbiota. Where are they usually found?

A

usually found sparsely in the seborrhoeic areas (scalp, face and chest) without causing a rash.

117
Q

What type of environment can trigger pityriasis versicolor?

A

Humid, warm environments (may clear in winter and recur in summer)

118
Q

What are the 2 types of pityriasis versicolor?

A

Brown → hyperpigmented (large melanosome within basal melanocytes)

White → hypopigmented

119
Q

Can pityriasis versicolor patches tan on sun exposure?

A

No

120
Q

Management for pityriasis versicolor?

A
  • Treat known triggers:
    • E.g. immunosuppressive condition
    • Warm, wet environment
  • Topical antifungals e.g. terbinafine
  • Oral antifungals if severe or widespread e.g. itraconazole
121
Q

Why should pityriasis versicolor not be treated with topical steroids?

A

Can cause tinea incognito

122
Q

What is candidiasis? Most common pathogen causing it?

A

Yeast infection (most common ‘candida albicans’). Can infect the mouth, GI tract, genitals, nails and skin in general:

  • Oral
  • Angular cheilitis
  • Vulvovaginal candidiasis
123
Q

Where is candida albicans a normal inhibitant of without problems?

A

GI tract

124
Q

Clinical features of candidiasis?

A
  • White plaques with erythema
  • Itchy
125
Q

Pharmacological management of oral candidiasis?

A

Nystatin

126
Q

What is scabies?

A

A highly contagious skin infection caused by mites.

Scabies is more common than you think. When someone presents with an itchy rash, ask whether anyone they live with has a similar rash and check between their finger webs for little red dots and track marks that may indicate scabies.

127
Q

What is the cause of scabies?

A

Parasite mites (Sarcoptes scabiei) burrow under skin.

128
Q

Transmission of scabies?

A
  • Close/direct contact (skin-to-skin contact with a person with scabies, can be brief e.g. holding hands or sexual contact)
  • Indirectly via fomites (less common) e.g. bedding, clothes, towels
  • Highly contagious
129
Q

Who is scabies more common amongst?

A

Seen more commonly among disadvantaged populations – is considered a neglected tropical disease

130
Q

Risk factors for scabies?

A
  • Children
  • Elderly
  • Living conditions (poverty, overcrowding)
  • Immunosuppression
131
Q

Pathophysiology of scabies?

A

A delayed type IV hypersensitivity reaction results in symptoms around 30 days or even up to 8 weeks) after the initial infection.

132
Q

What do the clinical features of scabies infection primarily result from?

A

from a local allergic reaction to the presence of the scabies mite, rather than directly being caused by the mite itself.

133
Q

Clinical features of scabies?

A
  • Intensely itchy rash that usually affects the inter-web spaces (between fingers), flexures of the wrist, axillae, abdomen, and groin
  • Itchy is classically worse at night – sleep disturbance
  • Rash usually papular or vesicular (with surrounding dermatitis)
  • Superficial burrows may often be seen – classically found in the webbed spaces between fingers
134
Q

What should you ask about in patient history in scabies?

A
  • Social history for risk factors e/g/ poor living conditions, overcrowding
  • Potential contacts
  • Additional holistic support
135
Q

What is Crusted (Norweigan) Scabies? Who is it typically seen in?

A
  • A severe variant of scabies where an individual is infected with thousands or millions or mites (compared with 5-20 in typical infection)
  • Often seen in immunocompromised
136
Q

1st line management of scabies?

A

Topical permethrin cream 5% (or malathion lotion)

137
Q

In scabies, how can the chance of reinfection be minimised?

A
  • Treat all members of household & all contacts on the same day
  • Good hygiene – wash all bed linen, toys, clothes etc
138
Q

Scabies can lead to a 2ary bacterial infection due to patients scratching the pruritic rash. What pathogens are most commonly responsible for this?

A

Most common S. pyogenes or S. aureus

Yr 3 - Core Conditions (33 decks)

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