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dermatology Flashcards

1
Q

cyst types

A

Epidermoid cyst - ‘Blackhead’
Sebaceous cyst - ‘Whitehead’
Dermoid cyst - Can contain hair (or teeth/other abnormal growths within -dependent on the location [ovaries])

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2
Q

what is tinea capitis

A

fungal infection of the scalp (scalp ringworm), which is a key cause of scarring hair loss in children

well-demarcated hair loss on the scalp

kerion- which are raised, pustular, boggy masses appearing as numerous bright yellow areas with the skin surface surrounded by regions of hair loss and flakiness.

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3
Q

what is Tinea corporis

A

dermatophyte fungal infections of the trunk / arms / legs
i.e ringworm

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4
Q

what is eczema

A

chronic atopic condition caused by defects in the normal continuity of the skin barrier, leading to inflammation in the skin
different types e.g. atopic dermatitis, contact dermatitis

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5
Q

how to dx atopic dermatitis

A

an itchy skin condition plus 3/+ of:
- hx of involvement of the skin creases (eg. folds of elbows/behind knees)
- personal hx of asthma or hay fever (/hx atopic dis in 1st deg rel if < 4)
- hx of general dry skin in last yr
- visible flexural eczema (elsewhere if <4)
- onset < 2 yrs (not if <4)

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6
Q

acute changes in atopic dermatitis

A

erythema
swelling
crusting
erosions
fissuring
scaling

unclear boarders

hyper/hypopigmentation in darker skin

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7
Q

chronic changes in atopic dermatitis

A

scaling
lichenification (thick skin)
prurigo like lesions (nodules from scratching)
xerosis (v dry)

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8
Q

atopic stigmata in dermatitis

A

dennie morgan folds (under eyes)
keratosis pilaris
peri-orbital darkening
xerosis

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9
Q

what is eczema herpeticum

A

viral skin infection in patients with eczema caused by the herpes simplex virus (HSV) or varicella zoster virus (VZV)

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10
Q

presentation eczema herpeticum

A

patient who suffers with eczema that has developed a widespread, painful, vesicular rash with systemic symptoms such as fever, lethargy, irritability and reduced oral intake
- there will usually be lymphadenopathy

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11
Q

mx eczema herpeticum

A

ADMIT FOR IV ACICLOVIR ASAP
opthal if near eye

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12
Q

quantity of emollients needed per week in <12s

A

250-500g (500g is one big tub)

oitments are thicker creams are thinner

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13
Q

emollient safety advice

A

they are flammable (careful in px who smoke)
slip risk in bath

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14
Q

steroid ladder

A

Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)

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15
Q

how to use topical steroids

A

use the weakest steroid for the shortest period required to get the skin under control

don’t use more than once daily

finger tip unit needed for area size of 2 palms

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16
Q

topical steroid SEs

A

skin thinning - can make the skin more prone to flares, bruising, tearing, stretch marks and telangiectasia
systemic absorption of the steroid
excessive hair growth

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17
Q

other options to steroid tx

A

topical calcineurin inhibitors
2dary care referral
- phototherapy
- systemic therapies (e.g. pred course, methotrexate, ciclosporin, axathioprin)
- biologics

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18
Q

2 types of contact dermatitis

A

irritant contact
allergic contact

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19
Q

what is irritant contact dermatitis

A

direct chemical / physical irritation to the skin
not a hypersensitivity reaction
do not need sensitisation
anyone affectedw

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20
Q

what is allergic contact dermatitis

A

type IV hypersensitivity reaction (delayed)
prior sensitisation needed
only ppl w allergy react

  • patch testing done (not prick testing - that is done for type I immediate reactions)
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21
Q

what is nummular dermatitis

A

a pruritic eczematous dermatosis characterized by multiple coin-shaped lesions

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22
Q

what is stasis dermatitis

A

type of eczema that develops in people who have poor blood flow
often near ankles
older ppl, venous insuff
tx w compression

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23
Q

what is seborrheic dermatitis

A

chronic form of eczema - appears on the body where there are a lot of oil-producing (sebaceous) glands like the upper back, nose and SCALP

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24
Q

what is psoriasis

A

T cell mediated abnormal immune response resulting in keratinocyte proliferation

  • dry, flaky, scaly, faintly erythematous skin lesions that appear in raised and rough plaques, over the extensor surfaces of the elbows and knees and on the scalp.
  • clear borders
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25
Q

Plaque psoriasis

A

thickened erythematous plaques with silver scales, commonly seen on the extensor surfaces and scalp. The plaques are 1cm – 10cm in diameter.

Most common form of psoriasis in adults

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26
Q

Guttate psoriasis

A

commonly occurs in children.
- many small raised papules across the trunk and limbs - mildly erythematous and can be slightly scaly.
- RAINDROPS
- over time the papules -> plaques.
- often triggered by a STREPTOCOCCAL THROAT INFECTION, stress or medications.
- resolves spontaneously within 3 – 4 months.

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27
Q

Pustular psoriasis

A

rare severe form of psoriasis where pustules form under areas of erythematous skin. The pus in these areas is not infectious. Patients can be systemically unwell.
Medical emergency -> admission to hx

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28
Q

psoriasis triggers

A

infection (espesh guttate)

local skin injury - Koebner phenomenon (KP) = is the appearance of new skin lesions on previously unaffected skin secondary to trauma

obesity
smoking
alcohol
stress
HIV

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29
Q

drugs that can induce psoriasis

A

BBs
lithium
antimalarials
abx
NSAIDs
ACEi
Anti TNFs
systemic steroid withdrawal

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30
Q

Auspitz sign

A

small points of bleeding when plaques are scraped off

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31
Q

nail changes in psoriasis

A

nail pitting
leukonychia (white nails)
thickening, discolouration, ridging
onycholysis (separation of the nail from the nail bed)

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32
Q

flexural psoriasis

A

ie. inverse psoriasis - in axilla, groin, breasts etc
well demarcated shiny smooth plaques often lacking scale
fissuring

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33
Q

co-morbidities assoc w psoriasis

A

things that increase the risk of CVD -particularly obesity, hyperlipidaemia, HTN and DMT2

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34
Q

tx psoriasis

A

topicals =
emollients
steroids
coal tar
vitamin D analogues
calcineurin inhib

phototherapy

conventional systemics =
ciclosporin
methotrexate
acitretin

biologics =
all the -umabs

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35
Q

how long break in between courses of topical corticosteroids in patients with psoriasis

A

4 weeks

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36
Q

what is Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

A

where a disproportional immune response causes epidermal necrosis
-> blistering and shedding of the top layer of skin.

Generally SJS affects <10% of body surface area + TEN affects >10%

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37
Q

causes of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

A

Medications =
Anti-epileptics
Antibiotics
Allopurinol
NSAIDs

Infections =
Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV

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38
Q

presentation of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

A

spectrum of severity
px start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin.
then develop a purple or red rash that spreads across the skin and starts to blister.
a few says after this skin starts to break away + shed leaving the raw tissue underneath

pain, erythema, blistering to lips + mucus membranes
irritates + ulcerated eyes
can also affect the urinary tract, lungs and internal organs

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39
Q

Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis mx

A

medical emergencies - admitted to a suitable dermatology or burns unit for treatment.

Supportive care - nutritional care, antiseptics, analgesia and ophthalmology input.
Treatment options include steroids, immunoglobulins and immunosuppressant medications guided by a specialist.

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40
Q

what is uticaria

A

hives - small itchy lumps that appear on the skin (maybe w rash, angioedema and flushing of the skin)

caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin (type 1 reaction - exaggerated IgE mediated immune responses)
- may be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.

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41
Q

causes of acute uticaria

A

triggered by something that stimulates the mast cells to release histamine. This may be:

Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications (common culprit drugs are the ‘As’: anticonvulsants, antibiotics, anti-inflammatories (NSAIDs), and allopurinol)
Viral infections
Insect bites
Dermatographism (rubbing of the skin)

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42
Q

types of chronic uticaria

A

an AI condition where autoantibodies target mast cells and trigger them to release histamines and other chemicals

Chronic idiopathic urticaria
Chronic inducible urticaria
Autoimmune urticaria (w other condition)

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43
Q

how can chronic inducible urticaria be triggered

A

Sunlight
Temperature change
Exercise
Strong emotions
Hot or cold weather
Pressure (dermatographism)

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44
Q

mx uticaria

A

non-sedating antihistamines (e.g. loratadine or cetirizine) - for up to 6 weeks following an episode

a sedating antihistamine (e.g. chlorphenamine) may be considered for night-time use (in addition to day-time non-sedating antihistamine) for troublesome sleep symptoms CKS

prednisolone is used for severe or resistant episodes

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45
Q

what is cellulitis

A

an infection of the skin and the soft tissues underneath
will be breach in skin barrier

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46
Q

cellulitis presentation

A

Erythema
Warm or hot to touch
Tense
Thickened
Oedematous
Bullae (fluid-filled blisters)
A golden-yellow crust indicates a staph aureus infection

systemically unwell - sepsis?

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47
Q

causes cellulitis

A

Staphylococcus aureus
Group A streptococcus (mainly streptococcus pyogenes)
Group C streptococcus (mainly streptococcus dysgalactiae)

consider MRSA

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48
Q

Eron classification 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 infection

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49
Q

mx cellulitis

A

class 3/4/v old/v young/immunocomp/near face= admission for IV abx

abx = FLUCLOXACILLIN (oral or IV)

alts = Clarithromycin
Clindamycin
Co-amoxiclav (the usual first choice for cellulitis near the eyes or nose)

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50
Q

what is melanoma

A

malignant neoplasm of melanocytes

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51
Q

RFs melanoma

A

age
UV exposure
skin type (paler)
>100 melanocytic naevi (having lots of moles)
>5 atypical naevi
multiple solar lentigines
FHx
personal hx

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52
Q

familial melanoma

A

CDKN2A

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53
Q

red flags skin lesion

A

asymmetry
irregular border
multiple colours
>7mm diameter
evolution

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54
Q

7 pt weighted checklist for skin lesions

A

need 3+ for referral

major features (2 pts each)
change in size
irreg shape
irreg colour

minor features (1)
largest diameter >7mm
inflam
oozing or crusting
change in sensation (inc itch)

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55
Q

what is acral lentiginous melanoma

A

palms soles or nails
no connection to UV
equal incidence in all skin (so most common for darker skin to get)
presents late so worse prog

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56
Q

what is lentigo maligna melanoma

A

elders
chronic accum sun exposure
on face
on sun damaged skin
(darkened bits)

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57
Q

what is nodular melanoma

A

red/black lump which bleeds/oozes
early vertical growth phase
most aggressive
males
trunk, head, neck

(can seem more symm w reg borders but is pigmented + growing)

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58
Q

what is superficial spreading melanoma

A

most common
prolonged radial growth phase
trunk in males
legs in females

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59
Q

what is amelanotic melanoma

A

hx rapid growth
residual pigment
look pink and stick out

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60
Q

what is used to help stage melanoma

A

breslow thickness

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61
Q

stage 0 melanoma

A

in situ

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62
Q

stage 1 melanoma

A

thinner tumours confined to skin (almost 100% 5+ yr survival)

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63
Q

stage 2 melanoma

A

thicker tumours confined to skin (80%)

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64
Q

stage 3 melanoma

A

lymph node involvement (70%)

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65
Q

stage 4 melanoma

A

distant mets (30%)

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66
Q

mx melanoma

A

GP 2 wk wait referral

diagnostic excision of pigmented skin lesion w 2mm peripheral margin
wide local excision

test for BRAF mutation (causes it to grow more aggressively)

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67
Q

what is a sentinel lymph node biopsy

A

take out nearest draining lymph node as well (use dye to see)

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68
Q

tx stage 3/4 melanomas

A

Targeted therapy:
BRAF (protein that helps control cell growth) inhibitors
- dabrafenib
MEK inhibitors
- trametinib

Immunotherapy
Anti CTLA4 antibody
Anti PD1 antibody

rarely use radio or chemo

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69
Q

RFs for non-melanoma skin cancer

A

UV exposure
- SCCs = chronic cumulative
- BCCs = intermittent intense
pale skin
age
immune suppression (SCC)
ionising radiation
chronic wounds (SCC)
smoking (SCC)
HPC (SCC)
genetic syndromes

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70
Q

what is actinic keratosis

A

dry, scaly patches of skin that have been damaged by the sun

partial thickness dysplasia of epidermal keratinocytes
begins in basal layer
no BM invasion

flesh-coloured, irregularly shaped, small macules/plaques
small
devs over yrs at sun exposed sites
v small no progress to SCC
no reg flag sx

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71
Q

tx actinic keratosis

A

prev further risk

topical tx
-fluorouracil cream
- diclofenac
- imiquimod
Photodynamic therapy (PDT)

discrete lesions:
cryotherapy
C&C

refer if does not resolve/unsure dx

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72
Q

what is bowen’s disease

A

precancerous dermatosis
SCC IN SITU
full thickness dysplasia of epidermal keratinocytes
more of a well defined plaque
cant met
develop over yrs at sun exposed sites

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73
Q

bowen’s disease tx

A

INITIAL = 5-flurouracil

cryotherpy
C&C
PDT

74
Q

what is squamous cell carcinoma (SCC)

A

2nd most common skin cancer
abnormal, accelerated growth of squamous cells
now invasion past BM
potential to met

75
Q

features of SCC

A

rapid growth - wks/mths
raised base
keratotic/scaly lesions
may ulcerate/bleed
may be painful
sun exposed sites - face, lips, ears, hands, forearms, lower legs

76
Q

tx SCC

A

surgery - standard excision, Mohs surgery (removes skin layers at a time)
radiotherapy

77
Q

what is basal cell carcinoma (BCC)

A

most common type of skin cancer
abnormal, accelerated growth of basal cells

78
Q

features BCC

A

slowly growing plaque/nodule
skin coloured, pink/pigmented, often shiny / pearly
rolled edges
telangiectasia
ulceration + spontan bleeding
rarely mets

79
Q

BCC tx

A

surgery
radiotherapy

80
Q

what to do Mohs surgery

A

if high risk :
tumour site = central face, eyes, nose, ears
size (>2cm)
histology sub type (morphoetic, infiltrative, micronodular, basosqaumous)
poor clinical definition of tumour margins
recurrent lesions
perineural/perivascular involvement

81
Q

tx of superficial BCC

A

C&C
Cryotherapy
Topical - imiquimod, 5-flurouracil
Photodynamic therapy

82
Q

what is polymorphic eruption of preg

A

pruritic condition associated with last trimester
lesions often first appear in abdominal striae
mx depends on severity: emollients, mild potency topical steroids and oral steroids

83
Q

what is atopic eruption of pregnancy

A

is the commonest skin disorder found in pregnancy
it typically presents as an eczematous, itchy red rash.
no specific tx needed

84
Q

what is pemphigoid gestationis

A

pruritic blistering lesions
often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms
usually presents 2nd or 3rd trimester and is rarely seen in the first pregnancy
oral corticosteroids are usually required

85
Q

how long does it take a pityriasis rosea rash to resolve

A

6-12 weeks

86
Q

presentation of pityriasis rosea

A

Minority may give a hx of a recent viral infection
herald patch (single larger pink/red oval 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 = ‘fir-tree’ appearance

87
Q

how is acne caused

A

chronic inflammation, with or without localised infection, in pockets within the skin known as the pilosebaceous unit (tiny dimples on skin that contain hair follicles + sebaceous glands - produce sebum)

There is increased sebum production, trapping of keratin + blockage -> swelling + inflam

Swollen and inflamed units are called comedones.

88
Q

acne tx

A

explore the psychosocial burden

No tx may be acceptable if mild

TOPICAL BENZOYL PEROXIDE reduces inflammation, helps unblock the skin and is toxic to the P. acnes bacteria

TOPICAL RETINOIDS (chemicals related to vitamin A) slow the production of sebum (women of childbearing age need effective contraception)
- e.g. ADAPALENE

TOPICAL antibiotics such as CLINDAMYCIN (prescribed with benzoyl peroxide to reduce bacterial resistance)
ORAL antibiotics such as LYMECYCLINE
use erythromycin in pregnancy
DONT USE ABX AS MONOTHERAPY

Oral contraceptive pill can help PX stabilise their hormones and slow the production of sebum

89
Q

tx severe acne

A

oral retinoid e.g. isotretinoin ie roaccutane (TERATOGENIC)
- only prescribed by specialist after other methods fail

90
Q

SEs isotretinoin ie roaccutane

A

Dry skin and lips
Photosensitivity of the skin to sunlight
Depression, anxiety, aggression and suicidal ideation. Patients should be screened for mental health issues prior to starting treatment.
Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis

91
Q

what are viral warts

A

common benign lesion caused by HPV

spread through direct skin contact

92
Q

specialist dermatology referral for acne

A

Severe acne (scarring, hyperpigmentation and widespread pustules)

93
Q

tx viral warts

A

none
soaking/paring
chemicals -salicyclic acid
cryotheraoy
c&c
laser

94
Q

what is molluscum contagiosum

A

a viral skin infection caused by the molluscum contagiosum virus, which is a type of poxvirus
self-resolving but can take yrs
spread through direct contact

95
Q

features of molluscum contagiosum

A

small, flesh coloured papules (raised individual bumps on the skin) that characteristically have a central dimple. They typically appear in “crops” of multiple lesions in a local area

96
Q

what is an epidermoid cyst

A

benign cyst derived from infundibulum of hair follicle
have a central punctum

97
Q

what is a pilar cyst

A

benign keratin filled cyst derived from outer hair root sheath
often runs in fams - AD

98
Q

what is seborrhoeic keratosis
+ how does it look

A

v common benign lesion

well-circumscribed plaques or papules with a ‘stuck on’ appearance
brown, black or light tan.
look waxy or scaly and slightly raised

They appear gradually, usually on the face, neck, chest or back

a sign of Leser-Trélat disorder

asx

99
Q

what is solar lentigo

A

from cumulative sun exposure on back of hand + face

100
Q

what is dermatofibroma

A

common benign lesion usually on legs
get at middle age
has a tethering/pinch sign
can get from mild trauma

101
Q

what is a lipoma

A

common benign tumour made of fat cells
soft/smooth dome shaped subcut lesion

102
Q

what is a pyogenic gruanuloma

A

acquired proliferation of BVs

103
Q

what is allergic rhinitis

A

inflammation of the inside of the nose caused by an allergen, such as pollen, dust, mould, or flakes of skin from certain animals
causes cold-like sx
tx w salt water rinsing/antihistamines

104
Q

what parasite are head lice

A

pediculus humanus capitis parasite

105
Q

tx head lice

A

dimeticone 4% lotion can be applied to the hair and left to dry. This is left on for 8 hours, then washed off. This process is repeated 7 days later to kill any head lice that have hatched since treatment.

fine combs

106
Q

what are scabies

A

tiny mites called Sarcoptes scabiei that burrow under the skin causing infection and intense itching
lay eggs in the skin
can take 8 wks to get sx/rash from initial infestation

107
Q

scabies presentation

A

incredibly itchy small red spots, possibly with track marks where the mites have burrowed.
The classic location of the rash is between the finger webs, can be whole body

does anyone they live w have similar rash?

108
Q

scabies tx

A

PERMETHRIN cream - apply to whole body when cool, leave for 8 – 12 hours then wash off
repeat 1 wk later

Oral IVERMECTIN as a single dose that can be repeated a week later is an option for difficult to treat or crusted scabies.

tx household + close contacts in the same way
wash clothes + bedding on hot, hoover carpets

109
Q

still itching after scabies tx?

A

Itching can continue for up to 4 weeks after successful treatment

Crotamiton cream and chlorphenamine at night at night can help with the itching.

110
Q

what is crusted scabies

A

serious infestation with scabies in px that are immunocompromised.

  • may have over a million mites in their skin
  • extremely contagious
  • patches of red skin that turn into scaly plaques - can be misdiagnosed as psoriasis
  • may not have an itch as they do not mount an immune response to the infestation
  • may need admission for tx as an inpatient with oral ivermectin and isolation.
111
Q

what is impetigo

A

superficial bacterial skin infection, usually caused by the staphylococcus aureus bacteria
contagious
non-bullous or bullous

112
Q

non-bullous impetigo presentation

A

typically occurs around the nose or mouth. The exudate from the lesions dries to form a “golden crust”. Do not usually cause systemic symptoms or make the person unwell.

113
Q

non-bullous impetigo tx

A

Antiseptic cream (hydrogen peroxide 1% cream) first line

Topical fusidic acid (abx)

Oral flucloxacillin is used to treat more wide spread or severe impetigo

114
Q

what is bullous impetigo

A

always s. aureus
this bacteria can produce epidermolytic toxins that break down the proteins that hold skin cells together -> 1–2 cm fluid filled vesicles to form on the skin. These vesicles grow in size and then burst, forming a “golden crust”. Eventually they heal without scarring. These lesions can be painful and itchy.

more common in neonates + <2yrs
more likely to get systemic sx

115
Q

tx bullous impetigo

A

Swabs of the vesicles can confirm the diagnosis, bacteria and antibiotic sensitivities.

Tx w antibiotics, usually flucloxacillin. This may be given orally or intravenously if they are very unwell or at risk of complications.

The condition is very contagious and patients should be isolated where possible.

116
Q

what is staphylococcal scalded skin syndrome (SSSS)

A

a condition caused by a type of s. aureus bacteria that produces epidermolytic toxins (they are protease enzymes that break down the proteins that hold skin cells together).

When a skin infection occurs and these toxins are produced, the skin is damaged and breaks down.

affects children under 5 years (older have developed immunity to the toxins)

117
Q

staphylococcal scalded skin syndrome (SSSS) presentation

A
  • generalised patches of erythema on the skin
  • then skin gets thin + wrinkled.
  • then the formation of fluid filled blisters (bullae) - burst + leave v sore, erythematous skin below
    similar appearance to a burn or scald.

Nikolsky sign = v gentle rubbing of the skin causes it to peel away

Systemic sx = fever, irritability, lethargy + dehydration.
If untreated it can lead to sepsis and potentially death.

118
Q

Staphylococcal scalded skin syndrome (SSSS) tx

A

admission + tx with IV abx.

Fluid and electrolyte balance is key to management as patients are prone to dehydration.

When adequately tx, usually make a full recovery without scarring.

119
Q

causes of erythema nodosum

A

infection
- streptococci
- tuberculosis
- brucellosis
systemic disease
– sarcoidosis
- inflammatory bowel disease
- Behcet’s
malignancy/lymphoma
drugs
- penicillins
- sulphonamides
- COCP
pregnancy

120
Q

features of rosacea

A

typically affects nose, cheeks and forehead
flushing is often first symptom
telangiectasia are common
later develops into persistent erythema with papules and pustules
rhinophyma (large bulbous nose)
ocular involvement: blepharitis
SUNLIGHT exacerbates symptoms

121
Q

what to avoid in rosacea

A

direct sunlight
oil based products
alcohol
spicy food
hot drinks
sudden temp changes
excessive exercise

122
Q

rosacea tx for:

predominant erythema/flushing:

mild-to-moderate papules and/or pustules:

moderate-to-severe papules and/or pustules:

A

daily application of a high-factor sunscreen

predominant erythema/flushing:
topical BRIMONIDINE gel
brimonidine (topical alpha-adrenergic agonist) - ‘as required basis’

mild-to-moderate papules and/or pustules:
topical IVERMECTIN is first-line
alternatives include: topical METRONIDAZOLE or topical azelaic acid

moderate-to-severe papules and/or pustules:
combination of topical ivermectin + oral DOXYCYCLINE

laser therapy may be appropriate for patients with prominent telangiectasia

avoid topical steroids

123
Q

what is shingles

A

(herpes zoster infection) is an acute, unilateral, painful blistering rash caused by reactivation of the varicella-zoster virus (VZV).

124
Q

RFs shingles

A

increasing age
HIV: strong risk factor, 15 times more common
other immunosuppressive conditions (e.g. steroids, chemotherapy)

125
Q

most common affected dermatomes in shingles

A

T1-L2

126
Q

shingles features

A

prodromal period
- burning pain over the affected dermatome for 2-3 days

rash
- initially erythematous, macular rash over the affected dermatome
- quickly becomes vesicular
- well demarcated by the dermatome and does not cross the midline. However, some ‘bleeding’ into adjacent areas may be seen

127
Q

shingles tx

A

infectious (avoid preg women + immunocomp ppl) until vesicles crusted over

analgesia - paracetamol + NSAIDs first line
- then neuropathic agents
- consider oral steroids in first 2 wks if immunocomp + no res

antivirals within 72 hours, unless the px is < 50 years and has a ‘mild’ truncal rash associated with mild pain and no underlying risk factors
- aciclovir, famciclovir, or valaciclovir

128
Q

what constitutes as severe acne + what do you do if a patient has it

A

scarring, hyperpigmentation and widespread pustules

requires specialist dermatology referral

129
Q

which bacteria contributes to dev of acne

A

Propionibacterium acnes

130
Q

what is a keloid

A

tumour-like lesions that arise from the connective tissue of a scar and extend BEYOND the dimensions of the original wound

131
Q

predisposing factors to keloid

A

ethnicity: more common in people with dark skin
occur more commonly in young adults, rare in the elderly
common sites (in order of decreasing frequency): sternum, shoulder, neck, face, extensor surface of limbs, trunk

132
Q

keloid tx

A

early keloids may be treated with intra-lesional steroids e.g. triamcinolone

133
Q

what is a hypertrophic scar

A

an grow following trauma and can present similarly to keloid, they do not extend past the margins of the damaged skin.

134
Q

tx seborrheic dermatitis

A

scalp = ketoconazole 2% shampoo

Face and body = topical antifungals: e.g. ketoconazole
topical steroids: best used for short periods

135
Q

red flags for drug reactions

A

mucosal involvement
blistering/skin peeling off
pain (common to be itchy but not usually pain)
lymphadenopathy
systemic upset - fever, abnormal LFTs, U&Es

136
Q

what to document in drug reaction

A

documentation of all drugs + dates administered (inc OTC + complementary)
dates of eruption
create a drug time-line
response to removal of suspected agent
response to re-challenge (only if mild reaction + unsure of cause)

137
Q

tx of mild drug eruption

A

withdraw drug
emollients
topical corticosteroids in short term for sx relief
antihistamines if urticaria

138
Q

what are steven johnson syndrome (SJS) + toxic epidermal necrolysis (TEN)

A

almost always caused by drugs
- drug eruption
TEN more severe
distinct from erythema multiforme (normally caused by infections - HSV / mycoplasma )
more common in px w HIV

139
Q

most common causes of SJS + TEN

A

allopurinol
carbamazepine
lamotrigine
phenobarbital
phenytoin
sulfasalazine
sulfur abx
NSAIDs
nevirapine (HIV tx - ART)

140
Q

presentation of SJS/TEN

A

new drug 7-21 days prev
prodrome of resp tract sx
fever
PAIN
dusky red lesions
atypical targets (ie not 3 concentric rings)
erythematous plaques

141
Q

difference between SJS + TEN

A

percentage of detachment of epidermis (which becomes necrotic + starts peeling off)

SJS <10%
TEN >30% - more likely to have systemic sx that are worse
10-30 = SJS-TEN crossover

both have mucosal involvement

142
Q

how to find prognosis in SJS + TEN

A

SCORTEN calc

143
Q

mx SJS/TEN

A

ABCDE
stop medication (all non-essential if don’t know)
admit to ICU / burn unit
correct fluid + electrolytes
caloric replacement
protect from 2ndary infections w topical abx ointments (but not routine)
ophthalmology consult + eye care
urology consult if urethral inflam
oral antacids + mouth care
pulmonary hygiene if resp syndrome
periodic cultures of mouth, eyes, skin, sputum
physical therapy to prev contractures
topical paraffin (50/50), non adherent dressings

don’t prescribe any meds w/o discussion w senior
get lots of specialists involved

144
Q

drug reaction with eosinophilia + systemic sx (DRESS)

A

15-40 days after exposure (anticonvulsants, sulfonamides etc)
high fever
rash: morbilliform eruption (measles-like) sometimes w oedema (espesh on face), infiltration, purpura and scaling
lymphadenopathy
atypical lymphocytes
eosinophilia
internal organ involvement

145
Q

mx DRESS

A

withdrawal of drug
systemic steroids for severe cases
supportive tx
- dressings
- topical steroids
- emollients - 50/50 (50% white soft paraffin 50 % liquid paraffin - v greasy!)
- oral antihistamines
- address: fluid status, electrolytes, temp, nutrition
- tx 2ndary infection

146
Q

acute generalised exanthematous pustulosis (AGEP)

A

<4 days after medication exposure - usually beta lactam abx
high fever
small sterile pustules arise within larger areas of oedematous erythema
oedema hands + face, purpura, vesicles, bulla, target lesions, mucosal involvement
marked leukocytosis w elevated neutrophils
(can look similar to acute pustular psoriasis)

147
Q

mx AGEP

A

withdraw the drug (sld be enough)
topical steroids
emollients
antihistamines
systemic therapy rarely indicated

148
Q

what is erythroderma

A

generalised erythema affecting >90% skin surface
due to rapid epidermal cell turnover

149
Q

causes of erythroderma

A

eczema - espesh topical dermatitis
psoriasis
drug eruption - sulphonureas, isoniazid, sulfonamide
cutaneous T cell lymphoma
idiopathic

150
Q

what comps do px w erythroderma need to be monitored for

A

dehydration, infection and high-output heart failure

151
Q

Erythrodermic psoriasis

A

may result from progression of chronic disease to an exfoliative phase with plaques covering most of the body. Associated with mild systemic upset

more serious form is an acute deterioration. This may be triggered by a variety of factors such as withdrawal of systemic steroids. Patients need to be admitted to hospital for management

152
Q

what is staphylococcal scalded skin syndrome (SSSS)

A

rare, severe, superficial blistering skin disorder which is characterised by epidermal detachment (more superficial than SJS/TEN)
triggered by exotoxin release from specific strains of s.aureus
normally in children <5

153
Q

presentation SSSS

A
  • usually starts with generalised patches of erythema on the skin
  • then the skin looks thin and wrinkled
  • then formation of fluid filled blisters called bullae, which burst and leave very sore, erythematous skin below.

Nikolsky sign (where very gentle rubbing of the skin causes it to peel away)

Systemic sx: fever, irritability, lethargy and dehydration.
If untreated -> sepsis, death.

154
Q

what is bullous pemphigoid

A

an AI condition causing sub-epidermal blistering of the skin
more common in the ELDERLY

a result of an attack on the BM of the epidermis by IgG +/- IgE immunoglobulins + activated T lymphocytes
target is protein BP180

155
Q

features of bullous pemphigoid

A

itchy, tense intact blisters typically around flexures
the blisters usually heal without scarring
there is stereotypically no mucosal involvement

156
Q

dx bullous pemphigoid

A

Skin biopsy
- immunofluorescence shows IgG and C3 at the dermoepidermal junction

157
Q

what is pemphigus vulgaris

A

AI blistering skin disease, painful blisters of the skin + mucus membranes
ages 30-60
jews + indians

antibodies directed against desmoglein 3 found on desmosomes

158
Q

features pemphigus vulgaris

A

mucosal ulceration is common and often the presenting symptom (often oral)

skin blistering - flaccid, easily ruptured vesicles and bullae
Lesions are typically painful but not itchy. These may develop months after the initial mucosal symptoms.
Nikolsky’s = spread of bullae following application of horizontal, tangential pressure to the skin

159
Q

dx pemphigus vulgaris

A

acantholysis on biopsy

160
Q

tx pemphigus vulgaris

A

steroids are first-line
immunosuppressants

161
Q

tx bullous pemphigoid

A

referral to a dermatologist for biopsy and confirmation of diagnosis
oral corticosteroids are the mainstay of treatment
topical corticosteroids, immunosuppressants and antibiotics are also used

162
Q

hyperhydrosis tx

A

Topical aluminium chloride

163
Q

cause of lichen planus

A

T-cell mediated AI disorder

164
Q

where wld you see lichen planus

A

mucus membranes of mouth + vagina (inside vagina)
nails
wrists

165
Q

characteristic feature of lichen planus

A

white lines on surface of the rash
- Wickham’s striae

is otherwise flat-topped, purple, polygonal papules and plaques
itchy

166
Q

histology of lichen planus

A

saw-tooth pattern of epidermal hyperplasia
t-cell infiltration of dermis
reduced melanocytes
globular deposits of IgM

167
Q

Lichen planus tx

A

potent topical steroids are the mainstay of treatment
e.g. betnovate

168
Q

presentation acanthosis nigricans

A

symmetrical, brown, velvety plaques that are often found on the neck, axilla and groin

169
Q

pathophysiology of acanthosis nigricans

A

insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)

170
Q

causes of acanthosis nigricans

A

T2DM
GI cancer
obesity
PCOS
acromegaly
Cushing’s disease
hypothyroidism
familial
Prader-Willi syndrome
drugs
- COCP, nicotinic acid

171
Q

tx pityriasis versicolor

A

topical antifungal - ketoconazole shampoo

172
Q

presentation pityriasis versicolor

A

pale white/brown/pink patches
well-demarcated
dry scaly

usually on trunk

173
Q

cause of pityriasis versicolor

A

fungal infection caused by Malassezia furfur

174
Q

what is dermatitis herpetiformis

A

autoimmune blistering skin disorder associated with coeliac disease

caused by deposition of IgA in the dermis

175
Q

Dermatitis herpetiformis features

A

itchy, vesicular skin lesions on the extensor surfaces (e.g. elbows, knees, buttocks)

176
Q

skin bipsy for dermatitis herpetiformis

A

direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis

177
Q

Hereditary haemorrhagic telangiectasia diagnostic criteria

A

epistaxis : spontaneous, recurrent nosebleeds

telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)

visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM

family history: a first-degree relative with HHT

178
Q

side effect of ketoconazole

A

gynecomastia

179
Q

sx in neonate who has got VZV from mother

A

dysfunc of bladder + bowel
eye defects - cataracts, chorioretinitis
limb hyperplasia
cortical atrophy
microcephaly

1 + = foetal varicella syndrome

180
Q

tx dermatophyte nail infections

A

oral terbinafine

finals (27 decks)

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