Derm Flashcards
1
Q
wht is skin and what are skin appendages?
A
skin = epidermis + dermis +overlying subcutaneous tissue.
skin appendages are structures formed by skin derived cells such as nails, hair, sweat glands and sebaceous glands
2
Q
major cell types of epidermis
A
there are 4
- keratinocytes- produce keratin as a protective barrier
- langerhans’ cells - present antigens and activeate T cells for immune protection
- melanocytes - produce melanin which gives pigment to skin and protects cell nuclei from UV radiation induced DNA damage
- merkel cells - contain specialised nerve endings for sensation
3
Q
average epidermal turnover time
A
migration of cells from basal layer to horny layer. it is about 30 days
4
Q
different epidermal layers and their composition
A
stratum basale (basal cell layer) -actively dividing deepest layer stratum spinosum (prickle cell layer)- differentiating cells stratum granulosum (granular cell layer)- cells here lose their nuclei and contain granules of keratohyaline. they secrete lipid into intercellular spaces stratum corneum (horny layer) - layer of keratin. most superficial layer
**in areas of thick skin such as palms, soles and digits there is a 5th layer called stratum lucidum beneath stratum corneum and it consists of paler, compact keratin.
5
Q
contents of dermis
A
mainly made of collagen along with elastin and glycosaminoglycans which are synthesised by fibroblasts. the dermis also contains immune cells, nerves, skin appendages as well as lymphatic and blood vessels.
6
Q
3 main types of hair
A
- lanugo hair (fine long hair in fetus)
- vellus hair (fine short hair on all body surfaces)
- terminal hair (coarse long hair on scalp, eyebrows, eyelashes and pubic areas)
7
Q
what does each hair consist of
A
each hair is made of modified keratin and has a shaft and hair bulb (actively dividing cells and ,melanocytes which give pigment to the hair)
8
Q
growth cycle of hair follicles
A
each hair follicle enters its own growth cycle -
- anagen - long growing phase
- catagen - short regressing phase
- telogen - resting/shedding phase
9
Q
types of sweat glands
A
eccrine sweat glands - distributed universally in the skin
apocrine sweat glands - found in the axillae, areolae, genitalia and anus, and modified sweat glands are found in the external auditory canal. they only function from puberty onwards and action of bacteria on the sweat produces body odour
10
Q
4 phases of wound healing
A
haemostasis
iflammation
prolifereation
remodelling
11
Q
causes of urticaria, angioedema and anaphylaxis
A
- idiopathic
- foods (nuts, sesame, shellfish, dairy products)
- drugs (penicillin, contrast media, NSAIDs, morphine, ACEis)
- insect bites
- contact (eg latex)
- viral or parasitic infections
- autoimmune
- hereditary - in some cases of angioedema
12
Q
what is the major mediator of urticaria?
A
histamine derived from skin mast cells
13
Q
urticaria presentation
A
itchy wheals. due to swelling involving superficial dermis, raising the epidermis
14
Q
angioedema presentation
A
swelling of tongue and lips - deeper swelling involving dermis and subcutaneous tissue
15
Q
presentation of anaphylaxis
A
can present initially with urticaria and angioedema
bronchospasm, hypotension, facial and laryngeal oedema
16
Q
management of urticaria, angioedema and anaphylaxis
A
mild-moderate urticaria - antihistamines
severe acute urticaria and angioedema - corticosteroids
anaphylaxis - adrenaline, corticosteroids and antihistamines
17
Q
complications of urticaria, angioedema and anaphylaxis
A
urticaria is usually uncomplicated
angioedmea and anaphylaxis can lead to asphyxia, cardiac arrest and death
18
Q
lesion?
A
an area of altered skin
19
Q
rash?
A
an eruption
20
Q
naevus?
A
a localised malformation of tissue structures
21
Q
A
naevus
pigmented melanocytic naevus (mole)
22
Q
comedone?
A
a plug in a sebaceous follicle containing altered sebum, bacteria and cellular debris. can present as either open (blackheads) or closed (whiteheads)
23
Q
A
open comedone (in acne)
24
Q
A
closed comedones (in acne)
25
generalised vs widespread pattern of distribution of lesions?
generalised= all over body
widespread= extensive spread
26
flexural areas
body folds - groin, neck, behind ears, antecubital fossa, popliteal fossa
27
extensor surfaces
knee, elbows, shins
28
pressure areas
saccrum, buttocks, ankles and heels
29
dermatome
A dermatome is **an area of skin in which sensory nerves derive from a single spinal nerve root**
30
photosensitive
affects sun exposed areas such as face, neck and back of hands
31
sunburn
32
Köebner phenomenon
a linear eruption arising at site of trauma
33
koebner phenomenon (in psoriasis)
34
target lesions (erythema multiforme)
35
annular lesion (tinea corporis)
36
discoid/nummular lesion (discoid eczema) ie coin shaped/round lesion
37
erythema?
redness which blanches on pressure
38
palmar erythema
39
purpura
40
petichiae vs ecchymoses
petechiae - small pinpoint purpuric macules
ecchymoses - large bruise like purpuric patches
remember purpura does not blanch
41
hypopigmentation
in this case - pityriasis versicolor (superficial fungal infection)
42
depigmentation
| (here vitiligo - loss of melanocytes)
43
hyperpigmentation
(here cause was melasma - increased melanin pigmentation)
44
macules (freckles)
45
patchy morphology - this is vascular malformation - naevus flammeus/ port wine stain
46
papules
here xanthomata
47
nodule?
solid raised lesion more than 0.5cm in diameter with a deeper component
48
nodule
here Pyogenic granuloma(granuloma telangiectaticum)
49
plaque
palpable scaling raised lesion \>0.5cm in diameter
50
psoriatic plaque
51
papule vs vesicle?
papule - raised solid lesion \<0.5cm in diameter
vesicle - raised clear fluid filled leasion \<0.5cm in diameter. aka small blister
52
vesicles in acute hand eczema (pompholyx)
53
bulla
raised clear fluid filled lesion \>0.5cm in diameter
aka large blister
54
bulla
55
pustule
pus containing lesion\<0.5cm in diameter
56
pustules in acne
57
abscess
localised accumulation of pus in the dermis or subcutaneous tissue
58
periungual abscess
59
wheal
transient raised lesion due to dermal oedema
60
wheal in urticaria
61
boil/furuncle
staphylococcal infection around or within a hair follicle
62
carbuncle
staphylococcal infection of adjacent hair follicles (multiple boils/furuncles)
63
excoriation
loss of epidermis following trauma
64
excoriations
65
lichenification
well defined roughening of skin with accentuation of skin markings
66
lichenification (here has happend due to chronic rubbing in eczema)
67
scales
flakes of stratum corneum
68
psoriatic scales
69
crust
Rough surface consisting of dried serum, blood, bacteria and cellular debris that has exuded through an eroded epidermis(e.g.from a burst blister)
70
crust (in impetigo)
71
scar
new fibrous tissue which occurs post wound healingand may be atrophic (thinning), hypertrophic (hyperproliferation within wound wall) or keloid (hyperproliferation beyond wound wall)
72
keloid scar
73
ulcers
loss of epidermis and dermis (heals with scarring)
74
leg ulcers
75
fissure
epidermal crack often due to excess dryness
76
fissure in eczema
77
striae
linear areas which progress from purple to pink to white with the histopathological appearance like a scar (associated with excessive steroid use, glucocorticoid production, pregnancy and growth spurts)
78
striae
79
alopecia areata (well defined patch of complete hair loss)
80
hirsutism
androgen dependent hair growth in females
81
hirsutism
82
hypertrichosis
non androgen dependent pattern of excessive hair growth eg in a pigmented naevii
83
hypertrichosis
84
clubbing?
loss of angle bw posterior nail fold and nail plate
associations include suppurative lung disease, cyanotic heart disease, idiopathic and IBD
85
clubbing
86
koilonychia - spoon shaped depression of the nail plate
associations include Fe deficiency anaemia, congenital and idiopathic
87
onycholysis - separation of the distal end of the nail plate from the nail bed
associated with fungal nail infection, trauma, psoriasis and hyperthyroidism
88
nail pitting - punctuate depressions on nail plate
associated with psoriasis, eczema and alopecia areata
89
what do sweat glands do?
regulate body temperature and are innervated by the sympathetic nervous system
90
what is the nail made of?
nail matrix
nail plate (which in turn arises from the nail matrix at the posterior nail fold) - hard keratin
nail bed - contains blood capillaries
91
pilosebaceous unit?
sebaceous gland + hair follicle are collectively called a pilosebaceous unit.
92
what are sebaceous glands stimulated by?
sebaceous glands are stimulated by conversion of androgens to dihydrotestosterone and therefore become active at puberty
93
what causes erythema nodosum
it is a hypersensitivity response to a variety of stimuli. some causes are - group A beta haemolytic streptococcus, malignancy, sarcoidosis, primary TB, pregnancy, IBD, chlamydia and leprosy
94
presentation of erythema nodosum
discrete erythematous tender nodules which may become confluent. the shins are the most common site. lesions continue to appear for 1-2 weeks and leave bruise like discolouration as they resolve. they do not ulcerate and resolve without atrophy or scarring.
95
erythema multiforme
an acute self limiting inflammatory condition presenting as target lesions. herpes simplex virus is the main precipitating factor but other causes include idiopathic, other infections and drugs.
mucosal involvement is absent or limited to 1 mucosal surface
96
stevens-johnson syndrome
characterised by mucocutaneous necrosis with at least 2 mucosal sites involved.
main associations are drugs or combinations of infections or drugs.
histopathology shows epithelial necrosis with few inflammatory cells
extensive necrosis differentiates it from erythema multiforme
97
toxic epidermal necrosis
an acute severe disease characterised by extensive skin and mucosal necrosis accompanied by systemic toxicity.
usually drug induced
histopathology shows full thickness epidermal necrosis with subepidermal detachement
98
mx of erythema multiforme, SJS and TEN?
early recognition and call for senior help
full supportive care to maintain haemodynamic stability
99
complications of of erythema multiforme, SJS and TEN?
mortality rates 5-12% with SJS and \>30% with TEN
death often due to sepsis, electlyte imbalance and multi-organ failure
100
how is acute meningococcaemia transmitted?
via respiratory secretions
101
cause of acute meningococcaemia
Neisseria meningitidis
102
presentation of
meningitis - headache, neck stiffness and fever
septicaemia - hypotension, fever, myalgia, etc
non-blanching purpuric rash on trunks and extremities, which may be preceeded by blanching maculopapular rash, and, can rapidly progress to echhymoses, haemorrhagic bullae and tissue necrosis
103
management of acute acute meningococcaemia
abx - eg benzylpenicillin
prophylactic abx for close contacts eg rifampicin (ideally within 14 days of exposure)
supportive care if required - IV fluids, analgesia, etc.
104
complications of acute acute meningococcaemia
septicaemic shock, DIC, multi organ failure and death
105
what is erythroderma? causes?
exfoliative dermatitis involving at least 90% of skin surface
causes - previous skin disease (eg eczema, psoriasis), lymphoma, drugs (sulphonylureas, gold, sulphonamides, allopurinol, penicillin, captopril) and idiopathic
106
presentation of erythroderma
skin appears inflammed, oedematous and scaly
systemically unwell with lymphadenopathy and malaise
107
mx of erythroderma
treat underlying cause where known
emollients and wet wraps to maintain skin moisture
topical steroids may help relieve inflammation
108
complications of erythroderma
secondary infection
fluid loss and electrolyte imbalance
hypothermia
high output cardiac failure
capillary leak syndrome (most severe)
prognosis depends on underlying cause. 20-40% mortality
109
erythema nodosum
110
erythema multiforme
111
Stevens-Johnson syndrome
112
erythroderma
113
eczema herpeticum?
aka kaposi's varicelliform eruption
it is a serious complication of atopic eczema or other skin conditions (less common) where there is widespread eruption caused by herpes simplex virus
114
presentation of eczema herpeticum
extensive crusted papules, blisters and erosions
systemically unwell with fever and malaise
115
mx of eczema herpeticum
antivirals (aciclovir) and antibiotics if secondary bacterial infection
116
complications of eczema herpeticum
herpes hepatitis, encephalitis, DIC and rarely death
117
eczema herpeticum
118
necrotising fasciitis? cause and RFs
rapidly spreading infection of the deep fascia with secondary tissue necrosis
caused by group a beta haemolytic strep, or a mix of anaerobic and aerobic bacteria
50% of cases occur in previously healthy individuals.
RFs include abdominal surgery and medical co-morbidities (diabetes, malignancy)
119
presentation of nec fasc
severe pain
systemically unwell with fever and tachycardia
erythematous, blistering and necrotic skin
presence of crepitus (subcutaneous emphysema)
x-ray may show soft tissue gas (absence does not exclude diagnosis)
120
mx of nec fas
urgent referral for extensive surgical debridement
IV abx
remember mortality up to 76%
121
what is this and what is imp to do in this pt?
herpes zoster (shingles) infection due to varicella zoster virus affecting the distribution of the ophthalmic division of the trigeminal nerve.
examination for eye involvement is important
122
what are erysipelas and cellulitis?
causes?
presentation?
Mx?
complications?
they are spreading bacterial infections of the skin
cellulitis involves the deep subcutaneous tissue
erysipelas is an acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue
they are caused by staphylococcus aureus and streptococcus pyogenes. RFs - minor skin injury, immunosuppresion, wounds, leg ulcers, toe web intertrigo
presentation - most commonly inflammation in the lower limbs. swelling, erythema, warmth, pain. may be associated with lymphangitis. sytemically unwell with fever, malaise or rigors. erysipelas is distinguished from cellulitis by a well defined, red raised border
mx - abx (fluclox or benzylpenicillin). supportive care including rest, leg elevation, sterile dressings and analgesia
complications - local necrosis, abscess and septicaemia
123
erysipelas
124
staphylococcal scalded skin syndrome
skin disorder seen in infancy and early childhood caused by the production of a circulating epidermolytic toxin from phage group II, benzylpenicillin resistant (coagulase +ve) staphylococci.
125
presentation of staphylococcal scalded skin syndrome
develops within a few hrs to a few days and may be worse over face, axillae, groins or neck.
a scald like appearance is followed by large flaccid bulla
perioral crusting is typical
there is intraepidermal blistering
lesions are very painful
sometimes the eruption is more localised
recovery is usually within 5-7 days
126
mx of staphylococcal scalded skin syndrome
abx - eg a systemic penicillinase-resistant penicillin (flucloxacillin), fusidic acid, erythromycin or appropriate cephalosporin
analgesia
127
staphylococcal scalded skin syndrome
128
superficial fungal infections and causes
common and mild infection of the superficial layers of skin, nails and hair but can be severe in immunocompromised individuals.
causes - 3 main groups -
dermatophytes (tinea/ringworm), yeast (candidiasis, malassezia) and moulds (aspergillus)
129
presentation of fungal skin infections (superficial)
varies with site of infection but usually itchy and unilateral
130
tinea corporis
tinea infection of trunk and limbs
itchy circular or annular lesions with a cleaarly defined, raised and scaly edge is typical
131
tinea cruris
tinea infection of groin and natal cleft
very itch, circular or annular lesions with clearly defined rasied and scaly edge is typical
132
tinea pedis
athlete's foot
moist scaling and fissuring in toe webs, spreading to sole and dorsal aspect of the foot
133
tinea manuum
tinea infection of the hand
scaling and dryness in the palmar creases
134
tinea capitis
scalp ringworm
patches of broken hair, scaling and inflamaation
135
tinea unguium
tinea infection of the nail
yellow discolouration, thickened and crumbly nail
136
tinea incognioto
inappropriate treatment of tinea infection with topical or systemic steroids leading to ill defined and less scaly lesions
137
candidiasis
candidal skin infection - white plaques on mucosal areas, erythema with satellite lesions in flexures
138
pityriasis/tinea versicolor
infection with malassezia furfur
scaly pale brown patches on upper trunk that fail to tan on sun exposure, usually asymptomatic
139
mx of fungal skin infections
establish diagnosis by skin scrapings, hair or nail clippings (for dermatophytes) or skin swabs (for yeasts)
general measures - treat known precipitating factor (eg underlying immunosuppressive condition, moist environment)
topical antifungal agents (eg terbinafine cream)
oral antifungal agents (eg itraconazole) for severe, widespread, or nail infections
AVOID topical steroids - can lead to tinea incognito
140
tinea infection
141
tinea capitis
142
tinea manuum of right hand
143
tinea pedis associated with tinea unguium
144
right axilla candidiasis
145
pityriasis versicolor
146
generally skin cancer are of 2 types?
non-melanoma (BCC and SCC) and melanoma (malignant melanoma)
147
which is the most life threatening type of skin cancer
malignant melanoma
it is one of the few cancers affecting the younger population
148
1 RF for skin cancer
sun exposure is the single most preventable risk factor for skin cancer
149
Basal cell carcinoma
a slow growing, locally invasive malignant tumour of the epidermal keratinocytes normally in older individuals. only rarely metastasises
it is the most common malignant skin tumour
150
RFs for BCC
increasing age
male sex
immunosuppression
previous hx of skin cancer
genetic predisposition
skin type I (always burns, never tans)
hx of frequent or severe sunburn in childhood
UV exposure
151
presentation of BCC
various morphological types - nodular (most common), superficial (plaque like), cystic, morphoeic (sclerosing), keratotic and pigmented
nodular basal cell carcinoma is a small skin coloured papule or nodule with surface telangiectasia, and a pearly rolled edge; the lesion may have a necrotic or ulcerated centre (rodent ulcer)
most common over head and neck
152
mx of BCC
surgical excision - tx of choice as it allows histological examination of tumor and margins
mohs micrographic surgery (excision of lesion and tissue borders are progressively excised until specimens are microscopically free of tumour) - for high risk, recurrent tumours
radiotherapy where surgery is not appropriate
other - cryotherapy, curretage and cautery, topical photodynamic therapy, and topical treatment (eg imiquimod cream) for small and low-risk lesions
153
complications of BCC and prognosis
local tissue invasion and destruction
prognosis depends on tumor size, site, type, growth pattern/histological subtype, failure of previous tx, recurrence and immunosuppression
154
basal cell carcinoma - nodular type
155
Squamous cell carcinoma
locally invasive malignant tumour of the epidermal keratinocytes or its appendages which has the potential to metastasise
156
RFs for SCC
genetic predisposition
immunosuppression
chronic inflammation (eg leg ulcers, wound scars)
pre-malignant skin conditions (eg actinic keratoses)
excessive UV exposure
157
presentation of SCC
keratotic (scaly, crusty), ill defined nodule which may ulcerate
158
mx of SCC
surgical excision is the tx of choice
mohs micrographic surgery may be necessary for ill defined, large, recurrent tumours
radiotherapy for large non-resectable tumours
159
prognosis of SCC
depends on tumour size, site, histological patttern, depth of invasion, perineural involvement and immunosuppression
160
SCC adjacent to ear
161
SCC on glans penis
162
malignant melanoma
an invasive malignant tumour of the epidermal melanocytes which has the potential to metastasise
163
RFs for malignant melanoma
family hx or previous hx of melanoma
hx of multiple moles or atypical moles
skin type I (always burns, never tans)
excessive UV exposure
164
presentation of malignant melanoma
"ABCDE symptoms" rule -
Asymmetrical shape
Border irregularity
Colour irregularity
Diameter\>6mm
Evolution of lesion (eg change in size and/or shape)
Symptoms (eg bleeding, itching)
MAJOR SUSPICIOUS FEATURES - asymmetrical shape, colour irregularity and evolution of lesion (ACE)
more common on the legs in women and trunk in men
165
types of malignant melanoma
1. superficial spreading melanoma (70%of all melanomas) - common on lower limbs, in young and middle aged adults; related to intermittent high-intensity UV exposure
2. nodular melanoma - common on the trunk, in young and middle aged adults; related to intermittent high intensity UV exposure
3. lentigo maligna melanoma - common on the face, in elderly population; related to long term cumulative UV exposure
1. acral lentiginous melanoma - common on the palms, soles and nail beds, in elderly population; no clear relation with UV exposure
166
mx of malignant melanoma
depends on staging of melanoma - currently used system in the UK is American Joint Committee of Cancer Staging System (AJCC).
satges I-IV are based on primary tumour Breslow thickness, lymph node involvement and evidence of metastases. stage I is the earliest and stage IV is the most advanced
In general, surgical excision is the definitive treatment (often a second surgery, wide local excision is needed after initial excision biopsy)
radiotherapy may sometimes be useful. chemotherapy is used for metastatic disease
167
prognosis of malignant melanoma
depends on stage of melanoma and breslow thickness
in general, 90% of ppl diagnosed with melanoma in England and Wales survived 10yrs or more
168
acral lentiginous melanoma
169
lentigo maligna melanoma
170
nodular melanoma
171
superficial spreading melanoma
172
what does management of inflammatory conditions such as eczema and psoriasis aim at?
management is aimed at achieving control and not providing a cure. important to address the psychosocial complications of the illnesses.
patient education is important in these chronic skin conditions
173
atopic eczema
eczema (or dermatitis) is characterised by papules and vesicles on an erythematous base
atopic eczema is the most common type - usually develops by early childhood and resolves during teenage years (but may recur). 20% prevalence in \<12 yr olds in UK.
174
cause of atopic eczema
+ve family hx of atopy (eczema, asthma, allergic rhinits) is often present
a primary genetic defect in skin barrier function (loss of functional variants of the protein filaggrin) appears to underlie atopic eczema
exacerbating factors - infections, allergens (eg chemicals, food, dust, pet fur), sweating, heat and severe stress
175
presentation of atopic eczema
commonly present as itchy, erythematous dry scaly patches
more common on face and extensor aspects of limbs in infants and flexor aspects in children and adults
acute lesions are erythematous, vesicular and weepy (exudative)
chronic scratching/rubbing can lead to excoriations and lichenification
may show nail pitting and ridging of nails
176
mx of atopic eczema
* general measures - avoid known exacerbating factors, frequent emollients +/- bandages and bath oil/soap substitute
* topical therapies - topical steroids for flare ups; topical immunomodulators (eg tacrolimus, pimecrolimus) can be used as steroid sparing agents
* oral therapies - antihistamines for symptomatic releif, abx (eg flucloxacillin) for 2ndary bacterial infection and antivirals (eg aciclovir) for 2ndary herpes infection
* phototherapy and immunosuppressants (eg oral prednisolone, azathioprine, ciclosporin) for severe non-responsvive cases
177
complications of atopic eczema
2ndary bacterial infection (crusted weepy lesions)
2ndary viral infection - eczema herpeticum, molluscum contagiosum (pearly with central umbilication) and viral warts
178
atopic eczema
179
atopic eczema
180
acne vulgaris
an inflammatory disorder of the pilosebaceous follicle
over 80% of teenagers aged 13-18 yrs
181
causes of acne vulgaris
hormonal (androgen)
contributing factors - increased sebum production, abnormal follicular keratinization, bacterial colonization (propionibacterium acnes) and inflammation
182
presentation of acne vulgaris
non-inflammatory lesions (mild acne) - open and closed comedones
inflammatory lesions (moderate and severe acne) - papules, pustules, nodules and cysts
commonly affects face, chest and upper back
183
mx of acne vulgaris
general measures - no specific food has been identified to cause acne.
tx needs to be continued for atleast 6 weeks to produce effect
topical therapies (mild acne) - benzoyl peroxide and topical abx and topical retinoids (comedolytic and anti-inflammatory properties)
oral therapies (mod to severe acne) - oral abx and anti-androgen (in females)
oral retinoids (for severe acne)
184
complications of acne
post inflammatory hyperpigmentation, scarring, deformity, psychological and social effects
185
acne vulgaris - comedones
186
acne vulgaris - papules and nodules
187
psoriasis
chronic inflammatory skin condition due to hyperproliferation of keratinocytes and inflammatory cell infiltration
affects abt 2% of UK population
188
types of psoriasis
chronic plaque psoriasis is the most common type
other types include guttate (raindrop lesions), seborrhoeic (naso-labial and retro-auricular), flexural (body folds), pustular (palmar-plantar) and eryhtrodermic (total body redness)
189
cause of psoriasis
complex interaction bw genetic, immunological and environmental factors
precipitating factors include trauma (which may produce a Koebner phenomenon), infection (eg tonsillitis), drugs, stress and alcohol
190
presentation of psoriasis
well demarcated erythematous scaly plaques
lesions can sometumes be itchy, burning or painful
common on the extensor surfaces of the body and over scalp
auspiz sign (scratch and gentle removal of scales causes capillary bleeding)
50% have assocaited nail changes (eg pitting, onycholysis)
5-8% suffer from associated psoriatic arthropathy - symmetrical polyarthritis, asymmetircal oligomonoarthritis, lone distal interphalangeal disease, psoriatic sondylosis and arthritis mutilans (flexion deformity of distal interphalangeal joints)
191
mx of psoriasis
general measures - avoid known precipitants. use emollients to reduce scales
topical therapies (localised and mild psoriasis)- vitamin D analogoues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics and scalp preparations
phototherapy (extensive disease) - UVB and photochemotherapy ie psoralen + UVA
oral therapies (extensive and sever psoriasis or psoriasis with systemic involvement) - methotrexate, retinoids, ciclosporin, mycophenolate mofetil, fumaric acid esters and biologics (etanercept, adalimumab, ustekinumab)
192
complications of psoriasis
erythroderma
psychological and social effects
193
plaque psoriasis
194
nail changes and arthropathy (in psoriasis)
195
psoriasis (with scalp involvement)
196
what can blistering skin disorders be divided into?
in general, blistering skin conditions can be divided into -
1. immunobullous diseases (eg bullous pemphigoid, pemphigus vulgaris)
1. blistering skin infections(eg herpes simplex)
1. other blistering disorders (eg porphyria cutanea tarda)
197
what does the fragility of blisters depend on?
depends on level of split within the skin -
an intra-epidermal split causes blisters to rupture easily
a sub-epidermal split (split bw epidermis and dermis) causes blisters to be less fragile
198
common causes of blisters
impetigo
insect bites
herpes simplex infection
herpes zoster infection
acute contact dermatitis
pompholyx (vesicular eczema of the hands and feet )
burns
\*\*bullous pemphigoid and pemphigus vulgaris are uncommon conditions due to immune reaction within the skin
199
bullous impetigo (in a new tatto)
200
pompholyx
201
bullous pemphigoid
blistering disorder which usually affects the elderly
caused by autoantibodies against antigens bw the epidermis and dermis causing a subepidermal split in the skin
202
presentation of bullous pemphigoid
tense fluid filled blisters on an erythematous base
lesions are often itchy
may be preceeded by a non-sepcific itchy rash
usually affects trunk and limbs (mucosal involvement less common)
203
mx of bullous pemphigoid
general measures - wound dressings where required and monitor for signs of infection
topical therapies for localised diseases - topical steroids
oral therapies for widespread disease - oral steroids, combination of oral tetracycline and nicotinamide, immunosuppressive agents (eg azathioprine, mycophenolate mofetil, methotrexate, etc)
204
bullous pemphigoid
205
pemphigus vulgaris
blistering skin disorder usually affecting the middle aged
caused by autoantibodies against antigens within the epidermis causing an intraepidermal split in the skin
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presentation of pemphigus vularis
flaccid easily ruptured blisters forming erosions and crusts
lesions often painful
usually affects the mucosal areas (can precede skin involvement)
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mx of pemphigus vulgaris
general measures - wound dressings where required, monitor for signs of infection and good oral care (if oral mucosa is involved)
oral therapies - high dose oral steroids, immunosuppressive agents (eg MTX, azathioprine, cyclophosphamide. mycophenolate mofetil, etc)
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pemphigus vulgaris
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pemphigus vulgaris affecting the oral mucosa
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types/ddx of leg ulcers
3 main types
1. venous
2. arterial
3. neuropathic
other causes - vasculitic ulcers (purpuric, punched out lesions), infected ulcers (prurulent discharge, may have systemic signs) and malignancy (eg SCC in long standing non-healing ulcers)
In clinical practice there can be mixture of arterial, venous and/or neuropathic components in an ulcer
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venous ulcer
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arterial ulcer
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neuropathic ulcer
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venous leg ulcers
1. hx - often painful, worse on standing. hx of venous disease - varicose veins, DVT
2. common sites - malleolar areas (more common over medial than lateral malleolus)
3. lesion - large, shallow irregular ulcer. exudative and granulating base
4. associated features - warm skin, normal peripheral pulses, leg oedema, haemosiderin and melanin deposition (brown pigment), lipodermatosclerosis, atrophie blanche (white scarring with dialted capillaries)
5. possible ix - normal ankle/brachial pressure index (ie ABPI 0.8-1)
6. management - compression bandaging (only after excluding arterial insufficiency)
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arterial leg ulcers
1. hx - painful esp at night, worse when legs elevated. hx of arterial disease eg atherosclerosis
2. common sites -pressure and trauma sites eg pretibial, supramalleolar (usually lateral), and at distal points eg toes
3. lesion - small, sharply defined, deep ulcer, necrotic base
4. associated features - cold skin, weak or absent peripheral pulses, shiny pale skin, loss of hair
5. possible ix - ABPI \<0.8 - presence of arterial insufficiency. doppler studies and angiography
6. mx - vascular reconstruction. \***compression bandaging is CONTRAINDICATED**\*
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neuropathic leg ulcer
1. hx - often painless, abnormal sensation, hx of diabetes or neurological disease
2. common sites - pressure sites eg soles, heels, metatarsal heads, toes
3. lesion - variable size and depth, granulating base, may be surrounded by or underneath a hyperkeratotic lesion (callus)
4. associated features - warm skin, normal peripheral pulses but cold weak/absent pulses if it is a neuroischaemic ulcer, peripheral neuropathy
5. possible ix - ABPI \<0.8 implies neuroischaemic ulcer, X-ray to exclude osteomyelitis
6. mx - wound debridement, regular repositioning, appropriate footwear and good nutrition
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causes/ddx for an itchy eruption
inflammatory condition (eg eczema), infection (eg varicella), infestation (eg scabies), allergic reaction (eg some cases of urticaria), idiopathic or autoimmune (eg lichen planus)
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(chronic fissured) hand eczema
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scabies
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urticaria
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lichen planus
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wickham's striae
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eczema
1. hx - personal or family hx of atopy. exacerbating factors (eg allergens, irritants)
2. common sites - variable (eg flexor aspects in children and adults but extensor aspects and face in infants)
3. lesion - dry erythematous patches. acute eczema is erythematous, vesicular and exudative
4. assoc features - 2ndary bacterial or viral infections
5. possible ix - patch testing. serum IgE lvls. skin swab
6. mx - emollients, corticosteroids, immunomodulators, antihistamines
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scabies
1. hx - pruritis worse at night. may have hx of contact with symptomatic individuals
2. common sites - sides of fingers, finger webs, wrists, elbows, ankles, feet, genitals, nipples
3. lesions - linear burrows (may be tortuous) or rubbery nodules
4. assoc features - 2ndary eczema and impetigo
5. ix- skin scrape, extraction of mite and view under microscope
6. mx - scabicide (eg permethrin or malathion). antihistamines
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urticaria
1. hx -precipitating factors (eg food, drugs, contact)
2. common sites - no specific tendency
3. lesions - pink wheals (transient). may be round, annular or polycyclic
4. assoc feautres - may be associated with angioedema or anaphylaxis
5. ix - bloods and urinalysis to exclude systemic cause
6. mx - antihistamines, corticosteroids
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lichen planus
1. hx -family hx in 10%. may be drug induced
2. common sites - forearms, wrists and legs. always examine oral mucosa
3. lesions - violaceous (lilac) flat topped papules. symmetrical distribution
4. assoc features - nail changes and hair loss. lacy white streaks on oral mucosa and skin lesions (wickham's striae)
5. ix - skin biopsy
6. mx - corticosteroids, antihistamines
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ddx/causes for a changing pigment lesion
benign - melanocytic naevi, seborrhoeic wart
malignant - malignant melanoma
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congenital naevus
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seborrhoeic keratosis
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malignant melanoma
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malignant melanoma
1. hx - tend to occur in adults or middle aged. hx of evolution of lesion. may be symptomatic (bleeding, itching). presence of RFs
2. common sites - more common on legs in women and trunk in men
3. lesions - features of ABCDE - asymmetrical shape, border irregularity, color irregularity, diameter \> 6mm, evolution of lesion
4. mx - excision
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melanocytic naevi
1. hx - not usually present at birth but develop during infancy, childhood or adolescence. asymptomatic.
2. common sites - variable
3. lesions - congenital naevi may be large, protuberant, hairy and pigmented. junctional naevi are small, flat and dark. intradermal naevi are usually dome shaped papules or nodules. compound naevi are usually raised, warty, hyperkeratotic, and/or hairy
4. mx - rarely needed
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seborrhoeic wart
1. hx - tend to arise in middle aged or elderly. often multiple and asymptomatic
2. common sites - face and trunk
3. lesions - warty greasy papules or nodules. ‘stuck on’ appearance with well defined edges
4. mx - rarely needed
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ddx/ causes of purpuric eruption
what ix are important?
thrombocytopaenic (meningococcal septicaemia, DIC, ITP)
non-thrombocytic causes (trauma, drug (eg steroids), aged skin, vasculitis (eg HSP))
platelet count and clotting screen is required to rule out coagulation disorders
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HSP
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senile purpura
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meningococcal septicaemia
1. hx - acute onset. sx of meningitis and septicaemia
2. common sites - extremities
3. lesion - petechiae, ecchymoses, haemorrhagic bullae and/or tissue necrosis
4. assoc features - systemically unwell
5. ix - bloods, LP
6. mx - abx
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disseminated intravascular coagulation
1. hx - hx of trauma, malignancy, liver failure, obstetric complications, transfusions or sepsis
2. common sites - spontaneous bleeding from ear, nose, throat, GI tract, respiratory tract or wound site
3. lesion - petechiae, ecchymoses, haemorrhagic bullae and/or tissue necrosis
4. assoc features - systemically unwell
5. ix - bloods (clotting screen is imp)
6. mx -treat underlying cause, transfuse for coagulation deficiencies and anticoagulants for thrombosis
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vasculitis
1. hx - painful lesions
2. common sites - dependent areas (eg legs, buttocks, flanks)
3. lesion - palpable purpura (often painful)
4. assoc features - systemically unwell
5. ix - bloods and urinalysis. skin biopsy
6. mx - treat underlying cause. steroids and immunosuppressants if there is systemic involvement
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senile purpura
1. hx - arise in the elderly population with sun damaged skin
2. common sites - extensor surfaces of hands and forearms. such skin is easily traumatised.
3. lesion- non-palpable purpura. surrounding skin is atrophic and thin
4. assoc features - systemically well
5. ix - none req
6. mx - none req
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ddx for red swollen leg
cellulitis
erysipelas
Venous thrombosis
chronic venous insufficiency
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cellulitis/erysipelas
1. hx - painful spreading rash. hx of abrasion or ulcer
2. lesion -erysipelas - well-defined edge. cellulitis - diffuse edge
3. assoc features - systemically unwell with fever and malaise. may have lymphangitis
4. ix - skin swab. anti-streptococcal O titre (ASOT)
5. mx - abx
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venous thrombosis
1. hx - pain with swelling and redness. hx of prolonged bed rest, long haul flights or clotting tendency
2. lesion - complete venous occlusion may lead to cyanotic discolouration
3. assoc features- usually systemically well. may present with PE
4. ix- d-dimer. doppler US and/or venography
5. mx - anticoagulants
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chronic venous insufficiency
1. hx - heaviness or aching of leg which is worse on standing and relieved by walking. hx of venous thrombosis
2. lesion - discoloured (purple-blue), oedema (improved in the morning), venous congestion and varicose veins
3. assoc features - lipodermatosclerosis (erythematous induration creating ‘champaigne bottle’ appearance). stasis dermatitis (eczema with inflammatory papules, scaly and crusted erosions). venous ulcer.
4. ix - doppler ultrasound and/or venography
5. mx - leg elevation and compression stockings. sclerotherapy or surgery for varicose veins
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what tx modalities exist for skin diseases
medical - topical and systemic
physical therapy (eg cryotherapy, phototherapy, photodynamic therapy, lasers and surgery)
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contents of topical treatments
active constituents which are transported into the skin by a base (aka vehicle)
active constituents eg - steroids, tar, immunomodulators, retinoids, abx
base eg - lotion(liquid), cream (oil in water), gel (organic polymers in liquid, transparent), ointment (oil with little or no water), paste (poder in ointment)
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emollients eg, indications, SEs
eg- Aqueous cream,emulsifying ointment,liquid paraffin and white soft paraffin in equal parts (50:50)
indications - to rehydrate skin and re-establish surface lipid layer.
useful for dry scaling conditions and as soap substitutes
SEs - reactions may be irritant or allergic (eg due to preservants or perfumes in creams)
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topical/oral corticosteroids eg, indications, SEs
topical steroids - classed as mildly potent (hydrocortisone), moderately potent (clobetasone butyrate (eumovate)), potent(betamethasone valerate(Betnovate)) and very potent (clobetasol propionate(dermovate))
oral steroids - prednisolone
indications - anti-inflammatory and anti-proliferative effects
useful for allergic and immune reactions, inflammatory skin conditions, vasculitis, blistering disorders, connective tissue diseases.
SEs -
local SEs - skin atrophy (thinning), telangiectasia, striae, may mask, cause or exacerbate skin infections, acne or perioral dermatitis, and allergic contact dermatitis
systemic SEs (from oral prednisolone) - cushing's syndrome, immunosuppression, diabetes, hypertension, osteoporosis, cataract and steroid induced psychosis
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oral aciclovir indications, SEs
indications - viral infections due to herpes simplex and herpes zoster virus
SEs - GI upset, raised liver enzymes, reversible neurological reactions, haematological disorders
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oral antihistamines eg, indications, SEs
eg - non sedative (cetirizine, loratadine)
sedative (chlorpheniramine, hydroxyzine)
indications - block histamine receptors producing an anti-pruritic effect
useful for type 1 hypersensitivity reactions and eczema (esp sedative antihistamines for children)
SEs - sedative antihistamines can cause sedation and anticholinergic effects (dry mouth, blurred vision, urinary retention, constipation)
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topical/oral abx eg, indications, SEs
topical abx: fusidic acid, mupirocin, neomycin
oral abx: u know them
indications: bacterial skin infections and some used for acne
SEs: local - local skin irritation/allergy
systemic: GI upset, rashes, anaphylaxis, vaginal candidiasis, abx-associated infection such as C.diff and abx resistance (rapidly appears to fusidic acid)
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topical antiseptics eg, indications, SEs
chlorhexidine, cetrimide, povidone-iodine
indications: tx and prevention of skin infection
SEs: local skin irritation/allergy
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oral retinoids eg, indications, SEs
eg: isotretinoin, acitretin
indications: acne, psoriasis, disorders of keratinisation
SEs: mucocutaneous reactions such as dry eyes, dry lips and dry skin, disordered liver function, hypercholesterolaemia, hypertrigylceridaemia, myalgia, arthralgia and depression
teratogenicity: effective contraception must be practiced at least 1 month before, during and 1 month after isotretinoin, but for 2 yrs after acitretin
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biological therapy eg, indications, SEs
eg - monoclonal antibodies (eg.,Infliximab,,Adalimumab,,Ustekinumab,,
Certolizumab,,Gorlilumab), Fusion,antibody proteins (eg.,Etanercept),
Recombinant human cytokines and growth factors (eg.,Interleukins)
indications: mainly for psoriasis, atopic eczema and hidradenitis suppurativa
SEs - local - redness, swelling and bruising at site of injection
systemic: allergic reactions, antibody formation, flu-like symptoms, infections, hepatitis, demyelinating disease, heart failure, blood problems, rare reports of cancers (non-melanoma skin cancers, lymphoma)
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functions of normal skin
i) protective barrier against environmental insults
ii) temp regulation
iii) Sensation
iv) Vitamin D synthesis
v) Immunosurveillance
vi) Appearance/cosmesis
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what does varicella-zoster virus cause?
Herpes zoster, also known as shingles, is caused by the reactivation of the varicella-zoster virus (**VZV**), the same virus that causes varicella (chickenpox). Primary infection with VZV causes varicella. Once the illness resolves, the virus remains latent in the dorsal root ganglia.
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shingles
In immunocompetent patients, the most frequent site of reactivation is the thoracic nerves followed by the ophthalmic division of the trigeminal nerve (ophthalmic shingles), which can progress to involve all structures of the eye. If the mucocutaneous division of the VII cranial nerve is involved, the lesions in the ear, facial paralysis and associated hearing and vestibulary symptoms are known as Ramsay Hunt syndrome
Chickenpox can rarely be acquired from a patient with active shingles, as the lesions shed virus (transmission is by direct contact or droplet spread) but shingles is not caught from contact with a person with chickenpox.
HIV, Hodgkin's lymphoma and bone marrow transplants all present a high risk
post herpetic neuralgia - PHN, is persistent or recurring pain lasting 30 days or more after the acute infection or after all lesions have crusted.
Ophthalmic herpes is a danger to sight and the patient should see an ophthalmologist the same day. Antiviral therapy is mandatory for this at any age.
If the tip of the nose has a rash, the nasociliary branch of the trigeminal nerve is involved. This branch supplies the globe and so it is very likely that the eye will be affected (at least 75% of cases). This is called Hutchinson's sign. The eye can be seriously affected with little evidence of a shingles rash.
Mx -
rash should be kept clean and dry to avoid secondary bacterial infection. If the rash can be covered, or if the lesions have all crusted, there is no need to avoid school or work. If the rash is weeping and not in a covered part of skin, however, the person should stay off school or work.
analgesia (paracetamol or co-codamol or nsaids)
Prescribe an oral antiviral treatment (**aciclovir, valaciclovir**) within 72 hours of rash onset for people with any of the following criteria:
Immunocompromise
Non-truncal involvement (such as shingles affecting the neck, limbs, or perineum).
Moderate or severe pain.
Moderate or severe rash.
**Consider prescribing oral antiviral treatment** within 72 hours of rash onset for all people aged over 50 years to reduce the incidence of [post-herpetic neuralgia](https://cks.nice.org.uk/topics/shingles/background-information/complications/)
In the UK, there is a shingles vaccination programme for people aged 70 years and above. The programme began in September 2013. It is not recommended for people aged 80 years or more.
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ramsay hunt syndrome
he Ramsay Hunt syndrome described here occurs when the varicella-zoster virus (chickenpox) becomes reactivated in the geniculate ganglion of the VIIth cranial nerve (facial nerve) causing facial paralysis, loss of taste, vestibulocochlear dysfunction and pain.
Presentation -
pain deep within the ear. after a day or two, the pain often radiates outward into the pinna and there is a more constant, diffuse and dull background pain.
The following may also be presenting features:
* [Vertigo](https://patient.info/doctor/vertigo) and ipsilateral hearing loss or hyperacusis.
* [Tinnitus](https://patient.info/doctor/tinnitus-pro).
* Facial weakness or face drop.
* Rash or blisters, which may be on the skin of the ear canal, auricle or both.
* A rash or herpetic blisters in the distribution of the nervus intermedius -
* The anterior two thirds of one side of the tongue.
* The soft palate.
* The external auditory canal, visible only with an otoscope.
* The pinna.
Mx - aciclovir and prednisolone asap
If there is problem with closing the eye, a pad will protect the cornea, and eye lubricants should be prescribed.
