derm Flashcards

1
Q

how to describe a skin lesion

A

SCAM
size (widest diameter) and shape
colour
associated secondary change
morphology and margin (border)

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2
Q

what is the ABCDE relating to pigmented skin lesions

A

increases likelihood of melanoma if any of these features are present
asymmetry
irrecular border
two or more colours within the lesion
diameter over 6mm
evolution (hx change in size, shape or colour)

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3
Q

what is a comedone

A

a plug in a sebaceous follicle containing altered sebum, bacteria and cellular debris, can present as either open (blackheads) or closed (whiteheads)

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4
Q

what is koebner phenomenon

A

a linear eruption arising at site of trauma

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5
Q

what is purpura

A

red or purple colour (due to bleeding into the skin or mucous membrane) which does not blach on pressure
petechiae (small pinpoint macules) and ecchymoses (larger bruise like patches)

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6
Q

what is a macule

A

a flat area of altered colour

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7
Q

what is a papule

A

solid raised lesion <0.5cm in diameter

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8
Q

what is a nodule

A

solid raised lesion >0.5cm in diameter with a deeper component

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9
Q

what is a plaque

A

palpable scaling raised lesion >0.5cm in diameter

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10
Q

what is a vesicle

A

raised, clear fluid-filled lesion <0.5cm in diameter

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11
Q

what is a bulla

A

large blister
raised, clear fluid filled lesion >0.5cm in diameter

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12
Q

what is a pustule

A

pus containing lesion <0.5cm in diameter

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13
Q

what is an abscess

A

localised accumulation of pus in the dermis or subcut tissue

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14
Q

what is a wheal?

A

transient raised lesion due to dermal oedema
e.g. urticaria

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15
Q

what is a boil/furuncle

A

staph infection around or within a heair follicle

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16
Q

what is a carbuncle

A

staph infection of adjacent hair follicles (multiple boils/furuncles)

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17
Q

what does excoriation mean

A

loss of epidermis following trauma

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18
Q

what is lichenification

A

well defined roughening of skin with accentuation of skin markings

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19
Q

what is hirsutism

A

androgen dependent hair growth in a femalw

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20
Q

what is hypertrichosis

A

non androgen dependent pattern of excessive hair growth

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21
Q

what is clubbing

A

loss of angle between the posterior nail fold and nail plate
suppurative lung disease, cyanotic heart disease, IBD

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22
Q

what is koilonychia

A

spoon shaped depression of nail plate
iron deficiency anaemia, congenital

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23
Q

what is oncholysis

A

separation of the distal end of the nail plate from the nail bed
trauma, psoriasis, fungal nail infection and hyperthyroidism

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24
Q

what is pitting of the nail

A

punctate depressions of the nail plate
psoriasis, eczema, alopecia areata

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25
functions of normal skin
proteacitve barrier against environmental insults temp regulation sensation vit D synthesis immunosurveillance appearance/cosmesis
26
what are the skin appendages
structures formed by skin derived cells hair, nails, sebaceous glands, sweat glands
27
cell types in the epidermis
keratinocytes langergans cells melanocytes merkel cells
28
function of keratinocytes
produce keratin as a protective barrier
29
functions of langerhans ells
present antigens and activate T-lymphocytes for immune protection
30
functions melanocytes
produce melanin, which gives pigment to skin and protects the cell nuclei from UV radiation induced DNA damage
31
function merkel cells
contain specialised nerve endings for sensation
32
layers of the epidermis
stratum basale: basal cell layer - cells actively dividing, deepest layer stratum spinosum: prickle cell layer - differentiating cells stratum granulosum: granular cell layer - cells lose nuclei and contain granules of keratohyaline, secrete lipid into the intercellular spaces stratum corneum: horny layer - layer of keratin, mose superficial in thick skin e.g. sole also the stratum lucidum (palyer compact keratin) beneath stratum corneum
33
what makes up the dermis
mainly collagen also elastin, glycosaminoglycans also immune cells, nerves, skin appendages and lymphatic and blood vessels
34
types of hair
lanugo: fine long hair in fetus vellus: fine short hair on all body surfaces terminal hair: coarse long hair on scalp, eyebrows, eyelashes and pubic areas
35
structure of hair
each hair consists of modified keratin and is divided into the hair shaft (keratinised tube) and hair bulb (actively dividing cells and melanocytes)
36
growth cycle of hair follicle
anagen: long growing phase catagen: short regressing phase telogen: resring/shedding phase
37
structure of nails
nail plate (hard keratin) which arises from the nail matrix at the posterior nail fold and rests on the nail bed nail bed contains blood capillaries - give pink colour
38
function of sebaceous glands
produce sebum via hair follicles (pilosebaceous unit). secrete sebum onto skin surface which lubricates and waterproofs stimulated by the conversion of androgens to dihydrotestosterone therefore activated in piberty
39
types of sweat glands
eccrine: universally distributed in skin apocrine: in axillae, areolae, genitalia and anus. only function from puberty and produce odour
40
phases of wound healing
haemostasis inflammation proliferation remodelling
41
what happens in haemostasis
vasoconstriction and platelet aggregation clot formation
42
what happens in inflammation stage healing
vasodilation migration of neutrophuls and macrophages phagocytosis of cellular debris and invading bacteria
43
what happens in proliferation stage of healing
granulation tissue formation (fibroblasts) and angiogenesis re-epithelialisation (epidermal cell proliferation and migration)
44
what happens in the remodelling stage of healing
collagen fibre re-organsiation scar maturation
45
what are the emergency presenations in derm
anaphylaxis and angiodema toxic epidermal necrolysis stevens-johnson syndrome acute meningococcaemia erythroderma eczema herpeticum necrotising fasciitis
46
common causes urticaria, angiodema, anaphylaxis
Idiopathic, food (e.g. nuts, sesame seeds, shellfish, dairy products), drugs (e.g. penicillin, contrast media, non-steroidal antiinflammatory drugs (NSAIDs), morphine, angiotensin-converting enzyme inhibitors (ACE-i)), insect bites, contact (e.g. latex), viral or parasitic infections, autoimmune, and hereditary (in some cases of angioedema)
47
features urticaria
Urticaria is due to a local increase in permeability of capillaries and small venules. A large number of inflammatory mediators (including prostaglandins, leukotrienes, and chemotactic factors) play a role but histamine derived from skin mast cells appears to be the major mediator. Local mediator release from mast cells can be induced by immunological or non-immunological mechanisms
48
presentation urticaria
(swelling involving the superficial dermis, raising the epidermis): itchy wheals
49
presentation angioedema
(deeper swelling involving the dermis
50
presentation anaphylaxis
bronchospasm, facial and laryngeal oedema, hypotension; can present initially with urticaria and angioedema
51
mx urticaria/angiodema/anaphylaxis
Corticosteroids for severe acute urticaria and angioedema Adrenaline, corticosteroids and antihistamines for anaphylaxis
52
what is erythema nodosum
A hypersensitivity response to a variety of stimuli
53
what causes erythema nodosum
Group A beta-haemolytic streptococcus, primary tuberculosis, pregnancy, malignancy, sarcoidosis, inflammatory bowel disease (IBD), chlamydia and leprosy
54
presentation erythema nodosum
Discrete tender nodules which may become confluent ● Lesions continue to appear for 1-2 weeks and leave bruise-like discolouration as they resolve ● Lesions do not ulcerate and resolve without atrophy or scarring ● The shins are the most common site
55
what is erythema multiforme
often of unknown cause, is an acute self- limiting inflammatory condition with herpes simplex virus being the main precipitating factor. Other infections and drugs are also causes. Mucosal involvement is absent or limited to only one mucosal surface.
56
what is stevens-johnson syndrome
characterised by mucocutaneous necrosis with at least two mucosal sites involved. Skin involvement may be limited or extensive. Drugs or combinations of infections or drugs are the main associations. Epithelial necrosis with few inflammatory cells is seen on histopathology. The extensive necrosis distinguishes Stevens- Johnson syndrome from erythema multiforme. Stevens-Johnson syndrome may have features overlapping with toxic epidermal necrolysis including a prodromal illness
57
what is toxic epidermal necrosis
usually drug-induced, is an acute severe similar disease characterised by extensive skin and mucosal necrosis accompanied by systemic toxicity. On histopathology there is full thickness epidermal necrosis with subepidermal detachment
58
mx Erythema multiforme, Stevens-Johnson syndrome and Toxic epidermal necrolysis
Early recognition and call for help ● Full supportive care to maintain haemodynamic equilibrium
59
what is acute meningococcaemia
A serious communicable infection transmitted via respiratory secretions; bacteria get into the circulating blood
60
cause accute meningococcameia
Gram negative diplococcus Neisseria meningitides
61
presentation acute meningococcaemia
Features of meningitis (e.g. headache, fever, neck stiffness), septicaemia (e.g. hypotension, fever, myalgia) and a typical rash ● Non-blanching purpuric rash on the trunk and extremities, which may be preceded by a blanching maculopapular rash, and can rapidly progress to ecchymoses, haemorrhagic bullae and tissue necrosis
62
mx acute meningococcaemia
Antibiotics (e.g. benzylpenicillin) ● Prophylactic antibiotics (e.g. rifampicin) for close contacts (ideally within 14 days of exposure)
63
what is erythroderma
Exfoliative dermatitis involving at least 90% of the skin surface
64
what causes erythroderma
Previous skin disease (e.g. eczema, psoriasis), lymphoma, drugs (e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol, captopril) and idiopathic
65
presentation erythroderma
● Skin appears inflamed, oedematous and scaly ● Systemically unwell with lymphadenopathy and malaise
66
mx erythroderma
● Treat the underlying cause, where known ● Emollients and wet-wraps to maintain skin moisture ● Topical steroids may help to relieve inflammation
67
what is kaposis varicelliform eruption
eczema herpticum
68
what is eczema herpeticum
Widespread eruption - serious complication of atopic eczema or less commonly other skin conditions
69
cause eczema herpticum
HSV
70
presentation eczema herpeticum
Extensive crusted papules, blisters and erosions ● Systemically unwell with fever and malaise
71
mx eczema herpeticum
Antivirals (e.g. aciclovir) ● Antibiotics for bacterial secondary infection
72
what is necrotising fascitis
● A rapidly spreading infection of the deep fascia with secondary tissue necrosis
73
causes necrotising fasciitis
Group A haemolytic streptococcus, or a mixture of anaerobic and aerobic bacteria ● Risk factors include abdominal surgery and medical co-morbidities (e.g. diabetes, malignancy)
74
presentation necrotising fasciitis
● Severe pain ● Erythematous, blistering, and necrotic skin ● Systemically unwell with fever and tachycardia ● Presence of crepitus (subcutaneous emphysema) ● X-ray may show soft tissue gas (absence should not exclude the diagnosis)
75
mx necrotising fasciitis
● Urgent referral for extensive surgical debridement ● Intravenous antibiotics
76
what is cellulitis
● Spreading bacterial infection of the deep subcutaneous tissue
77
what is erysipelas
acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue
78
causes Erysipelas and Cellulitis
● Streptococcus pyogenes and Staphylococcus aureus ● Risk factors include immunosuppression, wounds, leg ulcers, toeweb intertrigo, and minor skin injury
79
presentation erysipelas and cellulitis
● Most common in the lower limbs ● Local signs of inflammation – swelling (tumor), erythema (rubor), warmth (calor), pain (dolor); may be associated with lymphangitis ● Systemically unwell with fever, malaise or rigors, particularly with erysipelas ● Erysipelas is distinguished from cellulitis by a well-defined, red raised border
80
mx erysipelas and cellulitis
● Antibiotics (e.g. flucloxacillin or benzylpenicillin) ● Supportive care including rest, leg elevation, sterile dressings and analgesia
81
what is the cause of staph scalded skin syndrome
● Production of a circulating epidermolytic toxin from phage group II, benzylpenicillin-resistant (coagulase positive) staphylococci
82
presentation staph scalded skin syndrome
● Develops within a few hours to a few days, and may be worse over the face, neck, axillae or groins ● A scald-like skin appearance is followed by large flaccid bulla ● Perioral crusting is typical ● There is intraepidermal blistering in this condition ● Lesions are very painful ● Sometimes the eruption is more localised ● Recovery is usually within 5-7 days
83
mx staph scalded skin syndrome
● Antibiotics (e.g. a systemic penicillinase-resistant penicillin, erythromycin or appropriate cephalosporin) ● Analgesia
84
3 main groups of superficial fungal infection
dermatophytes (tinea/ringworm), yeasts (e.g. candidiasis, malassezia), moulds (e.g. aspergillus)
85
presentation tinea corporis
(tinea infection of the trunk and limbs) - Itchy, circular or annular lesions with a clearly defined, raised and scaly edge is typical
86
presentation tinea cruris
s (tinea infection of the groin and natal cleft) – very itchy, similar to tinea corporis
87
presentation tinea pedis
s (athlete’s foot) – moist scaling and fissuring in toewebs, spreading to the sole and dorsal aspect of the foot
88
presentation tinea manuum
Tinea manuum (tinea infection of the hand) – scaling and dryness in the palmar creases
89
presentation tinea capitis
(scalp ringworm) – patches of broken hair, scaling and inflammation
90
presentation tinea unguium
(tinea infection of the nail) – yellow discolouration, thickened and crumbly nail
91
presentation tinea incognito
(inappropriate treatment of tinea infection with topical or systemic corticosteroids) – Ill-defined and less scaly lesions
92
presentation candidiasis
(candidal skin infection) – white plaques on mucosal areas, erythema with satellite lesions in flexures
93
presentation pityriasis
Tinea versicolor (infection with Malassezia furfur) – scaly pale brown patches on upper trunk that fail to tan on sun exposure, usually asymptomatic
94
mx superficial fungal infections
● Establish the correct diagnosis by skin scrapings, hair or nail clippings (for dermatophytes); skin swabs (for yeasts) ● General measures: treat known precipitating factors (e.g. underlying immunosuppressive condition, moist environment) ● Topical antifungal agents (e.g. terbinafine cream) ● Oral antifungal agents (e.g. itraconazole) for severe, widespread, or nail infections ● Avoid the use of topical steroids – can lead to tinea incognito ● Correct predisposing factors where possible (e.g. moist environment, underlying immunosuppression)
95
main divisions of skin cancer
non-melanoma (basal cell carcinoma and squamous cell carcinoma) and melanoma (malignant melanoma).
96
what is basal cell carcinoma
A slow-growing, locally invasive malignant tumour of the epidermal keratinocytes normally in older individuals, only rarely metastasises ● Most common malignant skin tumour
97
causes basal cell carcinoma
● Risk factors include UV exposure, history of frequent or severe sunburn in childhood, skin type I (always burns, never tans), increasing age, male sex, immunosuppression, previous history of skin cancer, and genetic predisposition
98
presentation basal cell carcinoma
● Various morphological types including 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 the head and neck
99
mx basal cell carcinoma
● Surgical excision - treatment of choice as it allows histological examination of the tumour and margins ● Mohs micrographic surgery (i.e. excision of the lesion and tissue borders are progressively excised until specimens are microscopically free of tumour) - for high risk, recurrent tumours ● Radiotherapy - when surgery is not appropriate ● Other e.g. cryotherapy, curettage and cautery, topical photodynamic therapy, and topical treatment (e.g. imiquimod cream) - for small and low-risk lesions
100
what is squamous cell carcinoma
● A locally invasive malignant tumour of the epidermal keratinocytes or its appendages, which has the potential to metastasise
101
what causes squamous cell carcinoma
● Risk factors include excessive UV exposure, pre-malignant skin conditions (e.g. actinic keratoses), chronic inflammation (e.g. leg ulcers, wound scars), immunosuppression and genetic predisposition
102
presentation squamous cell carcinoma
● Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate
103
mx squamous cell carcinoma
● Surgical excision - treatment of choice ● Mohs micrographic surgery – may be necessary for ill-defined, large, recurrent tumours ● Radiotherapy - for large, non-resectable tumours
104
what is malignancy melanoma
● An invasive malignant tumour of the epidermal melanocytes, which has the potential to metastasise
105
what causes malignant melanoma
● Risk factors include excessive UV exposure, skin type I (always burns, never tans), history of > 100 moles or atypical neavus syndrome moles, family history in first degree relative or previous history of melanoma
106
presentation malignant melanoma
● The ‘ABCDE Symptoms’ rule (*major suspicious features): Asymmetrical shape* Border irregularity Colour irregularity* Diameter > 6mm Evolution of lesion (e.g. change in size and/or shape)* Symptoms (e.g. bleeding, itching) ● More common on the legs in women and trunk in men
107
what is superficial spreading melanoma
common on the lower limbs, in young and middle-aged adults; related to intermittent high- intensity UV exposure; around 70% of all melanomas are superficial spreading melanomas
108
what is nodular melanoma
common on the trunk, in young and middle- aged adults; related to intermittent high-intensity UV exposure
109
what is lentigo maligna melanoma
common on the face, in elderly population; related to long-term cumulative UV exposure
110
what is acral lentiginous melanoma
common on the palms, soles and nail beds, in elderly population; no clear relation with UV exposure
111
mx malingnat melanoma
● In general, surgical excision is the definitive treatment (often a second surgery, wide local excision is needed after the initial excision biopsy). Radiotherapy may sometimes be useful. Chemotherapy is used for metastatic disease.
112
causes atopic eczema
● Not fully understood, but a positive family history of atopy (i.e. eczema, asthma, allergic rhinitis) is often present ● A primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin) appears to underlie atopic eczema ● Exacerbating factors such as infections, allergens (e.g. chemicals, food, dust, pet fur), sweating, heat, occupation and severe stress
113
presentation atopic eczema
● Acute presentation consists of itchy papules and vesicle often weepy (exudative) ● Chronic lesions : dry scaly itchy patches can be erythematous in paler skin or grey/ brown in richly pigmented skin ▪ More common on the face and extensor aspects of limbs in infants, and the flexor aspects in children and adults ● In richly pigmented skin eczema may present as brown, grey or purple bumps (papular eczema or follicular eczema) ● Chronic scratching/rubbing leads to lichenification ● Across of skin types eczema can lead to pigmentary changes such as hypopigmentation (reduced pigmentation) and hyperpigmentation (increased pigmentation) ● Nail may show pitting and ridging of the nails
114
mx atopic eczema
● General measures - avoid known exacerbating agents, frequent emollients +/- bandages and bath oil/soap substitute ● Topical therapies – topical steroids for active areas; topical immunomodulators (e.g. tacrolimus, pimecrolimus) for maintenance therapy as steroid-sparing agents ● Oral therapies - antihistamines for symptomatic relief, antibiotics (e.g. flucloxacillin) for secondary bacterial infections, and antivirals (e.g. aciclovir) for secondary herpes infection ● Phototherapy and immunosuppressants (e.g. azathioprine, ciclosporin, methotrexate) for severe non- responsive cases, biologic therapy
115
complications atopic eczema
● Secondary bacterial infection (crusted weepy lesions) ● Secondary viral infection - molluscum contagiosum (pearly papules with central umbilication), viral warts and eczema herpeticum
116
what is acne vulgaris
An inflammatory disease of the pilosebaceous follicle
117
causes acne vulgaris
● Hormonal (androgen) ● Contributing factors include increased sebum production, abnormal follicular keratinization, bacterial colonization (Propionibacterium acnes) and inflammation
118
presentation acne vulgaris
● Non-inflammatory lesions (mild acne) - open and closed comedones (blackheads and whiteheads) ● Inflammatory lesions (moderate and severe acne) - papules, pustules, nodules, and cysts ● In richly pigmented skin: 1. Inflammatory lesions’ may not be so apparent, instead hyperpigmented lesions (‘acne hyperpigmented macules’) are seen. Hyperpigmented lesions may also signify ongoing inflammation 2. Non erythematous nodules may be present and detected by palpation ● Commonly affects the face, chest and upper back
119
mx acne vulgaris
● General measures - no specific food has been identified to cause acne, treatment needs to be continued for at least 6 weeks to produce effect ● Topical therapies (for mild acne) - benzoyl peroxide and topical antibiotics (antimicrobial properties), and topical retinoids ● Oral therapies (for moderate to severe acne) - oral antibiotics, and anti-androgens (in females) ● Oral retinoids (for severe acne)
120
complications acne vulgaris
● Post-inflammatory hyperpigmentation, scarring, deformity, psychological and social effects
121
what is psoriasis
● A chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration
122
types of psoraisis
● 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 erythrodermic (total body redness)
123
causes psoriasis
● Complex interaction between genetic, immunological and environmental factors ● Precipitating factors include trauma (which may produce a Köebner phenomenon), infection (e.g. tonsillitis), drugs, stress, and alcohol
124
presentation psoraisis
● Well-demarcated erythematous scaly plaques ● in richly pigmented skin psoriasis can present as dark brown, grey or purple patches or plaques ● Lesions can sometimes be itchy, burning or painful ● Common on the extensor surfaces of the body and over scalp ● Auspitz sign (scratch and gentle removal of scales cause capillary bleeding) ● 50% have associated nail changes (e.g. pitting, onycholysis) ● 5-8% suffer from associated psoriatic arthropathy - symmetrical polyarthritis, asymmetrical oligomonoarthritis, lone distal interphalangeal disease, psoriatic spondylosis, and arthritis mutilans (flexion deformity of distal interphalangeal joints)
125
mx psoriasis
● General measures - avoid known precipitating factors, emollients to reduce scales ● Topical therapies (for localised and mild psoriasis) - vitamin D analogues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics and scalp preparations ● Phototherapy (for extensive disease) - phototherapy i.e. UVB and photochemotherapy i.e. psoralen+UVA ● Oral therapies (for extensive and severe psoriasis, or psoriasis with systemic involvement) - methotrexate, retinoids, ciclosporin, mycophenolate mofetil, fumaric acid esters, and biological agents (e.g. etanercept, adalimumab, ustekinumab)
126
complications psoriasis
● Erythroderma, psychological and social effects
127
common causes of blisters
impetigo , insect bites, herpes simplex infection, herpes zoster infection, acute contact dermatitis, pompholyx (vesicular eczema of the hands and feet, see below) and burns.
128
what is bullous pemphigoid
A blistering skin disorder which usually affects the elderly
129
causes bullous pemphigoid
● Autoantibodies against antigens between the epidermis and dermis causing a sub-epidermal split in the skin
130
presentation bullous pemphigoid
● Tense, fluid-filled blisters on an erythematous base ● Lesions are often itchy ● May be preceded by a non-specific itchy rash ● Usually affects the trunk and limbs (mucosal involvement less common)
131
mx bullous pemphigoid
● General measures – wound dressings where required, monitor for signs of infection ● Topical therapies for localised disease - topical steroids ● Oral therapies for widespread disease – oral steroids, combination of oral tetracycline and nicotinamide, immunosuppressive agents (e.g. azathioprine, mycophenolate mofetil, methotrexate, and other)
132
what is pemphigus vulgaris
● A blistering skin disorder which usually affects the middle-aged
133
cause pemphigus vulgaris
● Autoantibodies against antigens within the epidermis causing an intra-epidermal split in the skin
134
presentation pemphigus vulgaris
● Flaccid, easily ruptured blisters forming erosions and crusts ● Lesions are often painful ● Usually affects the mucosal areas (can precede skin involvement)
135
mx pemphigus vulgaris
● General measures – wound dressings where required, monitor for signs of infection, good oral care (if oral mucosa is involved) ● Oral therapies – high-dose oral steroids, immunosuppressive agents (e.g. methotrexate, azathioprine, cyclophosphamide, mycophenolate mofetil, and other)
136
what is vitiligo
● An acquired depigmenting disorder, where there is complete loss of pigment cells (melanocytes)
137
cause vitiligo
● Thought to be an autoimmune disorder, where the innate immune system causes destruction or loss of melanocytes, leading to loss of pigment formation in the skin
138
presentation vitiligo
● Presentation at any age * A single patch or multiple patches of depigmentation (complete loss of pigment), often symmetrical ● Common sites are exposed areas such as face, hands, feet, as well as body folds and genitalia ● Favours sites of injury and this phenomenon is called the Koebner phenomenon
139
mx vitiligo
● Minimise skin injury as a cut, graze, or sunburn can potentially trigger a new patch of vitiligo ● Topical treatments such as topical steroids and calcineurin inhibitors (such as topical tacrolimus and pimecrolimus) ● Phototherapy such as UVB therapy, excimer laser ● Oral immunosuppressants such as methotrexate, ciclosporin and mycophenolate mofetil
140
what is melasma
● An acquired chronic skin disorder, where there is increased pigmentation in the skin
141
cause of melasma
● Thought to be due to genetic predisposition, and triggered by factors such as sun exposure, hormonal changes such as pregnancy and contraceptive pills ● The pigmentation is caused by an overproduction of pigment (melanin) by pigment cells (melanocytes)
142
presentation melasma
● Brown macules (freckle-like spots) or larger patches with an irregular border ● Symmetrical distribution ● Common sites are forehead, cutaneous upper lips and cheeks, rarely can occur on neck, shoulders and upper arms
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mx melasma
● Lifelong sun protection ● Discontinuation of hormonal contraceptive pills ● Cosmetic camouflage ● Topical treatments that aim at inhibiting the formation of new melanin such as hydroquinone, azelaic acid, kojic acid (a chelating agent) and vitamin C ● Laser treatments need to be used with caution as the heat generated by lasers can potentially cause post-inflammatory hyperpigmentation.
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features venous ulcer
- Often painful, worse on standing - History of venous disease e.g. varicose veins, deep vein thrombosis - Malleolar area (more common over medial than lateral malleolus) - Large, shallow irregular ulcer - Exudative and granulating base - Warm skin - Normal peripheral pulses - Leg oedema, haemosiderin and melanin deposition (brown pigment), lipodermatosclerosis, and atrophie blanche (white e scarring with dilated capillaries) - Normal ankle/brachial pressure index
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mx venous ulcers
- Compression bandaging (after excluding arterial insufficiency)
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features arterial ulcers
- Painful especially at night, worse when legs are elevated - History of arterial disease e.g. atherosclerosis - Pressure and trauma sites e.g. pretibial, supramalleolar (usually lateral), and at distal points e.g. toes - Small, sharply defined deep ulcer - Necrotic base - Cold skin - Weak or absent peripheral pulses - Shiny pale skin - Loss of hair
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ix for arterial ulcers
- ABPI < 0.8 - presence of arterial insufficiency - Doppler studies and angiography
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mx arterial ulcer
- Vascular reconstruction - Compression bandaging is contraindicated
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features neuropathic ulcer
- Often painless - Abnormal sensation - History of diabetes or neurological disease - Pressure sites e.g. soles, heel, toes, metatarsal heads - Variable size and depth - Granulating base - May be surrounded by or underneath a hyperkeratotic lesion (e.g. callus) - Warm skin - Normal peripheral pulses* *cold, weak or absent pulses if it is a neuroischaemic ulcer - Peripheral neuropathy
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ix neuropathic ulcers
- ABPI < 0.8 implies a neuroischaemic ulcer - X-ray to exclude osteomyelitis
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mx neuropathic ulcer
- Wound debridement - Regular repositioning, appropriate footwear and good nutrition
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causes itchy eruption
inflammatory condition (e.g. eczema), infection (e.g. varicella), infestation (e.g. scabies), allergic reaction (e.g. some cases of urticaria) or an unknown cause, possibly autoimmune (e.g. lichen planus)
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features lichen planus
- Family history in 10% of cases - May be drug-induced - Forearms, wrists, and legs - Always examine the oral mucosa - Violaceous (lilac) flat-topped Papules or hyperpigmented papules (in darker skin) - Symmetrical distribution - Nail changes and hair loss - Lacy white streaks on the oral mucosa and skin lesions (Wickham’s striae)
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mx lichen planus
- Corticosteroids - Antihistamines
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features melanocytic naevi
- Not usually present at birth but develop during infancy, childhood or adolescence - Asymptomatic - Congenital naevi may be large, pigmented, protuberant and hairy - Junctional naevi are small, flat and dark - Intradermal naevi are usually dome-shape papules or nodules - Compound naevi are usually raised, warty, hyperkeratotic, and/or hairy
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mx melanocytic naevi
- Only if symptomatic Shave or complete excision
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features seborrhoeic wart
- Tend to arise in the middle-aged or elderly - Often multiple and asymptomatic - Face and trunk - Warty greasy papules or nodules - ‘Stuck on’ appearance, with well-defined edges
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mx seborrhoeic wart
- Only if symptomatic Curette and cautery Cryotherapy
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causes purpuric eruption
thrombocytopenic (e.g. meningococcal septicaemia, disseminated intravascular coagulation, idiopathic thrombocytopenic purpura) or non-thrombocytopenic e.g. trauma, drugs (e.g. steroids), aged skin, vasculitis (e.g. Henoch-Schönlein purpura).
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features DIC
- History of trauma, malignancy, sepsis, obstetric complications, transfusions, or liver failure - Spontaneous bleeding from ear, nose and throat, gastrointestinal tract, respiratory tract or wound site - Petechiae, ecchymoses, haemorragic bullae and/or tissue necrosis - Systemically unwell
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ix DIC
- Bloods (a clotting screen is important)
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mx DIC
- Treat the underlying cause - Transfuse for coagulation deficiencies - Anticoagulants for thrombosis
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features vasculitis
Painful lesions - Dependent areas (e.g. legs, buttocks, flanks) - Palpable purpura (often painful) - Systemically unwell
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ix vasculitis
- Bloods and urinalysis - Skin biopsy
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mx vasculitis
- Treat the underlying cause - Steroids and immunosuppressants if there is systemic involvement
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features actinic purpura
- Arise in the elderly population with sun-damaged skin - Extensor surfaces of hands and forearms - Such skin is easily traumatised - Non-palpable purpura - Surrounding skin is atrophic and thin - Systemically well
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mx actinic purpur
nonw needed
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differentials ofr a red swollen leg
cellulitis, venous thrombosis, chronic venous insufficiency
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skin changes inchronic venous insufficeincy
- Discoloured (blue-purple) - Oedema (improved in the morning) - Venous congestion and varicose veins - Lipodermatosclerosis (erythematous induration, creating ‘champagne bottle’ appearance) - Stasis dermatitis (eczema with inflammatory papules, scaly and crusted erosions) - Haemosiderin deposition - Venous ulcer
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what are keloid scars
An overgrowth of scar tissue, which tends to be larger than the original wound itself
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cause keloid scars
● Thought to be due to overproduction of collagen during wound healing after minor injuries, skin surgery, insect bites and acne spots in genetically predisposed individuals ● More commonly seen in darker skin types
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presentation keloid scars
● Firm, smooth, hard nodule which can be itchy or painful ● Common sites are chest and shoulders
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mx keloid scars
● Avoidance of further trauma to the skin such as scratching ● Topical treatments such as topical steroids and silicone gel can potentially flatten the scar, and improve the symptoms ● Intralesional steroid injection if topical treatments are not effective ● Surgery such as excision needs to be carried out only as the last resort and with caution as the new wound may cause a larger keloid scar
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what is an emollient
● Aqueous cream, emulsifying ointment, liquid paraffin and white soft paraffin in equal parts (50:50)
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indications for emollients
● To rehydrate skin and re-establish the surface lipid layer ● Useful for dry, scaling conditions and as soap substitutes
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e.g. topical steroids in derm
classified as mildly potent (e.g, hydrocortisone), moderately potent (e.g. clobetasone butyrate (Eumovate)), potent (e.g.betamethasone valerate (Betnovate)), and very potent (e.g. clobetasol propionate (Dermovate))
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e.g. oral steroids derm
● Oral steroids: prednisolone
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indications steroids in derm
● Anti-inflammatory and anti-proliferative effects ● Useful for allergic and immune reactions, inflammatory skin conditions, blistering disorders, connective tissue diseases, and vasculitis
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SE steroids
● Local side effects (from topical corticosteroids): skin atrophy (thinning), telangiectasia, striae, may mask, cause or exacerbate skin infections, acne, or perioral dermatitis, and allergic contact dermatitis. ● Systemic side effects (from oral corticosteroids): Cushing’s syndrome, immunosuppression, hypertension, diabetes, osteoporosis, cataract, and steroid-induced psychosis
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indications oral aciclovir in derm
● Viral infections due to herpes simplex and herpes zoster virus
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SE aciclovir
● Gastrointestinal upsets, raised liver enzymes, reversible neurological reactions, and haematological disorders
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classes of oral antihistamines
● Classified into nonsedative (e.g. cetirizine, loratadine) and sedative antihistamines (e.g. chlorpheniramine, hydroxyzine)
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inidcations oral antihistamines derm
● Block histamine receptors producing an anti-pruritic effect ● Useful for type-1 hypersensitivity reactions and eczema (especially sedative antihistamines for children)
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SE oral antihistamines
● Sedative antihistamines can cause sedation and anticholinergic effects (e.g. dry mouth, blurred vision, urinary retention, and constipation)
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topical abx derm
fusidic acid, mupirocin (Bactroban), neomycin
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oral abx derm
penicillins, cephalosporins, gentamicin, macrolides, nitrofurantoin, quinolones, tetracyclines, vancomycin, metronidazole, trimethoprim
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indications abx derm
● Useful for bacterial skin infections, and some are used for acne
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topical antiseptics derm
Chlorhexidine, cetrimide, povidone-iodine
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indications topical antiseptics derm
● Treatment and prevention of skin infection
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oral retinoids derm
Isotretinoin, Acitretin
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indications oral retinoids derm
● Acne, psoriasis, and disorders of keratinisation
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SE oral retinoids
● Mucocutaneous reactions such as dry skin, dry lips and dry eyes, disordered liver function, hypercholesterolaemia, hypertriglyceridaemia, myalgia, arthralgia and depression ● Teratogenicity: effective contraception must be practised one month before, during and at least one month after isotretinoin, but for two years after Acitretin (
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biological therapy derm
Monoclonal antibodies (eg. Infliximab, Adalimumab, Ustekinumab, Certolizumab, Gorlilumab), Fusion antibody proteins (eg. Etanercept), Recombinant human cytokines and growth factors (eg. Interleukins)
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ndications biological therapy derm
psoriasis, atopic dermatitis and hidradenitis suppurativa
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SE biological therapy
● Local side effects: redness, swelling, bruising at the site of injection ● Systemic side effects: allergic reactions, antibody formation, flu-like symptoms, infections, hepatitis, demyelinating disease, heart failure, blood problems, rare reports of cancers (eg. non-melanoma skin cancers, lymphoma)
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how to use emollients
● Apply liberally and regularly
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how to use corticosteroids
● Apply thinly and only for short-term use (often 1 or 2 weeks only) ● In general, use 1% hydrocortisone or mild-moderate potent topical steroids on the face and thin skin areas eg. neck and flexures. ● Fingertip unit (advised on packaging) – strip of cream the length of a fingertip
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preventing pressure sores
● Pressure sores are due to ischaemia resulting from localised damage to the skin caused by sustained pressure, friction and moisture, particularly over bony prominences. ● Preventative measures involve frequent repositioning, nutritional support, and use of pressure relieving devices e.g. special beds
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how to prevent sun exposure
Spend time in the shade between 11am-3pm Make sure you never burn Aim to cover up with a t-shirt, wide-brimmed hat and sunglasses Remember to take extra care with children Then use Sun Protection Factor (SPF) 30+ sunscreen
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fitzpatrick skin phototype
I Always burns, never tans II Always burns, sometimes tans III Sometimes burns, always tans IV Never burns, always tans V Tans very easily, very rarely burns VI tans very easily, never burns
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bowens disease
=in situ SCC full thickness dysplasia epidermal keratinocytes
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acitinic keratoses
partial thickness dysplasia epidermal keratinocytes sun exposed sites=scaly erythema
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Derm red flags
Need urgent referral Blistering/skin peeling Pain Lymphadenopathy Mucosal involvement Systemic upset: fever, abnormal LFTs/U&E
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Mx mild drug rxn
Stop drug Emollients Topical corticosteroids Antihistamines if urticarial
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SJS and TEN
Steven Johnson syndrome and toxic epidermal necrolysis are on a scale SJS less severe, TEN more
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Cause SJS AND TEN
DRUGS
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Sx SJS and TEN
sx 7-21d after med given Prodrome=resp infection, fever, pain Dusky red lesions, atypical targets, erythematous plaques, mucosal involvement, systemic symptoms, detachment epidermis
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Mx SJS and TEN
stop med Dressings and emollient/paraffin ICU/burns unit Fluid and electrolytes Supportive: eyes, mouth, swabs for infection, physio
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DRESS
Drug rxn with eosinophilia and systemic sx
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Sx DRESS
15-40D after drug exposure- anticonvulsant and sulfonamodes Fever, oedema Rash=morbilloform, purpura, scaling Lymphadenopathy Eosinophilia Effects organs-LFTs
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Mx DRESS
Stop drug cause Systemic steroids if severe Supportive: dressings, topic steroids, emollients, oral antihistamines, fluids, tx secondary infection
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AGEP
Acute generalised exanthematous pustulosis
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Sx AGEP
Less than 4d after drug exposure - beta lactam abx Fever Small sterile pustules and oedematous erythema Increased WCC purpura Vesicles Target lesions Mucosal involvement
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Mx AGEP
Stop drug cause Topical corticosteroids, emollients, antihistamines
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What is erythroderma
Erythema over 90% skin surface
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Causes erythroderma
Dermatitis Psoriasis Drug eruption Cutaneous t cell lymphoma
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Features erythroderma
Hx: atopy, steroid withdrawal Clues underlying diagnosis=psoriasis, eczema
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Ix erythroderma
FBC U&E LFT CRP total IgE Blood film +/- skin biopsy, lymph node ix
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Mx erythroderma
Stop causative drugs Monitor vitals and fluid Dressings and emollients Tx cause Topical corticosteroids
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Symptoms bullous pemphigoid
Sub dermal blistering Usually elderly Tense intact blisters
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Bullous pemphigoid cause
AI drug eruption Attack on BM by IgE
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Diagnosis bullous pemphigoid
Skin biopsy and direct immunofluroescence
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Mx bullous pemphigoid
Specialist! Systemic and topical steroids
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Features staph scalded skin syndrome
Usually children Superficial skin blistering and crusting, often flexural No mucosal involvement
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Mx staph scalded skin
Tx infection Supportive- fluid, skin care
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Cause staph scalded skin
Staph aureus exotoxins
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Cause pemphigous vulgaris
AI IgG auto Ab
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Sx pemphigous vulgaris
Intra epidermal blisters=non tense, erosion Painful blisters skin and mucous membranes 30-60y, Jews, indians
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Mx pemphigous vulgaris
Specialist Topical and systemic steroids
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what is an acral distribution
distal areas- hands and feet
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cause dermatitis herpetiformis
coeliac and IgA defieincy
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biologic used in eczema
tacrolimus
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associations psoriasis
arthritis IBD uveitis coeliac T2DM gout
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prognosis melanoma
breslow depth >3mm = poor prognosis
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pathology psoriasis
autoimmune: T cell mediated keratinocyte proliferation