Dermatology Flashcards
1
Q
what are the functions of the skin?
A
- barrier to infection
- thermoregulation
- protection against trauma and UV
- vitamin D synthesis
- regulates H2O loss
2
Q
how is the normal balance of skin maintained?
A
- normal proliferation of the skin occurs just in basal layer
- in order to balance the introduction of new cells in the basal layer of the epidermis, mature corneocytes are shed from the surface of the stratum corneum in a process called desquamation
- desquamation involves the degradation of the extracellular corneo-desmosomes under the action of protease enzymes
3
Q
what is the pH of normal skin?
A
the pH of normal skin is 5.5; this allows the proteases to remain on the skin thereby enabling desquamation
4
Q
what are the 3 layers of the skin?
A
- epidermis
- dermis
- subcutaneous tissue
5
Q
what are the layers of the epidermis?
A
- stratum corneum (layer of keratin)
- stratum lucidum
- stratum granulosum
- stratum spinous
- stratum basale (dividing cells)
6
Q
what are features of the stratum corneum?
A
- outermost layer of the epidermis
- 15-20 layers of flattened cells with no nuclei or cell organelles
- cytoplasm shows filamentous keratin
- corneocytes are embedded in a lipid matrix composed of ceramides, cholesterol and fatty acids
- corneodesmosomes facilitate cellular adhesion by linking adjacent cells within this epidermal layer; they are degraded by proteases, allowing cells to be shed at the surface
7
Q
what are functions of the stratum corneum?
A
performs protective and adaptive physiological functions including:
- mechanical shear
- impact resistance
- water flux and hydration regulation
- microbial proliferation
- invasion regulation
- initiation of inflammation through cytokine activation and dendritic cell activity
- selective permeability to exclude toxins, irritants and allergens
8
Q
when are there increased numbers of corneodesmosomes?
A
diseases e.g. psoriasis in which there is a thickening of the stratum corneum
9
Q
when are there decreased numbers of corneodesmosomes?
A
diseases e.g. atopic eczema in which there is a thinning of the stratum corneum; there is increased risk of inflammation
10
Q
what are features and structure of the stratum lucidum?
A
- thin, clear layer of dead skin cells in the epidermis named for its translucent appearance under a microscope
- 3-5 layers of dead, flattened keratinocytes
- keratinocytes do not feature distinct boundaries and are filled with eleidin (intermediate form of keratin)
- surrounded by an oily substance that is the result of the exocytosis of lamellar bodies accumulated while keratinocytes are moving through the layers
11
Q
what determines the thickness and darkness of the stratum lucidum?
A
- thickness is controlled by rate of mitosis of the epidermal cells
- melanosomes in the stratum basale determine the darkness of the stratum lucidum
12
Q
what are features and structures of the stratum granulosum?
A
- thin layer of cells in the epidermis
- keratinocytes migrating from the stratum spinosum become known as granular cells in this layer
- granular cells contain keratohyalin granules, which are filled with histidine and cystein-rich proteins that bind the keratin filaments together
13
Q
what is contained in granular cells? where are they found? what is their function
A
- keratinocytes migrating from the stratum spinosum become known as granular cells in this layer
- granular cells contain keratohyalin granules, which are filled with histidine and cystein-rich proteins that bind the keratin filaments together
- main function of keratohyalin granules is to bind intermediate keratin filaments together
14
Q
what happens to cells at the transition between the stratum granulosum and the stratum corneum?
A
- cells secrete lamellar bodies (containing lipids and proteins) into the extracellular space
- this results in the formation of the hydrophobic lipid envelope responsible for the skin’s barrier properties
- cells lose their nuclei and organelles, causing the granular cells to become non-viable corneocytes in the stratum corneum
15
Q
what happens to the granular cells as they move up the layers of the skin?
A
cells lose their nuclei and organelles, causing the granular cells to become non-viable corneocytes in the stratum corneum
16
Q
what are the features of the stratum spinosum?
A
- layer of epidermis between the stratum granulosum and basale
- spiny appearance is due to shrinking of the microfilaments between desmosomes that occurs when stained with H and E
- keratinisation begins here
- composed of polyhedral keratinocytes
17
Q
what are the keratinocytes like in stratum spinosum? what happens to them?
A
- composed of polyhedral keratinocytes
- large pale-staining nuclei as they are active in synthesising fibrilar proteins, known as cytokeratin, which build up within the cells aggregating together, forming tonofibrils
18
Q
what causes the spiny appearance in the stratum spinosum?
A
spiny appearance is due to shrinking of the microfilaments between desmosomes that occurs when stained with H and E
19
Q
what are features of the stratum basale?
A
- single layer of columnar or cuboidal basal cells
- these cells are attached to eachother and to the overlying stratum spinosum by desmosomes and hemidesmosomes
20
Q
what cells are in the stratum basale? what are they like? what happens to them?
A
- single layer of columnar or cuboidal basal cells
- these cells are attached to eachother and to the overlying stratum spinosum by desmosomes and hemidesmosomes
- nucleus is large, ovoid and occupies most of the cell
- some act as stem cells
- others serve to anchor the epidermis glabrous skin and hyper-proliferative epidermis
- divide to form the keratinocytes of the spinosum, which migrate
- other cells here are melanocytes, Langerhans cells and Merkel cells
21
Q
what is the dermis?
A
layer of skin between the epidermis and subcutaneous tissues, that primarily consists of dense irregular connective tissue and cushions the body from stress and strain
22
Q
what can the dermis be divided into?
A
superficial area adjacent to the epidermis (papillary region) and a deep thicker area (reticular dermis)
23
Q
what are structural components of the dermis?
A
collagen, elastic fibres and extrafibrillar matrix
24
Q
what is contained in the dermis?
A
- Meissner’s corpuscle (light touch)
- Pacinian corpuscle (coarse touch/vibration)
- hair follicles
- sweat glands
- sebaceous glands
- apocrine glands
- lymphatics, nerves and blood vessels
25
what is the function of keratinocytes?
produce keratin as a protective barrier for the skin
26
what is the function of Langerhans cells?
present antigens and activate T cells
27
what is the function of melanocytes?
produce melanin, which protects from UV radiation
28
what are common causes of an itch with a rash?
- urticaria (hives, weals, welts - raised itchy rash)
- atopic eczema
- psoriasis
- scabies - burrows between fingers
29
what are common causes of an itch with no rash?
- renal failure
- jaundice
- iron deficiency
- lymphoma, particularly
Hodgkins
- polycythaemia - bath itch
- pregnancy alone
- drugs
- diabetes
- cholestasis
- as skin ages it itches more
30
what is acne? what are its typical features?
- common chronic skin disease that occurs when dead skin cells and oil from the skin clogs hair follicles
- affects hair follicle and sebaceous gland; there is expansion and blockage of the follicle and inflammation
- typical features include blackheads/whiteheads, pimples, oily skin and scarring
31
what is the most common variant of acne?
acne vulgaris
32
what is the epidemiology of acne?
- usually starts in adolescence
- often resolves in mid-20s
- prevalence ranges from 70-87% in teenagers
- affects the face, back and chest
- usually seen during puberty i.e. 13-20 yrs
33
what is the pathophysiology of acne?
- narrowing of the hair follicle due to hypercornification (corneodesmosomes blocking the entrance to hair follicles)
- results in increased sebum production, causing the skin to feel greasy
- some of the sebum becomes trapped in the narrow hair follicle
- sebum stagnates at the pit of the follicle where there is no oxygen
- this creates anaerobic conditions that allows Propionibacterium acnes
(P. acnes) to multiply in the stagnant sebum
- P. acne breaks down the triglycerides in sebum into free fatty acids resulting in irritation, inflammation and the attraction of neutrophils (due to chemoattractant release)
- this results in pus formation and further inflammation since the now full hair follicle is rapidly filled with attracted neutrophils
34
what organism causes acne? what are its effects?
- Propionibacterium acnes; P. acnes
- breaks down triglycerides into FFA, leading to irritation, inflammation and attraction of neutrophils
- there is pus formation and further inflammation as the now full hair follicle is rapidly filled with attracted neutrophils
35
what is the clinical presentation of acne?
- whiteheads: closed comedones
- blackheads: open comedones
- skin-coloured papules
- inflammatory lesions usually occurring when the closed wall of comedones (whitehead or blackhead) ruptures
- papules (small red bumps)
- pustules (white/yellow spots)
- nodules (large red bumps)
- commonly found on face, chest and upper back
36
what is a comedo?
- clogged hair follicle (pore) in the skin
| - keratin (skin debris) combines with oil to block the follicle
37
what is a whitehead?
closed comedo (by skin)
38
what is a pilosebaceous unit?
includes a hair follicle and a sebaceous gland
39
what is a blackhead?
- open comedo
| - being open to the air causes oxidation, which turns it black
40
how is acne diagnosed?
- usually clinical diagnosis
- skin swabs for microscopy and culture
- hormonal tests in females
41
what is treatment of mild acne?
- benzyl peroxide gel/cream
- topical antibiotics
- topical retinoids
42
what is the action of benzyl peroxide gel/cream in mild acne?
- increases skin turnover
- clears pores and reduces bacterial count
- causes dryness due to keratolytic effect
43
what are examples of topical antibiotics used in mild acne?
clindamycin gel or erythromycin gel
44
what are examples of topical retinoids? what is their action and side effects in mild acne?
e. g. tazarotene gel (irritating)
- inhibit formation and reduce the number of microcomedones
- side effects: burning, stinging, dryness and scaling, due to keratolytic effects
45
what is treatment of severe acne?
- in addition to topical therapy
- oral tetracyclines e.g. oral doxycycline then oral minocycline
- hormonal treatment
46
how are oral tetracyclines used to treat severe acne?
e. g. oral doxycycline (first line) then oral minocycline (second line)
- 4 month minimum use
- contraindicated in pregnancy and children
47
how is hormonal treatment used to treat severe acne?
- indicated when standard antibiotics treatments have failed or when control of menstruation is required
- anti-androgen treatment suppresses sebum production
- e.g. oral co-cyprindiol (contains acetate and ethinylestradiol)
48
what is dermatitis?
- group of disease that result in inflammation of the skin
- characterised by itchiness, red skin and a rash
- breakdown of the skin due to thinning of the stratum corneum
- includes atopic dermatitis, allergic contact dermatitis, irritant contact dermatitis and stasis dermatitis
49
what is the epidemiology of dermatitis?
- a genetically complex, familial disease with a strong maternal influence
- in the developed world, eczema may affect about 10% of the population at any one time
- up to 40% of people will experience an episode of eczema during their lifetime
- high prevalence in 15-30% of children and 2-10% of adults
- is nearly always itchy
50
what are the two types of dermatitis?
* endogenous (atopic); usually due to hypersensitivity (asthma and food allergy are also atopic)
* exogenous - contact dermatitis usually precipitated by chemicals, sweat and abrasives
51
what is the aetiology of dermatitis?
- pathophysiology is not fully understood
- thought to be caused by damaged filaggrin which is a skin barrier protein which, if damaged will increase the risk of eczema, as exogenous allergens will be able to invade more easily thereby resulting in inflammation
- exacerbated by chemicals, detergents and woollen clothes
- infection either in the skin or systemically, can lead to an exacerbation, possibly by a super-antigen effect
52
what is filaggrin? what is its role in dermatitis?
- filament-associated protein that binds to keratin fibres in epithelial cells
- 10-12 filaggrin units are post-translationally hydrolysed from a large profilaggrin precursor protein during terminal differentiation of epidermal cells
53
what is the genetic component of filaggrin?
encoded by FLG gene, which is part of the S100 fused-type protein family within the epidermal differentiation complex on chromosome 1q21
54
what is the pathophysiology of dermatitis?
- can be characterised by spongiosis which allows inflammatory mediators to accumulate
- different dendritic cells subtypes e.g. Langerhans cells, inflammatory dendritis epidermal cells and plasmacytoid dendritis cells have a role
55
what is the clinical presentation of dermatitis?
- commonly found on the face and flexure surfaces of the limbs
- itchy, erythematous and scaly patches especially in the flexure of the elbows, knees, ankles, wrists and around the neck
- increased dryness of skin
- in infants, eczema often starts on the cheeks before spreading to the body
- very acute lesions may weep or exude and can show small vesicles
- recurrent S. aureus infections may be common
56
what is the criteria of diagnosis of atopic dermatitis?
```
• clinical diagnosis
• high serum IgE in 80%
• must have an itchy skin condition in the past 6 months
• plus three or more of:
- history of involvement of skin creases
- personal history of asthma or hay fever (or family history)
- history of generally dry skin
- onset in childhood
```
57
what is the treatment of dermatitis?
- education and explanation
- avoidance of irritants/allergens e.g. soaps and furry animals, wearing
cotton clothes and not getting too hot
- keep nails short in children, so when they scratch it causes less damage!
- complete emollient therapy e.g. E45 cream
- topical therapies
58
what is the skin barrier like in healthy skin vs eczema?
in the healthy skin barrier there are:
• swelled corneocytes filled with natural moisturising factor (NMF) which retain moisture
• lipid bilayers prevent water loss between the corneocytes
defective barrier e.g. in eczema:
• loss of NMF leads to dry skin and the development of cracks
• has an abnormal lipid bilayer that provides an inadequate
permeability barrier
59
what is the action of emollient cream in eczema?
with emollients there is artificial restoration of the barrier in skin with defective barriers:
• occlusive emollients trap moisture in the skin and thus
transiently increase hydration
• an artificial permeability barrier is formed above the stratum corneum and thus prevents water loss between corneocytes
60
how should emollient cream be applied in dermatitis?
* application every 4 hours/3-4 times per day (x2 a day at least)
* 250-500g per week for a child
* 500-750g per week for an adult
* compliance is significantly correlated with clinical improvement
61
what is the first line treatment of dermatitis of topical therapies?
topical corticosteroids
62
what is the second line treatment of dermatitis of topical therapies?
topical calcineurin inhibitors
63
what is the classification of topical steroids for dermatitis?
- very potent; e.g. clobetasol propionate; use only on thick skin
- potent; e.g. flucinonide
- moderate e.g. clobetasol butyrate
- mild e.g. hydrocortisone
64
what is the mechanism of action and side effects of topical corticosteroids on dermatitis?
- directly & indirectly inhibit pro-inflammatory cytokines e.g. IL-1,-2,-6 & TNF-alpha
- side effects: skin atrophy, suppression of skin barrier homeostasis, telangiectasia (spider veins), thinning of the skin, acne, striae (lines on abdomen)
- only use steroids on inflamed skin!
65
what are examples of topical calcineurin inhibitors used in dermatitis?
pimecrolimus (mild) or tacrolimus (moderate) ointment
66
what is the mechanism of action and side effects of topical calcineurin inhibitors on dermatitis?
* slightly less effective but have less side effects and more useful for sensitive areas where you don’t want steroid side effects!!
* inhibits calcineurin which induces transcription factors for many interleukins e.g. IL-2 which activate T helper cells and induces production of other cytokines
* thus they reduce inflammation
* they do not cause skin atrophy and are a good option for treating eczema in sensitive areas e.g. face and eyelids
* side effects: burning/stinging following application
67
what is the treatment of moderate to severe/non-responsive dermatitis?
- oral immune-modulators
- oral steroids e.g. oral prednisolone
- antibiotics e.g. flucloxacillin
- phototherapy with UV A
- antihistamines e.g. chlorphenamine
68
what are examples of oral immune-modulators used in dermatitis?
- ciclosporin (calcineurin inhibitor)
- azothioprine
- be aware of immunosuppression effects
69
why are antihistamines used in dermatitis?
do not provide a clinical effect on eczema, instead they sedate patient so they are able to get good rest and better sleep
70
what is calcineurin?
calcium and calmodulin dependent serine/threonine protein phosphatase (3)
71
what is the action of calcineurin?
- activates T cells and can be blocked by drugs
- activates nuclear factor of activated T cell cytoplasmic (NFATc), a transcription factor, by phosphorylating it
- activated NFATc is translocated into the nucleus, where it upregulates expression of IL-2
- IL-2 stimulates growth and differentiation of T cell response
72
what are examples of calcineurin inhibitors?
ciclosporin, voclosporin, pimecrolimus and tacrolimus
73
what is psoriasis?
- chronic, inflammatory, autoimmune skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration
- characterised by patches of abnormal skin which are typically red, dry, itchy and scaly
74
what are the types of psoriasis?
- plaque
- guttate
- inverse
- pustular
- erythrodermic
75
what is the epidemiology of psoriasis?
- affects around 2% of UK population
- onset is at any age:
• uncommon in children
• peak prevalence in early adulthood
• second peak between 50-60yrs
- occurs equally in men and women
- essentially it is the opposite to eczema (where there is break-down of skin) since there is hyper-proliferation of skin leading to thickened plaques
76
what is the aetiology/risk factors of psoriasis? what are some environmental triggers?
- appears to be polygenic
- also dependent on certain environmental triggers:
• infection with group A Streptococcus
• drugs e.g. lithium
• UV light
• high alcohol use
• stress
- family history
77
what is the pathophysiology of psoriasis?
- psoriasis is a T-lymphocyte driven disorder to an unidentified antigen
- T cell activation results in upregulation of Th1 types T cell cytokines e.g. interferon-gamma, interleukins (-1,-2,-8), growth factors and adhesion
molecules
- upregulation of these cytokines results in increased uncontrolled hyperproliferation of the keratinocytes in the epidermis with an increase in
the epidermal cell turnover rate
78
what is a general clinical presentation of psoriasis?
associated with nail changes; pitting and onycholysis (separation of fingernail from nail bed)
79
what is the clinical presentation of chronic plaque psoriasis?
• most common
• well-demarcated disc-shaped, salmon-pink silvery plaques occur on the exterior surface of the limbs, particularly the elbows and knees
• scalp involvement is common and is most seen
at the hair margin
• thickened epidermis
• new plaques of psoriasis occur at sites of skin trauma
80
what are treatments of chronic plaque psoriasis?
- emollients e.g. E45
- topical vitamin D analogues
- topical corticosteroids e.g. hydrocortisone cream
- topical retinoids e.g. tazarotene gel (irritating)
- UV B
- coal tar
- anti-mitotic e.g. dithranol cream (use on large plaques only)
81
what are examples of topical vitamin D analogues? what is their mechanism of action on psoriasis?
• inhibit cell proliferation and stimulate keratinocyte differentiation
• e.g. calcipotriol cream (irritating - not for face) or
calcitriol ointment (less irritating)
82
what is the treatment of extensive plaques in chronic plaque psoriasis?
* phototherapy with UV A
* disease modifying anti-rheumatic drug (DMARD)
* immunosuppressant e.g. ciclosporin
83
what is the mechanism of action of DMARDs?
- inhibits folic acid metabolism thus inhibits DNA replication
- leads to anti-proliferative and anti-inflammatory effect
- must give folic acid supplements 48hrs after treatment
84
what is an example of a DMARD?
oral methotrexate
85
what are side effects and contraindications of oral methotrexate (a DMARD)?
* side effects: hepatotoxic
* contraindications: pregnancy/breast feeding, hepatic disease/alcoholism, renal impairment, active infection, live vaccines
86
what is the clinical presentation of flexural psoriasis? where does it often occur?
* tends to occur later in life
* well-demarcated red, glazed, non-scaly plaques
* scaling is absent
* confined to flexures e.g. groin, natal cleft and sub-mammary areas
* can be mistaken for candida intertrigo - but this will normally show satellite lesions
87
what is first line treatment of flexural psoriasis?
- topical mild to moderate corticosteroids e.g. hydrocortisone or clobetasol butyrate
- short course to avoid atrophy
88
what is the second line treatment of flexural psoriasis?
topical vitamin D analogue e.g. calcipotriol cream (irritating - not for face)
89
what is the clinical presentation of guttate psoriasis?
* raindrop-like
* most common in children and young adults
* generalised, concentrating on the trunk, upper arms and legs
* an explosive eruption of very small circular or oval plaques appears over the trunk about 2 weeks after a streptococcal sore throat
90
what is the treatment of guttate psoriasis?
- topical mild-moderate corticosteroids e.g. hydrocortisone or clobetasol butyrate
- ultraviolet B
- coal tar
91
what is the clinical presentation of palmoplantar psoriasis?
thickening of the palms and soles
92
what is the treatment of palmoplantar psoriasis?
- emollients e.g. greasy/ointments
- keratolytic agents e.g. salicylic acid
- potent topical corticosteroids e.g. flucononide
- phototherapy with UV A
- oral retinoid e.g. oral acitretin
93
what are oral retinoids? what are their mechanism of action/side effects? give an example?
- e.g. oral acitretin
- vitamin A derivative
- binds to nuclear receptors that regulate gene transcription. induce keratinocyte differentiation and reduce epidermal hyperplasia, leading to slowing of cell reproduction
- used alongside phototherapy
- side effects: dry lips, eyes and mucosa, hyperlipidaemia, disturbed liver functions
- teratogenic - contraindicated in pregnancy
94
how are anti-TNF biologics used in psoriasis? give some examples of drugs
- only used once systemic therapy has failed
| - IV infliximab, IV etanercept, IV adalimumab
95
what are venous ulcers?
• wounds that are thought to occur due to improper functioning of venous valves, usually of the legs
• defined as a loss of skin below the knee on the leg or foot that takes more than 2
weeks to heal
• they are the result of sustained venous hypertension in the superficial veins
96
what is the epidemiology of venous ulcers?
- venous ulcers are the most common type of leg ulcer in the developed world
- common in later life and are costly as they are often chronic and recurrent
- they affect 1% of the population over the age of 70 yrs
- most commonly found on the lower leg in a triangle above the ankles
97
what is the aetiology of venous ulcers?
sustained venous hypertension that is caused by:
• incompetent valves in the deep or perforating veins
• previous deep vein thrombosis (DVT)
• atherosclerosis
• vasculitis e.g. RA, SLE
98
what are risk factors for venous ulcers?
varicose veins or DVT
99
what is the pathophysiology of venous ulcers?
increased pressure causes extravasation of fibrinogen through the capillary
walls, giving rise to perivascular fibrin deposition, which leads to poor oxygenation of the surrounding skin
100
what is the clinical presentation of venous ulcers?
- sloping and gradual edges
- ulcer is large, shallow, irregular and exudative
- usually minimal pain
- oedema of the lower leg
- venous eczema
- brown pigmentation from haemosiderin
- varicose veins
- pulses present
- warm skin
101
how are venous ulcers diagnosed?
- ankle brachial pressure index (ABPI) is normal
| - doppler ultrasound to exclude significant arterial disease
102
what is the treatment of venous ulcers?
- high compression 4 layered bandage
- leg elevation to reduce venous hypertension
- antibiotics for infection
- analgesia e.g. ibuprofen or even morphine
- support stockings for life
103
what are arterial ulcers? what is their appearance?
- present as punched-out, painful ulcers higher up the leg or on the feet
- grey or yellow fibrotic base and undermining skin margins
- pulses not palpable
- thin shiny skin and absence of hair
104
what as the epidemiology of arterial ulcers?
commonly a history of claudication, hypertension, angina or smoking
105
what are risk factors for arterial ulcers?
- arterial disease e.g. atherosclerosis
- smoking
- hypercholesterolaemia
- diabetes mellitus
106
what is the clinical presentation of arterial ulcers?
- typically present as punched-out ulcers higher up the leg or on the feet
- intense pain that is worse when elevated (more pain than venous ulcer)
- leg is cold and pale
- ulcer is small, sharply defined and has a necrotic base
- shiny pale skin and loss of hair
- absent peripheral pulses
- arterial bruits - murmurs heard caused by turbulent blood flow often due to
partial obstruction in artery
- no oedema
107
how are arterial ulcers diagnosed?
- doppler ultrasound will confirm arterial disease
| - ankle brachial pressure index (ABPI) suggest arterial insufficiency
108
what is the treatment of arterial ulcers?
- keep ulcer clean and covered
- analgesia e.g. ibuprofen or even morphine
- vascular reconstruction if appropriate
- never use compression bandaging
109
what is a neuropathic ulcer?
major complication of diabetes, due to disturbed wound healing process
110
what is the clinical presentation of neuropathic ulcers?
* often painless
* tend to be seen over pressure areas of the feet, such as the metatarsal heads, or heels owing to repeated trauma
* ulcers tend to have a variable size and may be surrounded by callus
* there is warm skin and normal peripheral pulses
111
what is the epidemiology of neuropathic ulcers?
• most commonly found in diabetes and neurological disease due to peripheral
neuropathy
• in some developing countries, leprosy is the common cause
112
what is the treatment of neuropathic ulcers?
- keep ulcer clean and remove pressure or trauma from the affected area
- correctly fitting shoes and specialist podiatrist help for diabetics
113
what is vasculitis?
* vasculitis is an inflammatory disorder of blood vessels that causes endothelial damage
* cutaneous vasculitis (confirmed by skin biopsy) may be an isolated problem or part of a systemic disease with involvement of other organs
114
what is leucocytoclastic vasculitis/angiitis?
- cutaneous small-vessel vasculitis
- inflammation of small blood vessels (usually post-capillary venules in the dermis)
- most common cutaneous vasculitis affecting small vessels
- usually appears on the lower legs as a symmetrical palpable purpura
- rarely associated with systemic involvement
- often settles spontaneously
115
what are causes of leucocytoclastic vasculitis?
* majority idiopathic (55-60%)
* drugs (15%)
* infection (15%)
* inflammatory disease (10%)
* malignant disease (<5%)
116
what is the clinical presentation of leucocytoclastic vasculitis?
```
- cutaneous features which may erode and ulcerate are:
• haemorrhagic papules
• pustules
• nodules
• plaques
- these purpuric lesions do not blanch with pressure
from a glass slide
- pyrexia and arthralgia are common
```
117
what is the treatment of leucocytoclastic vasculitis?
- analgesia
- support stockings
- dapsone (antibiotic) or prednisolone
118
what is the epidemiology of squamous cell carcinoma?
• tends to present in later life
• locally invasive, malignant tumour of the squamal
keratinocytes (keratinocytes in the outermost part of
the epidermis)
• more aggressive than basal cell carcinoma (BCC/rodent ulcer) and has a higher
metastatic potential - particularly to the lymph nodes (but still rare to metastasise)
• second most common skin cancer just below BCC
• in situ SCC that is confined to the epidermis is known as Bowen’s disease
119
what are risk factors for squamous cell carcinoma?
- UV exposure
| - chronic inflammation e.g. wound scars and immunosuppression
120
what is the clinical presentation of squamous cell carcinoma?
- most common on sun-exposed sites in later-life
- lesions are often keratotic, rather ill-defined nodules that may ulcerate
- they can grow very rapidly
- ulcerated lesions on the lower lip or ear are often more aggressive
- examination of the regional lymph nodes is essential to look for metastases
121
what is the treatment of squamous cell carcinoma?
- surgical excision with a minimal margin of 5mm
| - radiotherapy is also used, especially if it is non-resectable
122
what is the most common malignant skin cancer?
basal cell carcinoma
123
what is the second most common malignant skin cancer?
squamous cell carcinoma
124
what is the epidemiology and behaviour of basal cell carcinoma?
* most common malignant skin cancer
* non-pigmented in 95%
* occasionally can resemble melanoma when pigmented
* majority occur in the elderly on the head and neck
* may ulcerate - when it does it's called ‘Rodent Ulcer’
* tumour of the basal keratinocytes (keratinocytes of the deepest part of the epidermis)
* also tends to present in later life
* less aggressive and metastatic than SCC
* rarely metastasises but is locally destructive
* slow growing
* locally invasive
125
what are risk factors for basal cell carcinoma?
- UV exposure
- skin type 1: skin that burns and doesn’t tan
- ageing
126
what is the clinical presentation of basal cell carcinoma?
- border of ulcerated lesions is raised with a pearly appearance
- slowly enlarging, shiny nodule on the head and neck area, which bleeds following minor trauma and does not heal
- slowly causes local tissue destruction if not treated
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what is the treatment of basal cell carcinoma?
- surgically excised with wide borders and histology to ensure clear and adequate tumour margins
- superficial BCCs can be managed with non-surgical treatment: cryotherapy or photodynamic therapy
- radiotherapy in those unable to tolerate surgery
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what is the most malignant form of skin cancer?
malignant melanoma
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what is a malignant melanoma?
malignant tumour of the melanocytes
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what is the epidemiology of malignant melanoma?
- commonly affects younger patients, thus early diagnosis is essential!!
- responsible for the most deaths caused by cancer in men
- incidence is rising due to excessive sun exposure and sunburn in childhood
- common in more affluent people and those who do heavy alcohol drinking
(the combination of sun exposure and alcohol in blood is carcinogenic to
melanocytes)
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what are risk factors for malignant melanoma?
- UV exposure e.g. suntanning and sunbed use
- red hair
- high density freckles
- skin type 1: skin tends to burn and not tan
- atypical moles
- multiple melanocytic naevi (benign)
- sun sensitivity
- immunosuppression
- family history
- pale skin
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what is the commonest site for malignant melanoma in men?
back/chest
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what is the commonest site for malignant melanoma in women?
lower legs
134
what is the usual colour of malignant melanomas?
>95% of melanomas show very dark colour, black or almost black in part of lesion
135
what are the symptoms and criteria used for diagnosis of malignant melanoma?
ABCDE symptoms & criteria used for diagnosis:
• A - Asymmetrical shape
• B - Border irregularity
• C - Colour irregularity e.g. non-uniform
• D - Diameter > 6 mm
• E - Elevation/Evolution - change of lesion
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what are major signs of malignant melanoma?
change in size, shape or colour (usually darkening)
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what are minor signs of malignant melanoma?
* inflammation, crusting or bleeding
* sensory change
* itching
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what are types of melanoma?
- superficial spreading (SSMM)
- nodular - most aggressive type!
- lentigo maligna - usually on the face
- acral - restricted to palms/soles
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what are differential diagnoses of malignant melanoma?
- benign pigmented naevus
- seborrhoeic wart (most common pigmented lesion in elderly)
- pyogenic granuloma
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what are features of a pyogenic granuloma?
* presents as a small warty lesion that bleeds easily
* non-pigmented and occurs where there is minor trauma e.g. shaving cut
* benign lesion that grows quickly
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what is treatment of malignant melanoma? what is done for metastatic disease?
- surgical excision is curative in early cases
- very wide excision does not improve survival
- has limited sensitivity to radiotherapy so this has limited role
- for metastatic disease (30-50%):
• removal of regional lymph nodes, isolated limb perfusion, radiotherapy, immunotherapy and chemotherapy
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what are the commonest metastases of malignant melanoma?
distant metastases is commonest to lung, liver, CNS - but any tissue/organ can be affected
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what is the prognosis of malignant melanoma?
- thin lesions (<1mm - Breslow lesion) have best prognosis
- if over 60 then lower than 5 year survival
- generally there is a female advantage in prognosis
- ulceration is usually a late-stage sign
- poor prognosis if present on trunk vs. limbs
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what is cellulitis?
- bacterial infection involving the inner layers of the skin
| - specifically affects the dermis and subcutaneous fat
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what is the epidemiology of cellulitis?
usually involves lower extremities
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what is the aetiology of cellulitis?
- Group A Beta-haemolytic streptococcus e.g. streptococcus pyogenes - most common!
- Staphylococcus aureus
- sometimes MRSA
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what are risk factors for cellulitis?
- lymphoedema
- leg ulcer
- immunosuppression
- traumatic wounds - normally an obvious port of entry of pathogen
- athletes
- leg oedema
- obesity
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what is the pathophysiology of cellulitis?
- typically affects the lower leg or arm and spreads proximally
- other sites that may be affected include the abdomen, perianal and peioribital areas
- can also affect just one side of the face
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what is the clinical presentation of cellulitis?
- local inflammation; proximally spreading
- hot erythema in the affected area
- poorly demarcated margins, swelling, warmth and tenderness
- occasionally will blister especially if oedema is prominent
- systemically unwell with pyrexia
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how is cellulitis diagnosed?
- clinical
- skin swabs are usually negative unless taken from broken skin
- serological testing to confirm a streptococcal infection e.g. antistreptolysin O titre (ASOT)
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what is the treatment of cellulitis?
- antibiotics e.g. oral phenoxymethylpenicillin or oral flucloxacillin
• oral erythromycin if penicillin allergic
- if infection is widespread then antibiotics should be given IV for 3-5 days followed by at least 2 weeks of oral therapy
- if recurrent then give prophylaxis low-dose antibiotics e.g. oral phenocymethylpenicillin twice daily
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what antibiotics are given in cellulitis?
oral phenoxymethylpenicillin or oral flucloxacillin
| • oral erythromycin if penicillin allergic
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what is necrotising fasciitis?
• this is a deep-seated infection of the subcutaneous tissue that results in a
fulminant and spreading destruction of fascia and fat but initially spares the skin (eventually the skin is also destroyed)
• there is high mortality
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what is type 1 necrotising fasciitis?
caused by a mixture of aerobic and anaerobic bacteria following abdominal surgery or in diabetics
155
what is type 2 necrotising fasciitis?
caused by group A beta-haemolytic streptococci e.g. S. pyogenes; most common cause, arises in previously healthy patients
156
what are risk factors for necrotising fasciitis?
- abdominal surgery
| - immunosuppression
157
what is the clinical presentation of necrotising fasciitis?
- severe pain that is out of proportion to the skin findings at the initial site of
infection that is rapidly followed by tissue necrosis
- infection tracks rapidly along the tissue planes, causing spreading erythema, pain and sometimes crepitus (crackling sound when joint moves)
- in patients with fever, toxicity and pain that is out of proportion to the skin findings - necrotising fasciitis should be suspected
- multi-organ failure is common and mortality is high
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how is necrotising fasciitis?
- soft tissue gas is seen on X-ray
- raised CRP
- very raised white cell count
- if necrotising fasciitis is suspected then it must be treated aggressively and promptly
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what is the treatment of necrotising fasciitis?
- aggressive and prompt antibiotics for confirmed group A streptococci (GAS) - type 2: IV benzylpenicillin and IV clindamycin
- if unknown aetiology e.g. type 1: broad spectrum IV antibiotics with the inclusion of IV metronidazole
- urgent surgical exploration with extensive debridement or amputation if necessary
160
what are examples of topical corticosteroids?
hydrocortisone, betamethasone
161
what are indications for topical corticosteroids?
used in inflammatory skin conditions such as eczema to treat disease flares or to control chronic disease where emollients alone are ineffective
162
what are mechanisms of action of topical corticosteroids?
- corticosteroids have immunosuppressive, metabolic and mineralocorticoid effects
- effects are mostly limited to site of application
- can be prescribed as mild, moderate, strong and very strong i.e. hydrocortisone 0.1-2.5% is mild and betamethasone 0.1% is strong
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what are adverse effects/contraindications of topical corticosteroids?
- adverse effects are uncommon with mild or moderately strong topical
corticosteroids
- stronger ones can cause skin thinning, stir, telangiectasia (spider veins) and contact dermatitis
- can cause perioral dermatitis and acne on the face
- withdrawal can cause rebound worsening initially
- contraindicated if infection is present at the site or other lesions
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what are examples of emollients?
aqueous cream, liquid paraffin, E45
165
what are indications for emollients?
- as a topical treatment for dry and scaling skin disorders e.g. psoriasis
- used alone or in combination with topical corticosteroids in the treatment of eczema
- can reduce skin dryness and cracking in psoriasis
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what are mechanisms of action of emollients?
- help to replace water content in dry skin
- contain oils or paraffin based products that help to soften the skin and can reduce water loss by protecting against evaporation from the skin surface
- can be used as a soap substitute or moisturiser
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what are adverse effects/contraindications of emollients?
main tolerability issue is that they cause greasiness of the skin and can exacerbate acne on the face
168
what are examples of keratolytics?
Salicylic acid, Lactic acid, Allantoin
169
what are indications for keratolytics?
- removal of warts and other lesions of excess skin growth
- treatment of dry skin
- treatment of acne
170
what are mechanisms of action of keratolytics?
- for lesions: keratolytic therapy thins the skin on and around the lesion and causes the outer layer of skin to loosen and shed
- can also be used to soften keratin in the skin, which improves the skin’s moisture binding capacity which is beneficial in dry skin conditions
- for acne, it causes the cells of the epidermis to shed more rapidly which opens clogged pores and neutralises bacteria within
- produces anti-inflammatory effects by suppressing cyclo-oxygenase
171
what are adverse effects/contraindications of keratolytics?
- at very high concentrations, can produce chemical burns on skin and damage pores
- hypersensitivity reactions can occur
- sun protection should be used with the treatment as it makes the skin more
susceptible to UV damage
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what are examples of retinoids?
acitretin, tazarotene
173
what are indications for retinoids?
- can be used in a range of inflammatory skin disorders such as severe cystic acne and disorders of skin turnover such as psoriasis
- can also be used in skin cancers
174
what are the mechanisms of action of retinoids?
- incompletely understood - has been shown to induce apoptosis in various cells especially sebaceous gland cells
- may amplify production of certain skin proteins that reduce sebum production and exhibit an antimicrobial effect
175
what are adverse effects/contraindications of retinoids?
- most common adverse effect is a transient worsening of acne, dry and
fragile skin, increased susceptibility to sunburn and anaemia
- rarely may cause myalgia, headaches and severe depression
- use is contraindicated in pregnancy as it is a severe teratogen
