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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
Q

functions of normal skin

A

proteacitve barrier against environmental insults
temp regulation
sensation
vit D synthesis
immunosurveillance
appearance/cosmesis

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26
Q

what are the skin appendages

A

structures formed by skin derived cells
hair, nails, sebaceous glands, sweat glands

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27
Q

cell types in the epidermis

A

keratinocytes
langergans cells
melanocytes
merkel cells

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28
Q

function of keratinocytes

A

produce keratin as a protective barrier

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29
Q

functions of langerhans ells

A

present antigens and activate T-lymphocytes for immune protection

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30
Q

functions melanocytes

A

produce melanin, which gives pigment to skin and protects the cell nuclei from UV radiation induced DNA damage

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31
Q

function merkel cells

A

contain specialised nerve endings for sensation

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32
Q

layers of the epidermis

A

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

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33
Q

what makes up the dermis

A

mainly collagen
also elastin, glycosaminoglycans
also immune cells, nerves, skin appendages and lymphatic and blood vessels

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34
Q

types of hair

A

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

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35
Q

structure of hair

A

each hair consists of modified keratin and is divided into the hair shaft (keratinised tube) and hair bulb (actively dividing cells and melanocytes)

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36
Q

growth cycle of hair follicle

A

anagen: long growing phase
catagen: short regressing phase
telogen: resring/shedding phase

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37
Q

structure of nails

A

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

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38
Q

function of sebaceous glands

A

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

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39
Q

types of sweat glands

A

eccrine: universally distributed in skin
apocrine: in axillae, areolae, genitalia and anus. only function from puberty and produce odour

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40
Q

phases of wound healing

A

haemostasis
inflammation
proliferation
remodelling

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41
Q

what happens in haemostasis

A

vasoconstriction and platelet aggregation
clot formation

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42
Q

what happens in inflammation stage healing

A

vasodilation
migration of neutrophuls and macrophages
phagocytosis of cellular debris and invading bacteria

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43
Q

what happens in proliferation stage of healing

A

granulation tissue formation (fibroblasts) and angiogenesis
re-epithelialisation (epidermal cell proliferation and migration)

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44
Q

what happens in the remodelling stage of healing

A

collagen fibre re-organsiation
scar maturation

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45
Q

what are the emergency presenations in derm

A

anaphylaxis and angiodema
toxic epidermal necrolysis
stevens-johnson syndrome
acute meningococcaemia
erythroderma
eczema herpeticum
necrotising fasciitis

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46
Q

common causes urticaria, angiodema, anaphylaxis

A

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)

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47
Q

features urticaria

A

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

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48
Q

presentation urticaria

A

(swelling involving the superficial dermis, raising the
epidermis): itchy wheals

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49
Q

presentation angioedema

A

(deeper swelling involving the dermis

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50
Q

presentation anaphylaxis

A

bronchospasm,
facial and laryngeal oedema, hypotension; can present initially
with urticaria and angioedema

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51
Q

mx urticaria/angiodema/anaphylaxis

A

Corticosteroids for severe acute urticaria and angioedema
Adrenaline, corticosteroids and antihistamines for anaphylaxis

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52
Q

what is erythema nodosum

A

A hypersensitivity response to a variety of stimuli

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53
Q

what causes erythema nodosum

A

Group A beta-haemolytic streptococcus, primary tuberculosis,
pregnancy, malignancy, sarcoidosis, inflammatory bowel disease
(IBD), chlamydia and leprosy

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54
Q

presentation erythema nodosum

A

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

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55
Q

what is erythema multiforme

A

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.

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56
Q

what is stevens-johnson syndrome

A

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

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57
Q

what is toxic epidermal necrosis

A

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

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58
Q

mx Erythema multiforme, Stevens-Johnson syndrome and Toxic epidermal necrolysis

A

Early recognition and call for help
● Full supportive care to maintain haemodynamic equilibrium

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59
Q

what is acute meningococcaemia

A

A serious communicable infection transmitted via respiratory
secretions; bacteria get into the circulating blood

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60
Q

cause accute meningococcameia

A

Gram negative diplococcus Neisseria meningitides

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61
Q

presentation acute meningococcaemia

A

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

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62
Q

mx acute meningococcaemia

A

Antibiotics (e.g. benzylpenicillin)
● Prophylactic antibiotics (e.g. rifampicin) for close contacts (ideally
within 14 days of exposure)

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63
Q

what is erythroderma

A

Exfoliative dermatitis involving at least 90% of the skin surface

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64
Q

what causes erythroderma

A

Previous skin disease (e.g. eczema, psoriasis), lymphoma, drugs
(e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol,
captopril) and idiopathic

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65
Q

presentation erythroderma

A

● Skin appears inflamed, oedematous and scaly
● Systemically unwell with lymphadenopathy and malaise

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66
Q

mx erythroderma

A

● Treat the underlying cause, where known
● Emollients and wet-wraps to maintain skin moisture
● Topical steroids may help to relieve inflammation

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67
Q

what is kaposis varicelliform eruption

A

eczema herpticum

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68
Q

what is eczema herpeticum

A

Widespread eruption - serious complication of atopic eczema or
less commonly other skin conditions

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69
Q

cause eczema herpticum

A

HSV

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70
Q

presentation eczema herpeticum

A

Extensive crusted papules, blisters and erosions
● Systemically unwell with fever and malaise

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71
Q

mx eczema herpeticum

A

Antivirals (e.g. aciclovir)
● Antibiotics for bacterial secondary infection

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72
Q

what is necrotising fascitis

A

● A rapidly spreading infection of the deep fascia with secondary
tissue necrosis

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73
Q

causes necrotising fasciitis

A

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)

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74
Q

presentation necrotising fasciitis

A

● 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)

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75
Q

mx necrotising fasciitis

A

● Urgent referral for extensive surgical debridement
● Intravenous antibiotics

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76
Q

what is cellulitis

A

● Spreading bacterial infection of the deep subcutaneous tissue

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77
Q

what is erysipelas

A

acute superficial form of cellulitis and involves
the dermis and upper subcutaneous tissue

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78
Q

causes Erysipelas and Cellulitis

A

● Streptococcus pyogenes and Staphylococcus aureus
● Risk factors include immunosuppression, wounds, leg ulcers,
toeweb intertrigo, and minor skin injury

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79
Q

presentation erysipelas and cellulitis

A

● 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

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80
Q

mx erysipelas and cellulitis

A

● Antibiotics (e.g. flucloxacillin or benzylpenicillin)
● Supportive care including rest, leg elevation, sterile dressings and
analgesia

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81
Q

what is the cause of staph scalded skin syndrome

A

● Production of a circulating epidermolytic toxin from phage group
II, benzylpenicillin-resistant (coagulase positive) staphylococci

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82
Q

presentation staph scalded skin syndrome

A

● 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

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83
Q

mx staph scalded skin syndrome

A

● Antibiotics (e.g. a systemic penicillinase-resistant penicillin,
erythromycin or appropriate cephalosporin)
● Analgesia

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84
Q

3 main groups of superficial fungal infection

A

dermatophytes (tinea/ringworm), yeasts (e.g.
candidiasis, malassezia), moulds (e.g. aspergillus)

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85
Q

presentation tinea corporis

A

(tinea infection of the trunk and limbs) - Itchy,
circular or annular lesions with a clearly defined, raised and scaly
edge is typical

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86
Q

presentation tinea cruris

A

s (tinea infection of the groin and natal cleft) – very
itchy, similar to tinea corporis

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87
Q

presentation tinea pedis

A

s (athlete’s foot) – moist scaling and fissuring in
toewebs, spreading to the sole and dorsal aspect of the foot

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88
Q

presentation tinea manuum

A

Tinea manuum (tinea infection of the hand) – scaling and dryness
in the palmar creases

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89
Q

presentation tinea capitis

A

(scalp ringworm) – patches of broken hair, scaling
and inflammation

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90
Q

presentation tinea unguium

A

(tinea infection of the nail) – yellow discolouration,
thickened and crumbly nail

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91
Q

presentation tinea incognito

A

(inappropriate treatment of tinea infection with
topical or systemic corticosteroids) – Ill-defined and less scaly
lesions

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92
Q

presentation candidiasis

A

(candidal skin infection) – white plaques on mucosal
areas, erythema with satellite lesions in flexures

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93
Q

presentation pityriasis

A

Tinea versicolor (infection with Malassezia furfur) – scaly
pale brown patches on upper trunk that fail to tan on sun
exposure, usually asymptomatic

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94
Q

mx superficial fungal infections

A

● 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)

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95
Q

main divisions of skin cancer

A

non-melanoma (basal cell carcinoma and
squamous cell carcinoma) and melanoma (malignant melanoma).

96
Q

what is basal cell carcinoma

A

A slow-growing, locally invasive malignant tumour of the
epidermal keratinocytes normally in older individuals, only rarely
metastasises
● Most common malignant skin tumour

97
Q

causes basal cell carcinoma

A

● 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
Q

presentation basal cell carcinoma

A

● 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
Q

mx basal cell carcinoma

A

● 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
Q

what is squamous cell carcinoma

A

● A locally invasive malignant tumour of the epidermal
keratinocytes or its appendages, which has the potential to
metastasise

101
Q

what causes squamous cell carcinoma

A

● 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
Q

presentation squamous cell carcinoma

A

● Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate

103
Q

mx squamous cell carcinoma

A

● Surgical excision - treatment of choice
● Mohs micrographic surgery – may be necessary for ill-defined,
large, recurrent tumours
● Radiotherapy - for large, non-resectable tumours

104
Q

what is malignancy melanoma

A

● An invasive malignant tumour of the epidermal melanocytes,
which has the potential to metastasise

105
Q

what causes malignant melanoma

A

● 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
Q

presentation malignant melanoma

A

● 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
Q

what is superficial spreading melanoma

A

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
Q

what is nodular melanoma

A

common on the trunk, in young and middle-
aged adults; related to intermittent high-intensity UV exposure

109
Q

what is lentigo maligna melanoma

A

common on the face, in elderly
population; related to long-term cumulative UV exposure

110
Q

what is acral lentiginous melanoma

A

common on the palms, soles and nail
beds, in elderly population; no clear relation with UV exposure

111
Q

mx malingnat melanoma

A

● 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
Q

causes atopic eczema

A

● 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
Q

presentation atopic eczema

A

● 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
Q

mx atopic eczema

A

● 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
Q

complications atopic eczema

A

● Secondary bacterial infection (crusted weepy lesions)
● Secondary viral infection - molluscum contagiosum (pearly
papules with central umbilication), viral warts and eczema
herpeticum

116
Q

what is acne vulgaris

A

An inflammatory disease of the pilosebaceous follicle

117
Q

causes acne vulgaris

A

● Hormonal (androgen)
● Contributing factors include increased sebum production,
abnormal follicular keratinization, bacterial colonization
(Propionibacterium acnes) and inflammation

118
Q

presentation acne vulgaris

A

● 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
Q

mx acne vulgaris

A

● 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
Q

complications acne vulgaris

A

● Post-inflammatory hyperpigmentation, scarring, deformity,
psychological and social effects

121
Q

what is psoriasis

A

● A chronic inflammatory skin disease due to hyperproliferation of
keratinocytes and inflammatory cell infiltration

122
Q

types of psoraisis

A

● 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
Q

causes psoriasis

A

● 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
Q

presentation psoraisis

A

● 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
Q

mx psoriasis

A

● 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
Q

complications psoriasis

A

● Erythroderma, psychological and social effects

127
Q

common causes of blisters

A

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
Q

what is bullous pemphigoid

A

A blistering skin disorder which usually affects the elderly

129
Q

causes bullous pemphigoid

A

● Autoantibodies against antigens between the epidermis and
dermis causing a sub-epidermal split in the skin

130
Q

presentation bullous pemphigoid

A

● 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
Q

mx bullous pemphigoid

A

● 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
Q

what is pemphigus vulgaris

A

● A blistering skin disorder which usually affects the middle-aged

133
Q

cause pemphigus vulgaris

A

● Autoantibodies against antigens within the epidermis causing an
intra-epidermal split in the skin

134
Q

presentation pemphigus vulgaris

A

● Flaccid, easily ruptured blisters forming erosions and crusts
● Lesions are often painful
● Usually affects the mucosal areas (can precede skin involvement)

135
Q

mx pemphigus vulgaris

A

● 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
Q

what is vitiligo

A

● An acquired depigmenting disorder, where there is complete loss
of pigment cells (melanocytes)

137
Q

cause vitiligo

A

● 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
Q

presentation vitiligo

A

● 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
Q

mx vitiligo

A

● 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
Q

what is melasma

A

● An acquired chronic skin disorder, where there is increased
pigmentation in the skin

141
Q

cause of melasma

A

● 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
Q

presentation melasma

A

● 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

143
Q

mx melasma

A

● 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.

144
Q

features venous ulcer

A
  • 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
145
Q

mx venous ulcers

A
  • Compression bandaging
    (after excluding arterial insufficiency)
146
Q

features arterial ulcers

A
  • 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
147
Q

ix for arterial ulcers

A
  • ABPI < 0.8 - presence of arterial
    insufficiency
  • Doppler studies and angiography
148
Q

mx arterial ulcer

A
  • Vascular reconstruction
  • Compression bandaging is
    contraindicated
149
Q

features neuropathic ulcer

A
  • 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
150
Q

ix neuropathic ulcers

A
  • ABPI < 0.8 implies a neuroischaemic
    ulcer
  • X-ray to exclude osteomyelitis
151
Q

mx neuropathic ulcer

A
  • Wound debridement
  • Regular repositioning, appropriate
    footwear and good nutrition
152
Q

causes itchy eruption

A

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)

153
Q

features lichen planus

A
  • 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)
154
Q

mx lichen planus

A
  • Corticosteroids
  • Antihistamines
155
Q

features melanocytic naevi

A
  • 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
156
Q

mx melanocytic naevi

A
  • Only if symptomatic
    Shave or complete excision
157
Q

features seborrhoeic wart

A
  • 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
158
Q

mx seborrhoeic wart

A
  • Only if symptomatic
    Curette and cautery
    Cryotherapy
159
Q

causes purpuric eruption

A

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).

160
Q

features DIC

A
  • 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
161
Q

ix DIC

A
  • Bloods (a clotting screen is
    important)
162
Q

mx DIC

A
  • Treat the underlying cause
  • Transfuse for coagulation
    deficiencies
  • Anticoagulants for thrombosis
163
Q

features vasculitis

A

Painful lesions
- Dependent areas (e.g. legs,
buttocks, flanks)
- Palpable purpura (often
painful)
- Systemically unwell

164
Q

ix vasculitis

A
  • Bloods and urinalysis
  • Skin biopsy
165
Q

mx vasculitis

A
  • Treat the underlying cause
  • Steroids and
    immunosuppressants if there
    is systemic involvement
166
Q

features actinic purpura

A
  • 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
167
Q

mx actinic purpur

A

nonw needed

168
Q

differentials ofr a red swollen leg

A

cellulitis, venous thrombosis, chronic venous insufficiency

169
Q

skin changes inchronic venous insufficeincy

A
  • 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
170
Q

what are keloid scars

A

An overgrowth of scar tissue, which tends to be larger than the original wound itself

171
Q

cause keloid scars

A

● 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

172
Q

presentation keloid scars

A

● Firm, smooth, hard nodule which can be itchy or painful
● Common sites are chest and shoulders

173
Q

mx keloid scars

A

● 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

174
Q

what is an emollient

A

● Aqueous cream, emulsifying ointment, liquid paraffin and white soft
paraffin in equal parts (50:50)

175
Q

indications for emollients

A

● To rehydrate skin and re-establish the surface lipid layer
● Useful for dry, scaling conditions and as soap substitutes

176
Q

e.g. topical steroids in derm

A

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))

177
Q

e.g. oral steroids derm

A

● Oral steroids: prednisolone

178
Q

indications steroids in derm

A

● Anti-inflammatory and anti-proliferative effects
● Useful for allergic and immune reactions, inflammatory skin conditions,
blistering disorders, connective tissue diseases, and vasculitis

179
Q

SE steroids

A

● 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

180
Q

indications oral aciclovir in derm

A

● Viral infections due to herpes simplex and herpes zoster virus

181
Q

SE aciclovir

A

● Gastrointestinal upsets, raised liver enzymes, reversible neurological
reactions, and haematological disorders

182
Q

classes of oral antihistamines

A

● Classified into nonsedative (e.g. cetirizine, loratadine) and sedative
antihistamines (e.g. chlorpheniramine, hydroxyzine)

183
Q

inidcations oral antihistamines derm

A

● Block histamine receptors producing an anti-pruritic effect
● Useful for type-1 hypersensitivity reactions and eczema (especially
sedative antihistamines for children)

184
Q

SE oral antihistamines

A

● Sedative antihistamines can cause sedation and anticholinergic effects
(e.g. dry mouth, blurred vision, urinary retention, and constipation)

185
Q

topical abx derm

A

fusidic acid, mupirocin (Bactroban), neomycin

186
Q

oral abx derm

A

penicillins, cephalosporins, gentamicin, macrolides,
nitrofurantoin, quinolones, tetracyclines, vancomycin, metronidazole,
trimethoprim

187
Q

indications abx derm

A

● Useful for bacterial skin infections, and some are used for acne

188
Q

topical antiseptics derm

A

Chlorhexidine, cetrimide, povidone-iodine

189
Q

indications topical antiseptics derm

A

● Treatment and prevention of skin infection

190
Q

oral retinoids derm

A

Isotretinoin, Acitretin

191
Q

indications oral retinoids derm

A

● Acne, psoriasis, and disorders of keratinisation

192
Q

SE oral retinoids

A

● 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 (

193
Q

biological therapy derm

A

Monoclonal antibodies (eg. Infliximab, Adalimumab, Ustekinumab,
Certolizumab, Gorlilumab), Fusion antibody proteins (eg. Etanercept),
Recombinant human cytokines and growth factors (eg. Interleukins)

194
Q

ndications biological therapy derm

A

psoriasis, atopic dermatitis and hidradenitis suppurativa

195
Q

SE biological therapy

A

● 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)

196
Q

how to use emollients

A

● Apply liberally and regularly

197
Q

how to use corticosteroids

A

● 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

198
Q

preventing pressure sores

A

● 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

199
Q

how to prevent sun exposure

A

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

200
Q

fitzpatrick skin phototype

A

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

201
Q

bowens disease

A

=in situ SCC
full thickness dysplasia epidermal keratinocytes

202
Q

acitinic keratoses

A

partial thickness dysplasia epidermal keratinocytes
sun exposed sites=scaly erythema

203
Q

Derm red flags

A

Need urgent referral

Blistering/skin peeling
Pain
Lymphadenopathy
Mucosal involvement
Systemic upset: fever, abnormal LFTs/U&E

204
Q

Mx mild drug rxn

A

Stop drug
Emollients
Topical corticosteroids
Antihistamines if urticarial

205
Q

SJS and TEN

A

Steven Johnson syndrome and toxic epidermal necrolysis are on a scale
SJS less severe, TEN more

206
Q

Cause SJS AND TEN

A

DRUGS

207
Q

Sx SJS and TEN

A

sx 7-21d after med given
Prodrome=resp infection, fever, pain
Dusky red lesions, atypical targets, erythematous plaques, mucosal involvement, systemic symptoms, detachment epidermis

208
Q

Mx SJS and TEN

A

stop med
Dressings and emollient/paraffin
ICU/burns unit
Fluid and electrolytes
Supportive: eyes, mouth, swabs for infection, physio

209
Q

DRESS

A

Drug rxn with eosinophilia and systemic sx

210
Q

Sx DRESS

A

15-40D after drug exposure- anticonvulsant and sulfonamodes
Fever, oedema
Rash=morbilloform, purpura, scaling
Lymphadenopathy
Eosinophilia
Effects organs-LFTs

211
Q

Mx DRESS

A

Stop drug cause
Systemic steroids if severe
Supportive: dressings, topic steroids, emollients, oral antihistamines, fluids, tx secondary infection

212
Q

AGEP

A

Acute generalised exanthematous pustulosis

213
Q

Sx AGEP

A

Less than 4d after drug exposure - beta lactam abx
Fever
Small sterile pustules and oedematous erythema
Increased WCC
purpura
Vesicles
Target lesions
Mucosal involvement

214
Q

Mx AGEP

A

Stop drug cause
Topical corticosteroids, emollients, antihistamines

215
Q

What is erythroderma

A

Erythema over 90% skin surface

216
Q

Causes erythroderma

A

Dermatitis
Psoriasis
Drug eruption
Cutaneous t cell lymphoma

217
Q

Features erythroderma

A

Hx: atopy, steroid withdrawal
Clues underlying diagnosis=psoriasis, eczema

218
Q

Ix erythroderma

A

FBC
U&E
LFT
CRP
total IgE
Blood film
+/- skin biopsy, lymph node ix

219
Q

Mx erythroderma

A

Stop causative drugs
Monitor vitals and fluid
Dressings and emollients
Tx cause
Topical corticosteroids

220
Q

Symptoms bullous pemphigoid

A

Sub dermal blistering
Usually elderly
Tense intact blisters

221
Q

Bullous pemphigoid cause

A

AI
drug eruption
Attack on BM by IgE

222
Q

Diagnosis bullous pemphigoid

A

Skin biopsy and direct immunofluroescence

223
Q

Mx bullous pemphigoid

A

Specialist!
Systemic and topical steroids

224
Q

Features staph scalded skin syndrome

A

Usually children
Superficial skin blistering and crusting, often flexural
No mucosal involvement

225
Q

Mx staph scalded skin

A

Tx infection
Supportive- fluid, skin care

226
Q

Cause staph scalded skin

A

Staph aureus exotoxins

227
Q

Cause pemphigous vulgaris

A

AI
IgG auto Ab

228
Q

Sx pemphigous vulgaris

A

Intra epidermal blisters=non tense, erosion
Painful blisters skin and mucous membranes
30-60y, Jews, indians

229
Q

Mx pemphigous vulgaris

A

Specialist
Topical and systemic steroids

230
Q

what is an acral distribution

A

distal areas- hands and feet

231
Q

cause dermatitis herpetiformis

A

coeliac and IgA defieincy

232
Q

biologic used in eczema

A

tacrolimus

233
Q

associations psoriasis

A

arthritis
IBD
uveitis
coeliac
T2DM
gout

234
Q

prognosis melanoma

A

breslow depth >3mm = poor prognosis

235
Q

pathology psoriasis

A

autoimmune: T cell mediated keratinocyte proliferation

finals (31 decks)

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