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Y4: Dermatology > Infective diseases > Flashcards

Infective diseases Flashcards

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Dermatology Board Prep flashcards
1
Q

primary infection with HSV usually occurs when? what symptoms will they present with?

A

in childhood - asymptomatic or gingivostomatitis

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2
Q

herpes simplex infection occurs when there is reactivation of the HSV from a __ __ __ or __ __ __

A

dorsal root ganglion

cranial nerve ganglion

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3
Q

T/F: after initial infection with the herpes simplex virus, HSV becomes dormant and lies in the dorsal root ganglia of the spinal nerves for life

A

true

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4
Q

characteristic lesion with HSV?

A

localised painful vesicular rash preceding by tingling (esp if recurrent)

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5
Q

HSV-1 is most commonly associated with ___ lesions, whereas HSV-2 is most commonly associated with ___ lesions

A

1- oral

2- genital

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6
Q

Presentation of herpes labialis?

A

(aka coldsore)

Prodromal burning/ itching > small crop of vesicles arise on lips/ perioral > burst to leave a crust

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7
Q

Presentation of herpes genitalis?

A

Prodromal burning/ itching > small crop of acutely painful vesicles arise on the genitalia (+ rarely anal)

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8
Q

Presentation of herpetic whitlow?

A

paronychia

most common in dentists and other healthcare workers

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9
Q

diagnosis of HSV?

A

clinical diagnosis

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10
Q

management of HSV infection?

A

topical aciclovir

oral if widespread/ systemic upset

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11
Q

complications of HSV infection?

A

eczema herpeticum (pt with atopic eczema - urgent IV therapy + hospitalisation)
erythema multiforme
herpes simplex encephalitis

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12
Q

what virus causes chicken pox

A

varicella zoster virus (90% of population infected before adolescence)

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13
Q

transmissions of varicella zoster virus?

A

via airborne droplets and/ or direct contact with the lesions of an infected person

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14
Q

Varicella zoster virus:

1) Once in contact with pt, the virus travels where to replicate?
2) after several days, virus spreads to the __ and __ and continues to multiply
3) 1-2 weeks later, migrates to skin and mucous membranes causing characteristic ____ rash
4) on exposure to virus, large number of ___ are released throughout the body
5) the virus becomes dormant in the __ __ __
6) it can then reactive in later life as ____

A

1) regional lymph nodes (primary viraema)
2) spleen and liver
3) vesicular (vesicles are filled with highly contagious viral fluid)
4) Abs (providing lifelong immunity - chicken pox for 2nd time v rare)
5) dorsal root ganglia of the spine
6) shingles (herpes zoster)

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15
Q

presentation of chicken pox?

A

1) prodrome (1-2 days before cutaneous features): pyrexia, HA, malaise, abdo pain
2) widespread vesicular rash: begins on trunk, quickly spreads to the rest of the body. Extreme pruritis, vesicles burst leaving a crust.

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16
Q

diagnosis of chicken pox?

A

clinical diagnosis

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17
Q

Rx of chicken pox?

A

self-limiting. Supportive treatment (paracetamol, NSAIDs, emollients)

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18
Q

aietology of shingles?

A

reactivation of varicella zoster virus from DRG or CNG

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19
Q

shingles

1) T/F: can arise in anyone
2) more common in elderly
3) more common in patients who are _____

A

1) as long as they’ve been preivously infected with varicella zoster
2) true (unsuual in children)
3) immunocompromised

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20
Q

differentiating shingles from chickenpox?

A

shingles: arises in a single dermatome (relating to the ganglion the virus has reactivated in)

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21
Q

3 stages of shingles?

A

1) pre-eruptive: prodromal pruritis or burning for 1-2 days
2) eruptive: maculopapular rash developing in a single dermatome. Clusters of small vesicles >burst and form crust. Severe neuritic pain and allodynia.
3) chronic: post-herpetic neuralgia. Can be recurrent/ last >1 month after the rash has cleared

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22
Q

diagnosis of shingles?

A

clinical diagnosis (vesicular rash confined to single dermatome)

if uncertain > viral swab for PCR

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23
Q

Rx shingles?

A

aciclovir (early oral therapy may reduce length of illness and risk of post-herpetic neuralgia)

symptomatic: rest, paracetamol, NSAIDs
prevention: shingles vaccine. If infection = avoid contact with pregnant women and immunocompromised

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24
Q

Complications of shingles?

A

Ramsay hunt syndrome

Herpes zoster opthalmicus

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25
Q

what is ramsay hunt syndrome?

A

aka herpes zoster oticus
virus reactivates in geniculate gangloin, causing it to migrate down CNVII and VIII
Rash/ vesicles develop in the auditory canal and throat. Facial palsy, deafness, vertigo, tinnitus.

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26
Q

what is herpes zoster opthalmicus

A

virus reactivates in the ophthalmic division of the trigeminal nerve (CN V1). +ve Hutchinson sign: indicates involvement of the nasociliary branch + potential ocular complications - keratitis, uveitis, conjuncitivis, iritis, optic neuritis

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27
Q

what is impetigo

A

contagious bacterial infection common in childhood (2-5)

can occur later in life if pts are immunocompromised

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28
Q

most commonly develops during what sort of weather?

A

hot and humid

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29
Q

most common pathogens in impetigo

A

most often s. aureus.

Less commonly strep pyogenes or MRSA

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30
Q

2 types of impetigo?

A

impetigo (non-bullous)

bullous impetigo

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31
Q

how does impetigo form

A

small breaks in skin/ minor abrasions allow bacteria to enter skin from another infected individual

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32
Q

presentation of impetigo

A

most often the face (esp around mouth+ nose)
erythematous macules > small crop of vesicles/ pustules > rupture releasing exudate > dries forming golden yellow/ brown crust (honey comb)

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33
Q

impetigo infection lasts how long?

A

2-3 weeks

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34
Q

diagnosis of impetigo?

A

clinical diagnosis

swab if uncertain

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35
Q

Rx of impegito?

A

wound care: regular cleaning, topical antiseptic or Abx
Oral fluclox if infection extensive
Measures to reduce spread (not sharing towels etc)

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36
Q

what is this describing:

a pyogenic infection of the s/c fat and lower dermis

A

cellulitis

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37
Q

causative pathogen in cellulitis?

A 
step pyogenes (2/3)
staph aureus (1/3)
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38
Q

risk factors for cellulitis?

A 
prev cellulitis
venous stasis
lymphodema
obesity
elderly
IVDU
alcoholism
inflammatory dermatoses
insect bites
pregnancy 
immunosupression
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39
Q

how does cellulitis form?

A

bacteria penetrate the skin through disruptions to the normal barrier

they make their way to the deep dermal and s/c layers where they proliferate

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40
Q

presentation of cellulitis?

A

often unilateral, affecting a limb
localised, painful, erythematous and swollen
systemic features (fever, rigors, malaise)

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41
Q

diagnosis of cellulitis

A

clinical diagnosis

confirm with: raised WCC, raised CRP, swab and culture causative organism

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42
Q

Rx of cellulitis?

A

analgesia (WHO ladder)

fluclox 1st line Abx

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43
Q

what is molluscum contagiosum

A

viral skin infection that presents as cluster of papules (mollucsa)

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44
Q

who gets molluscum contagiosum?

A

almost exclusively childhood infection (1-4)

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45
Q

what causes molluscum contagiosum?

A

infection with Poxvirus
methods of transmission: direct skin-skin contact, indirect (fomite), autoinucolation (scratching, shaving), sexual transmission

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46
Q

presentation of molluscum contagiosum?

A

clusters of small, shiny, round, umbilcated papules most often on limbs
usually flesh coloured (can be white, pink or pigmented)

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47
Q

diagnosis of molluscum contagiosum?

A

clinical (skin biopsy if unusual presentation - rare)

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48
Q

Rx of molluscum contagiosum?

A

no treatment to eradicte the virus
self limiting mostly, not actively treatment (often lasts 12-18 months)
To speed up disappearance of each papule: squeeze out the soft, white core of the papule, cryothereapy, gentle curettage, antiseptics, wart paints/ salicylic acid

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49
Q

what is pityriasis versicolor?

A

a common cutaneous yeast infection

50
Q

pityriasis versicolor more common in what climate?

A

hot/ humid

51
Q

what causes pityriasis versicolor?

A

infection with the fungus Malassezia (makes up part of normal cutaneous flora)
> changes from its usual form to a pathological form that proliferates and causes infection

52
Q

pityriasis versicolor presentation:

1) most commonly presents on the ___ initially
2) describe the lesions
3) are the lesions symptomatic?

A

1) trunk
2) multiple hypopigmented macules with a fine scale
4) may be slightly pruritic

53
Q

diagnosis of pityriasis versicolor?

A

clinical

if uncertain: wood’s lamp (yellow/ green fluorescence). Skin scraping for microscopy.

54
Q

Rx of pityriasis versicolor?

A

topical anti-yeast e.g. clotrimazole or ketoconazole

55
Q

what is this describing:

Also known as slapped cheek/ fifths disease.
A common infective paediatric condition.

A

erythema infectiosum

56
Q

erythema infectiosum - most common in who? and when?

A

children

winter months

57
Q

what causes erythema infectiosum?

A

infection with parovirus B19/ erythrovirus

- spread via respiratory droplets

58
Q

presentation of erythema infectiosum?

A

non-specific prodrome (HA, malaise, fever)
biphasic rash
- erythema over cheeks, sparing nasal bridge and periorbital region. 1-4 days.
- pink, lace-like rash trunk and limbs. 5-9 days. Can recur in the following months following trigger e.g. sunlight, stress etc

59
Q

when are pts with erythema Infectiosum no longer infectious?

A

when erythematous rash over cheeks forms

60
Q

complications of erythema Infectiosum?

A

small joint polyarthropathy
spontaneous abortion (hydrops foetalis)
aplastic crisis
chronic anaemia

61
Q

diagnosis of erythema Infectiosum?

A

clinical

if uncertain -Ab testing (paravirus B19 IgM)

62
Q

rx of erythema infectiosum?

A

self-limiting

supportive Rx

63
Q

hand, foot and mouth disease occurs following infection with what?

A

cocksackie virus A16, cocksackie virus A10, enterovirus 71 (usually more severe)

64
Q

transmission of hand, foot and mouth disease?

A

often faecal-oral route

65
Q

presentation of hand, foot and mouth disease?

A

non-specific prodrome: HA, malaise, fever
painful oral lesions (vesicles and ulcers)
vesicles on palms of hands, soles of feet and in between fingers (grey in colour, have tendency to ulcerate/ crust. Typically resolve in 10 days. May be painful

66
Q

complications of hand, foot and mouth disease?

A

neuro involvement/ meningitis risk - usually when enterovirus 71 is the causative virus

67
Q

Rx of hand, foot and mouth disease?

A

self-limiting

supportive treatment as required

68
Q

what is Pitted Keratolysis?

A

a bacterial skin infection mainly affecting the feet

69
Q

Pitted Keratolysis

1) more common in what weather?
2) high incidence in what occupations?

A

1) hot and humid

2) farmers, athletes, industrial/ construction workers

70
Q

causative organism in Pitted Keratolysis?

A

Corynebacterium infection.

71
Q

Pitted Keratolysis risk factors?

A
  • hot, humid weather (bacteria proliferative)
  • poorly breathable footwear
  • excessive perspiration
  • poor hygeine
  • immunosupression
72
Q

Pitted Keratolysis pathophysiology

1) bacteria rapidly proliferative in optimum conditions
2) they produce protease enzymes that work to destroy the __ __
3) ____ compounds released by the bacteria cause a potent malodour

A

2) stratum corneum (>characteristic pitted appearance)

3) sulfur

73
Q

Pitted Keratolysis almost always affects where?

A

plantar aspect of foot (+ rarely the hands)

74
Q

how does Pitted Keratolysis present?

A

extremely unpleasant, malodorous feet
multiple small pits covering the feet. Usually asymptomatic, may rarely cause pain or itching. May coalesce to form a large crater-like lesion

75
Q

diagnosis of Pitted Keratolysi?

A

clinical

skin scraping to rule out fungal infection

76
Q

Rx of Pitted Keratolysi?

A

encourage breathable, light footwear and foot hygeine
topical fusidic acid
oral Abx therapy if severe erythromycin)

77
Q

lice are obligate ____ found living on the human body

how are they spread?

A

ectoparasites

spread via human contact

78
Q

what are the names for

1) head louse
2) body louse
3) pubid louse

A

1) Pediculus capitis
2) Pediculus corporis (aka Vagabond’s disease when chronic)
3) Phthirus pubis

79
Q

presentation of lice

A

intense pruritis

often visible lice and eggs

80
Q

diagnosis of lice?

A

clinical

81
Q

Rx of lice?

A

malothion lotion of other insecitide

hygeine to avoid spread/ reinfection

82
Q

what is tinea?

A

a fungal infection with a dermatophyte

aka ringworm of the skin

83
Q

subtypes of tinea?

A 
Tinea capitis = Scalp.
Tinea barbae = Beard.
Tinea corporis = Body.
Tinea manuum = Hands.
Tinea unguium = Nails.
Tinea cruris = Groin.
Tinea pedis = Feet.
84
Q

how is tinea spread?

A

can be human contact (most common) animal contact, soil contact

85
Q

organism responsible for tinea?

A

trichophyton rubrum (>70%) and Trichophyton mentagraphytes (>20%) spread by human contact

Microsporum canis spread through animal contact (cats and dogs)

86
Q

presentation of tinea?

A

expanding lesions with central clearing and red scaly serpignous edge, thickened and crumbling nail

87
Q

diagnosis of tinea?

A

clinical

skin scraping/ nail clippings for microscopy and culture

88
Q

Rx of tinea?

A

small and localised infection: clotrimazole cream
extensive/ stubborn infection: oral terbinafine or intraconazole
affecting nails: oral terbinafine

89
Q

what is the most common fungal infections affecting the skin?

A

candida skin infection

most common type of yeast infection

90
Q

candida infection of the skin is most often with candida _____

A

albicans

91
Q

risk factors for candida infection?

A 
extremes of life
warm, humid climate
immunodeficient
broad-spec Abx
certain underlying skin conditions
Fe deficiency
COCP use/ pregnancy
92
Q

Candida makes up part of the normal flora of the human ___ ___ and ____.

A

digestive tract

vagina

93
Q

T/F: candida is a commensal of the skin

A

not typically, but can colonise areas temporarily

94
Q

Candida skin infection presentation?

A

typically affects the folds of the skin (groin, under breasts, abdo skin folds etc - candida intertrigo)
Skin in red, can look shiny in skin folds and there are often spotty ‘satellites’ around the edges
Also commonly affects the oral cavity (white plaques on buccal mucosa/ tongue)

95
Q

diagnosis?

A

clinical

if uncertain skin swabs and scrapings for microscopy and culture

96
Q

Rx of candida skin infection?

A

clotrimazole cream

oral fluconazole

97
Q

what causes scabies

A

infection with a parasitic mite Sarcoptes scabiei, variety hominis

98
Q

transmission of scabies?

A

skin-skin contact between individuals

99
Q

scabies:
Mite burrows through the epidermis and lies in the ___ ____
Here, it lays 2-4 eggs each day.
The symptoms experienced by infected individuals are due to what?

A

stratum corneum

the host immune response

100
Q

presentation of scabies?

A

extreme pruritus (worse at night, often distrurbing sleep)
affects whole body, almost always scalp-sparing
burrows: irregular tracks, usually grey. Most often in webspaces. Also around waist, axillae and groin.
Erythematous papules, vesicles and excoriations

101
Q

diagnosis of scabies?

A

clinical

microscopic examination of scabies burrow

102
Q

Rx of scabies?

A 
permethrin cream (malothion as alternative)
antihistamines, crotamiton cream and hydrocortisone cream to reduce pruritis
avoid contact with others
103
Q

what is necrotising fasciitis?

A

acutely life-threatning infection of one of more of the deep soft tissue compartments (dermis, adipose tissue, fascia, muscle)

104
Q

T/F: necrotising fasciitis has a high mortality rate

A

true

risk of serious complications

105
Q

type 1 vs type 2 nec fascitis?

A

1) polymicrobial infection. Both anaerobic and aerobic bacteria. Most common in patients who are immunocomprimised/ chronically ill
2) infection with strep pyogenes (GAS)

106
Q

how does nec fas form?

A

Bacteria enter skin through sites of trauma (small puncture wounds, surgical incisions…etc).
Often the primary site is not identified.
The infection spreads along the fascial plane to infect the deep soft tissues.

107
Q

presentation of necrotising Fasciitis?

A

severe pain out of proportion to what is seen
erythema with well-defined edge
oedema
skin surface may appear relatively normal (while underlying tissue is extremely necrotic)
systemic upset

108
Q

what signs/ symptoms would suggest necrotising Fasciitis with streptococcal infection?

A

ulceration, haemorrhagic bullae, lymphangitis

109
Q

what signs/ symptoms would suggest necrotising Fasciitis with anaerobe infection?

A

foul smelling wound

110
Q

diagnosis of necrotising Fasciitis?

A

‘dishwater fluid’ on wound washout
bloods: FBC, CRP, U&E, CK, lactate
blood and wound cultures
surgical exploration ASAP

111
Q

treatment of necrotising Fasciitis?

A

urgent surgical debridement
broad spec abx
admission to ICU

112
Q

what is Orf

A

a viral skin infection transferring to humans from sheep and goats

relatively common in sheep/ goat farmers

113
Q

Orf causative pathogen?

A

parapox virus: contracted through direct contact with infected sheep/ goats

114
Q

Orf presentation?

A

development of a single lesion at the site of inoculation

  • mutiple lesions rare
  • most often on hands/ forearm
  • lesion arises as small, firm papule which is initially very tender and irritating
  • the lesion enlarges to become a flat-topped pustule/ blister with a white centre and red periphery
115
Q

Orf diagnosis?

A

clinical

116
Q

Orf treatment?

A

self-limiting (6 weeks)

117
Q

What is lyme disease

A

rare bacterial infection contracted from ticks

118
Q

lyme disease is most common in what region?

A

temperate - scottish highlands most common in UK

peak incidence in summer

119
Q

what causes lyme disease?

A

infection with bacteria, Borrelia (spirochete bacterium)

Ixodes ticks act as a vector for the bacteria

120
Q

presentation of lyme disease?

A

erythema migrans
- 1-2 weeks post bite
- ‘bulls eye’
- usually painful
- possible associated malaise, myalgia, pyrexia
- resolves within 3-4 weeks
disseminated disease, days-weeks post bite
- arthritis, cardiac complications, nerve palsies, rheum complications
chronic lyme disease
- chronic arthritis/ pain

121
Q

diagnosis?

A

high clinical suspicion required

blood sample for ELISA testing

122
Q

Rx of lyme disease?

A

oral antibiotic therapy (amox/ doxy)

cure rate decreases as treatment delayed

Y4: Dermatology (3 decks)

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