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Phase 2A > Dermatology > Flashcards

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
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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
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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

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4
Q

what are the 3 layers of the skin?

A
  • epidermis
  • dermis
  • subcutaneous tissue
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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)
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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
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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
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8
Q

when are there increased numbers of corneodesmosomes?

A

diseases e.g. psoriasis in which there is a thickening of the stratum corneum

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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

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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
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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
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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
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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
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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
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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

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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
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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
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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

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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

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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
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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

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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)

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23
Q

what are structural components of the dermis?

A

collagen, elastic fibres and extrafibrillar matrix

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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
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25
Q

what is the function of keratinocytes?

A

produce keratin as a protective barrier for the skin

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26
Q

what is the function of Langerhans cells?

A

present antigens and activate T cells

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27
Q

what is the function of melanocytes?

A

produce melanin, which protects from UV radiation

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28
Q

what are common causes of an itch with a rash?

A
  • urticaria (hives, weals, welts - raised itchy rash)
  • atopic eczema
  • psoriasis
  • scabies - burrows between fingers
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29
Q

what are common causes of an itch with no rash?

A
  • renal failure
  • jaundice
  • iron deficiency
  • lymphoma, particularly
    Hodgkins
  • polycythaemia - bath itch
  • pregnancy alone
  • drugs
  • diabetes
  • cholestasis
  • as skin ages it itches more
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30
Q

what is acne? what are its typical features?

A
  • 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
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31
Q

what is the most common variant of acne?

A

acne vulgaris

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32
Q

what is the epidemiology of acne?

A
  • 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
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33
Q

what is the pathophysiology of acne?

A
  • 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
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34
Q

what organism causes acne? what are its effects?

A
  • 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
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35
Q

what is the clinical presentation of acne?

A
  • 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
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36
Q

what is a comedo?

A
  • clogged hair follicle (pore) in the skin

- keratin (skin debris) combines with oil to block the follicle

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37
Q

what is a whitehead?

A

closed comedo (by skin)

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38
Q

what is a pilosebaceous unit?

A

includes a hair follicle and a sebaceous gland

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39
Q

what is a blackhead?

A
  • open comedo

- being open to the air causes oxidation, which turns it black

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40
Q

how is acne diagnosed?

A
  • usually clinical diagnosis
  • skin swabs for microscopy and culture
  • hormonal tests in females
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41
Q

what is treatment of mild acne?

A
  • benzyl peroxide gel/cream
  • topical antibiotics
  • topical retinoids
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42
Q

what is the action of benzyl peroxide gel/cream in mild acne?

A
  • increases skin turnover
  • clears pores and reduces bacterial count
  • causes dryness due to keratolytic effect
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43
Q

what are examples of topical antibiotics used in mild acne?

A

clindamycin gel or erythromycin gel

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44
Q

what are examples of topical retinoids? what is their action and side effects in mild acne?

A

e. g. tazarotene gel (irritating)
- inhibit formation and reduce the number of microcomedones
- side effects: burning, stinging, dryness and scaling, due to keratolytic effects

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45
Q

what is treatment of severe acne?

A
  • in addition to topical therapy
  • oral tetracyclines e.g. oral doxycycline then oral minocycline
  • hormonal treatment
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46
Q

how are oral tetracyclines used to treat severe acne?

A

e. g. oral doxycycline (first line) then oral minocycline (second line)
- 4 month minimum use
- contraindicated in pregnancy and children

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47
Q

how is hormonal treatment used to treat severe acne?

A
  • 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)
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48
Q

what is dermatitis?

A
  • 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
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49
Q

what is the epidemiology of dermatitis?

A
  • 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
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50
Q

what are the two types of dermatitis?

A
  • endogenous (atopic); usually due to hypersensitivity (asthma and food allergy are also atopic)
  • exogenous - contact dermatitis usually precipitated by chemicals, sweat and abrasives
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51
Q

what is the aetiology of dermatitis?

A
  • 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
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52
Q

what is filaggrin? what is its role in dermatitis?

A
  • 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
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53
Q

what is the genetic component of filaggrin?

A

encoded by FLG gene, which is part of the S100 fused-type protein family within the epidermal differentiation complex on chromosome 1q21

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54
Q

what is the pathophysiology of dermatitis?

A
  • 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
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55
Q

what is the clinical presentation of dermatitis?

A
  • 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
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56
Q

what is the criteria of diagnosis of atopic dermatitis?

A 
• 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
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57
Q

what is the treatment of dermatitis?

A
  • 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
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58
Q

what is the skin barrier like in healthy skin vs eczema?

A

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

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59
Q

what is the action of emollient cream in eczema?

A

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

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60
Q

how should emollient cream be applied in dermatitis?

A
  • 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
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61
Q

what is the first line treatment of dermatitis of topical therapies?

A

topical corticosteroids

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62
Q

what is the second line treatment of dermatitis of topical therapies?

A

topical calcineurin inhibitors

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63
Q

what is the classification of topical steroids for dermatitis?

A
  • very potent; e.g. clobetasol propionate; use only on thick skin
  • potent; e.g. flucinonide
  • moderate e.g. clobetasol butyrate
  • mild e.g. hydrocortisone
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64
Q

what is the mechanism of action and side effects of topical corticosteroids on dermatitis?

A
  • 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!
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65
Q

what are examples of topical calcineurin inhibitors used in dermatitis?

A

pimecrolimus (mild) or tacrolimus (moderate) ointment

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66
Q

what is the mechanism of action and side effects of topical calcineurin inhibitors on dermatitis?

A
  • 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
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67
Q

what is the treatment of moderate to severe/non-responsive dermatitis?

A
  • oral immune-modulators
  • oral steroids e.g. oral prednisolone
  • antibiotics e.g. flucloxacillin
  • phototherapy with UV A
  • antihistamines e.g. chlorphenamine
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68
Q

what are examples of oral immune-modulators used in dermatitis?

A
  • ciclosporin (calcineurin inhibitor)
  • azothioprine
  • be aware of immunosuppression effects
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69
Q

why are antihistamines used in dermatitis?

A

do not provide a clinical effect on eczema, instead they sedate patient so they are able to get good rest and better sleep

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70
Q

what is calcineurin?

A

calcium and calmodulin dependent serine/threonine protein phosphatase (3)

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71
Q

what is the action of calcineurin?

A
  • 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
Q

what are examples of calcineurin inhibitors?

A

ciclosporin, voclosporin, pimecrolimus and tacrolimus

73
Q

what is psoriasis?

A
  • 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
Q

what are the types of psoriasis?

A
  • plaque
  • guttate
  • inverse
  • pustular
  • erythrodermic
75
Q

what is the epidemiology of psoriasis?

A
  • 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
Q

what is the aetiology/risk factors of psoriasis? what are some environmental triggers?

A
  • 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
Q

what is the pathophysiology of psoriasis?

A
  • 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
Q

what is a general clinical presentation of psoriasis?

A

associated with nail changes; pitting and onycholysis (separation of fingernail from nail bed)

79
Q

what is the clinical presentation of chronic plaque psoriasis?

A

• 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
Q

what are treatments of chronic plaque psoriasis?

A
  • 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
Q

what are examples of topical vitamin D analogues? what is their mechanism of action on psoriasis?

A

• inhibit cell proliferation and stimulate keratinocyte differentiation
• e.g. calcipotriol cream (irritating - not for face) or
calcitriol ointment (less irritating)

82
Q

what is the treatment of extensive plaques in chronic plaque psoriasis?

A
  • phototherapy with UV A
  • disease modifying anti-rheumatic drug (DMARD)
  • immunosuppressant e.g. ciclosporin
83
Q

what is the mechanism of action of DMARDs?

A
  • 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
Q

what is an example of a DMARD?

A

oral methotrexate

85
Q

what are side effects and contraindications of oral methotrexate (a DMARD)?

A
  • side effects: hepatotoxic
  • contraindications: pregnancy/breast feeding, hepatic disease/alcoholism, renal impairment, active infection, live vaccines
86
Q

what is the clinical presentation of flexural psoriasis? where does it often occur?

A
  • 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
Q

what is first line treatment of flexural psoriasis?

A
  • topical mild to moderate corticosteroids e.g. hydrocortisone or clobetasol butyrate
  • short course to avoid atrophy
88
Q

what is the second line treatment of flexural psoriasis?

A

topical vitamin D analogue e.g. calcipotriol cream (irritating - not for face)

89
Q

what is the clinical presentation of guttate psoriasis?

A
  • 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
Q

what is the treatment of guttate psoriasis?

A
  • topical mild-moderate corticosteroids e.g. hydrocortisone or clobetasol butyrate
  • ultraviolet B
  • coal tar
91
Q

what is the clinical presentation of palmoplantar psoriasis?

A

thickening of the palms and soles

92
Q

what is the treatment of palmoplantar psoriasis?

A
  • 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
Q

what are oral retinoids? what are their mechanism of action/side effects? give an example?

A
  • 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
Q

how are anti-TNF biologics used in psoriasis? give some examples of drugs

A
  • only used once systemic therapy has failed

- IV infliximab, IV etanercept, IV adalimumab

95
Q

what are venous ulcers?

A

• 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
Q

what is the epidemiology of venous ulcers?

A
  • 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
Q

what is the aetiology of venous ulcers?

A

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
Q

what are risk factors for venous ulcers?

A

varicose veins or DVT

99
Q

what is the pathophysiology of venous ulcers?

A

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
Q

what is the clinical presentation of venous ulcers?

A
  • 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
Q

how are venous ulcers diagnosed?

A
  • ankle brachial pressure index (ABPI) is normal

- doppler ultrasound to exclude significant arterial disease

102
Q

what is the treatment of venous ulcers?

A
  • 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
Q

what are arterial ulcers? what is their appearance?

A
  • 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
Q

what as the epidemiology of arterial ulcers?

A

commonly a history of claudication, hypertension, angina or smoking

105
Q

what are risk factors for arterial ulcers?

A
  • arterial disease e.g. atherosclerosis
  • smoking
  • hypercholesterolaemia
  • diabetes mellitus
106
Q

what is the clinical presentation of arterial ulcers?

A
  • 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
Q

how are arterial ulcers diagnosed?

A
  • doppler ultrasound will confirm arterial disease

- ankle brachial pressure index (ABPI) suggest arterial insufficiency

108
Q

what is the treatment of arterial ulcers?

A
  • keep ulcer clean and covered
  • analgesia e.g. ibuprofen or even morphine
  • vascular reconstruction if appropriate
  • never use compression bandaging
109
Q

what is a neuropathic ulcer?

A

major complication of diabetes, due to disturbed wound healing process

110
Q

what is the clinical presentation of neuropathic ulcers?

A
  • 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
Q

what is the epidemiology of neuropathic ulcers?

A

• most commonly found in diabetes and neurological disease due to peripheral
neuropathy
• in some developing countries, leprosy is the common cause

112
Q

what is the treatment of neuropathic ulcers?

A
  • keep ulcer clean and remove pressure or trauma from the affected area
  • correctly fitting shoes and specialist podiatrist help for diabetics
113
Q

what is vasculitis?

A
  • 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
Q

what is leucocytoclastic vasculitis/angiitis?

A
  • 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
Q

what are causes of leucocytoclastic vasculitis?

A
  • majority idiopathic (55-60%)
  • drugs (15%)
  • infection (15%)
  • inflammatory disease (10%)
  • malignant disease (<5%)
116
Q

what is the clinical presentation of leucocytoclastic vasculitis?

A 
- 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
Q

what is the treatment of leucocytoclastic vasculitis?

A
  • analgesia
  • support stockings
  • dapsone (antibiotic) or prednisolone
118
Q

what is the epidemiology of squamous cell carcinoma?

A

• 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
Q

what are risk factors for squamous cell carcinoma?

A
  • UV exposure

- chronic inflammation e.g. wound scars and immunosuppression

120
Q

what is the clinical presentation of squamous cell carcinoma?

A
  • 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
Q

what is the treatment of squamous cell carcinoma?

A
  • surgical excision with a minimal margin of 5mm

- radiotherapy is also used, especially if it is non-resectable

122
Q

what is the most common malignant skin cancer?

A

basal cell carcinoma

123
Q

what is the second most common malignant skin cancer?

A

squamous cell carcinoma

124
Q

what is the epidemiology and behaviour of basal cell carcinoma?

A
  • 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
Q

what are risk factors for basal cell carcinoma?

A
  • UV exposure
  • skin type 1: skin that burns and doesn’t tan
  • ageing
126
Q

what is the clinical presentation of basal cell carcinoma?

A
  • 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
127
Q

what is the treatment of basal cell carcinoma?

A
  • 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
128
Q

what is the most malignant form of skin cancer?

A

malignant melanoma

129
Q

what is a malignant melanoma?

A

malignant tumour of the melanocytes

130
Q

what is the epidemiology of malignant melanoma?

A
  • 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)
131
Q

what are risk factors for malignant melanoma?

A
  • 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
132
Q

what is the commonest site for malignant melanoma in men?

A

back/chest

133
Q

what is the commonest site for malignant melanoma in women?

A

lower legs

134
Q

what is the usual colour of malignant melanomas?

A

> 95% of melanomas show very dark colour, black or almost black in part of lesion

135
Q

what are the symptoms and criteria used for diagnosis of malignant melanoma?

A

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

136
Q

what are major signs of malignant melanoma?

A

change in size, shape or colour (usually darkening)

137
Q

what are minor signs of malignant melanoma?

A
  • inflammation, crusting or bleeding
  • sensory change
  • itching
138
Q

what are types of melanoma?

A
  • superficial spreading (SSMM)
  • nodular - most aggressive type!
  • lentigo maligna - usually on the face
  • acral - restricted to palms/soles
139
Q

what are differential diagnoses of malignant melanoma?

A
  • benign pigmented naevus
  • seborrhoeic wart (most common pigmented lesion in elderly)
  • pyogenic granuloma
140
Q

what are features of a pyogenic granuloma?

A
  • 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
141
Q

what is treatment of malignant melanoma? what is done for metastatic disease?

A
  • 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
142
Q

what are the commonest metastases of malignant melanoma?

A

distant metastases is commonest to lung, liver, CNS - but any tissue/organ can be affected

143
Q

what is the prognosis of malignant melanoma?

A
  • 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
144
Q

what is cellulitis?

A
  • bacterial infection involving the inner layers of the skin

- specifically affects the dermis and subcutaneous fat

145
Q

what is the epidemiology of cellulitis?

A

usually involves lower extremities

146
Q

what is the aetiology of cellulitis?

A
  • Group A Beta-haemolytic streptococcus e.g. streptococcus pyogenes - most common!
  • Staphylococcus aureus
  • sometimes MRSA
147
Q

what are risk factors for cellulitis?

A
  • lymphoedema
  • leg ulcer
  • immunosuppression
  • traumatic wounds - normally an obvious port of entry of pathogen
  • athletes
  • leg oedema
  • obesity
148
Q

what is the pathophysiology of cellulitis?

A
  • 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
149
Q

what is the clinical presentation of cellulitis?

A
  • 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
150
Q

how is cellulitis diagnosed?

A
  • clinical
  • skin swabs are usually negative unless taken from broken skin
  • serological testing to confirm a streptococcal infection e.g. antistreptolysin O titre (ASOT)
151
Q

what is the treatment of cellulitis?

A
  • 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
152
Q

what antibiotics are given in cellulitis?

A

oral phenoxymethylpenicillin or oral flucloxacillin

• oral erythromycin if penicillin allergic

153
Q

what is necrotising fasciitis?

A

• 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

154
Q

what is type 1 necrotising fasciitis?

A

caused by a mixture of aerobic and anaerobic bacteria following abdominal surgery or in diabetics

155
Q

what is type 2 necrotising fasciitis?

A

caused by group A beta-haemolytic streptococci e.g. S. pyogenes; most common cause, arises in previously healthy patients

156
Q

what are risk factors for necrotising fasciitis?

A
  • abdominal surgery

- immunosuppression

157
Q

what is the clinical presentation of necrotising fasciitis?

A
  • 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
158
Q

how is necrotising fasciitis?

A
  • 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
159
Q

what is the treatment of necrotising fasciitis?

A
  • 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
Q

what are examples of topical corticosteroids?

A

hydrocortisone, betamethasone

161
Q

what are indications for topical corticosteroids?

A

used in inflammatory skin conditions such as eczema to treat disease flares or to control chronic disease where emollients alone are ineffective

162
Q

what are mechanisms of action of topical corticosteroids?

A
  • 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
163
Q

what are adverse effects/contraindications of topical corticosteroids?

A
  • 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
164
Q

what are examples of emollients?

A

aqueous cream, liquid paraffin, E45

165
Q

what are indications for emollients?

A
  • 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
166
Q

what are mechanisms of action of emollients?

A
  • 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
167
Q

what are adverse effects/contraindications of emollients?

A

main tolerability issue is that they cause greasiness of the skin and can exacerbate acne on the face

168
Q

what are examples of keratolytics?

A

Salicylic acid, Lactic acid, Allantoin

169
Q

what are indications for keratolytics?

A
  • removal of warts and other lesions of excess skin growth
  • treatment of dry skin
  • treatment of acne
170
Q

what are mechanisms of action of keratolytics?

A
  • 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
Q

what are adverse effects/contraindications of keratolytics?

A
  • 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
172
Q

what are examples of retinoids?

A

acitretin, tazarotene

173
Q

what are indications for retinoids?

A
  • 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
Q

what are the mechanisms of action of retinoids?

A
  • 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
Q

what are adverse effects/contraindications of retinoids?

A
  • 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

Phase 2A (28 decks)

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