dermatology core diseases

Question 1

acanthosis

Answer 1

temporary thickening of the epidermis due to an increase in keratinocytes
may be caused by rubbing

Question 2

acantholysis

Answer 2

keratinocytes separating from each other

eg pemphigus where the autoimmune process inactivates desmosomal structures within the epidermis so that the cells float free from each other

Question 3

alopecia

Answer 3

loss of hair

Question 4

scarring alopecia

Answer 4

loss of hair due to destruction of the follicles (hair cannot regrow as the follicles are destroyed)

Question 5

atrophy

Answer 5

loss of volume
eg loss of dermal substance you see in sun damaged skin on the dorsum of the hand in elderly lady

atrophy secondary to a disease process such as Discoid lupus erythematous where the dermis is reduced in volume as a result of inflammatory processes

Question 6

epidermal atrophy

Answer 6

much harder to detect as the epidermis is usually thin and many people use the term to describe different things

-means a reduction in the spindle cell layer, and a reduction in the rete ridges and dermal papillae

Question 7

atrophy of the dermis

Answer 7

also may mean that the vascular component of the dermis is more visible to the eye
-because the loss of collagen means you are better able to see the normal vascular structure because there is less collagen blocking the transmission of incident light

Question 8

papule

Answer 8

small <1cm solid elevated palpable lesion

Question 9

nodule

Answer 9

a papule larger then >1cm

Question 10

macule

Answer 10

small non-palpable area of colour change

flat focal

Question 11

patches

Answer 11

larger macule

Question 12

plaque

Answer 12

flat palpable lesion

Question 13

vesicle

Answer 13

<0.5cm fluid filled sac

Question 14

pustule

Answer 14

pus filled sac

Question 15

blisters or bulla

Answer 15

collection of fluid in epidermis >0.5cm

due to either cell to cell or cell to basement membrane or basement membrane to dermis loss of attachment

Question 16

weal

Answer 16

localised oedema

Question 17

crust

Answer 17

refers to dry exudate

commonly seen in eczema and impetigo

Question 18

diascopy

Answer 18

means pressing on the lesion with a glass
eg to check that it blanches on pressure
if it blanches you know the colour is due to blood in vessels

Question 19

erythema

Answer 19

redness of skin due to an increase in intravascular blood

Question 20

fissure

Answer 20

a narrow ulcer

common on hands in hand eczema

Question 21

hyperkeratosis

Answer 21

refers to thickening of the stratum corneum so that there are more layers of corneocytes then there should be

Question 22

parakeratosis

Answer 22

thickening of stratum corneum but with corneum cells that have nuclei (usually anuclei)

Question 23

hyperplasia

Answer 23

same as acanthosis

Question 24

lichenoid

Answer 24

typically if lesions are small papules that are flat topped and resemble lichen planus- then it is lichenoid

also used to describe exaggerated skin markings and thickening seen in lichenification

Question 25

milium (plural milia)

Answer 25

small epidermoid cyst | seen in newborns, on face of adults and secondary to some diseases eg PCT porphyria cutanea tarda

Question 26

necrobiosis

Answer 26

degeneration of collagen which is found within palisading granulomas -necrobiosis lipoidica - rash most commonly seen on diabetics shins, and granuloma annulare

Question 27

nikolsky sign

Answer 27

refers to the ability to induce a blister on apparently normal skin by applying simple frictional force across the skin feature of pemphigus and TEN

Question 28

oncholysis

Answer 28

distal lifting away of nail plate from nail bed | commonly seen in psoriasis or dermatophyte tinea nail infections

Question 29

panniculitis

Answer 29

inflammation of subcutaneous fat | eg erythema nodosum

Question 30

pompholyx

Answer 30

skin on palms and soles has a different organisation in terms of tethering of the epidermis and dermis, as the epidermis is much thicker oedema due to spongiosis, more readily forms vesicles that are relatively robust to trauma vesicular appearance in eczema at these sites is known as pompholyx

Question 31

petechiae

Answer 31

non blanching mm petechiae

Question 32

purpura

Answer 32

non blanching >petechiae

Question 33

ecchymosis

Answer 33

bruise

Question 34

palpable purpura is a sign of

Answer 34

vasculitits

Question 35

scale

Answer 35

small piece of stratum corneum

Question 36

sclerosis

Answer 36

refers to change in dermis when the tissue feels harder and stiffer than normal and may relate to increases in collagen production

Question 37

spongiosis

Answer 37

intercellular oedema within the epidermis | one of the cardinal signs of eczema

Question 38

telangiectasia

Answer 38

small visible blood vessels

Question 39

ulcer

Answer 39

full thickness break in dermis and epidermis

Question 40

erosion

Answer 40

superficial- epidermis

Question 41

psoriasis other presentation

Answer 41

inflammatory polyarthropathy | increase CVD risk and metabolic

Question 42

presentation psoriasis

Answer 42

scaly red plaques extensor surfaces, nails and scalp waxing and waning course some itch but not as itchy as eczema

Question 43

pathology of psoriasis

Answer 43

1. Epidermal hyperproliferation- keratinocytes | 2. inflammatory infiltrate

Question 44

epidermal hyperproliferation in psoriasis

Answer 44

- epidermal differentiation is derranged in psorasis with hyperproliferation - parakeratosis- retention on nulcei - absence of granular layer - acanthosis: thickening of epidermis - time taken for epidermal differentiation is shortened-rushed through in an immature state

Question 45

inflammation in psoriasis

Answer 45

oedema in the dermis T cell rich inflammatory infiltrate in dermis polymorphs in dermis and epidermis capillaries in dermis are increased

Question 46

munro microabscesses

Answer 46

epidermis polymorph collection in psoriasis

Question 47

psoriasis causes

Answer 47

mostly unknown- and based on what drugs works for what -highly heritable - genes involved in innate, adaptive immune system and skin barrier function and keratinocyte -APC, T cells, HLA, TNF, IL HLA cw6 HLA B27 Linkage disequilibrium -MHC on chromosome 6

Question 48

risk of developing psoriasis if one parent affected | risk if both

Answer 48

15% | 40-50%

Question 49

% psoriasis prevalence

Answer 49

2%

Question 50

2 peaks of onset of psoriasis

Answer 50

type1= starts in later teen years. early adulthood and more linked to HLA groups type 2- onset in 5th or 6th decade

Question 51

Triggering factors for psoriasis

Answer 51

- often presents first time after a strep sore throat- immune system - HIV can aggrevate - certain drugs: lithium, betablockers, INF a and chloroquine - receiving a bone marrow transplant - obesity, smoking and alcohol - psychogenic- stress

Question 52

koebner phenomenon

Answer 52

in some situations injury or damage to the skin causes the development of a psoriatic plaque at the site of the insult -usually lag of 2 weeks eg sunburn, surgery, exathema, accupuncture

Question 53

Types of psoriasis 7

Answer 53

``` stable plaque guttate erythrodermic pustular flexuaral or inverse palmoplantar nail ```

Question 54

stable chronic plaque psoriasis features

Answer 54

- scaly red well demarcated plaque, mostly seen on extensor surfaces of elbow and knees - can occur also on genitals and scalp - usually red unless obscured by an excess of silvery scale seen in plaque psoriasis - called stable as tends not too change week to week - well defined

Question 55

how can scale of stable plaque psoriasis be removed

Answer 55

with keratolytic agents eg salicylic acid | emolients

Question 56

why does psoriasis look white

Answer 56

untreated plaque psoriasis looks white is because of the light refracted at the stratum corneum - in psoriasis the sc is thickened and disorganised so contains more air so more light is reflected than usually so the skin looks white - increase refractive index

Question 57

Auschpitz sign

Answer 57

bleeding when scratch off the plaque

Question 58

guttate psoriasis

Answer 58

characterised by several hundred small lesions, which often follow a strep sore throat by 2-3 weeks - most common on the trunk - often first episode of psoriasis an individual develops and can then go onto develop stable - raindrops - usually resolves as guttate 6 months later

Question 59

erythrodermic psoriasis

Answer 59

``` most of the skin is affected looks less like psoraisis red all over erythroderma refers to any rash >90% can be difficult to diagnose on first episode as many causes of erythroderma medial emergency as can get hypothermia as skin feels hot, dehydration -need admitting to hospital -dehydration ```

Question 60

causes of erythroderma

Answer 60

- psoriasis - eczema - iatrogenic - cutaneous T cell lymphoma

Question 61

pustular psoriasis

Answer 61

pustules present due to collections of polymprophs (munro micro-abscesses) in epidermis which become large enough so can see if pustules are all over the body- generalised can become quite unwell

Question 62

2 forms of pustular psoriasis

Answer 62

1. palmoplantar pustular psoriasis-- palms and soles mostly affected 2. generalised pustular psoriasis - can become very ill although pustules are sterile - pyrexia, rigors, severe malaise

Question 63

other states in which pustules in psoriasis can be seen 2- induced

Answer 63

1. plaques that are continually treated with steroids may become pustular- steroid induced pustular 2. patients with very acute psoriasis if treated with strong concentrations of dithranol or tar, may develop pustular psoriasis

Question 64

flexual or inverse psoriasis

Answer 64

-some patients get psoriasis predominantly in flexures eg natal cleft, under boob, antecubital fossa -red and shiny generally lack the scale -needs different treatment and can be harder to target with phototherapy

Question 65

nail psoriasis 3 changes

Answer 65

1. pitting of nail plate 2. oncholysis- separation of distal nail bed 3. oily spots/ salmon patches = yellowy brown

Question 66

cause of nail pitting in psoriasis

Answer 66

parakeratosis in dorsal nail matrix

Question 67

scalp psoriasis

Answer 67

``` Scalp is very commonly affected lesions are usually discrete and spread beyond the hair line on to the borders of the scalp scales usually adhere to the hair shafts very rarely alopecia may develop itch can be a big problem ```

Question 68

palmoplantar psoriasis

Answer 68

some patients with psoriasis have chronic hyperkeratotic psoriasis without pustules that is often indistinguishable from chronic hand eczema

Question 69

systemic aspects of psoriasis

Answer 69

- inflammatory seronegative arthropathy -patients can present with psoriatic arthritis and develop psoraisis later on more usually other way round -cardiovascular- increase risk of MI, peripheral vascular disease and emboli more common

Question 70

diagnosis of psoriasis

Answer 70

clinical diagnosis - describe as discomfort, irritation or pain - rarely itch

Question 71

differential scalp psoriasis

Answer 71

sebhorreic dermatitis

Question 72

solitary plaques of psoriasis differentials

Answer 72

bowen disease- intra epithelial carcinoma | eczema- chronic hand eczema

Question 73

assessment score for psoraisis

Answer 73

PASI | psoriasis area severity index

Question 74

management of psoriasis

Answer 74

1. Avoid precipitants- smoking and alcohol?, treat HIV infections, drugs 2. Active treatments in psoriasis - Topical- creams and ointments - UVR- UVB or PUVA - Older systemic- methotrexate, ciclosporin - newer eg biologics

Question 75

bad drugs in psoriasis

Answer 75

lithium chloroquine beta blockers antimalarials

Question 76

which type of psoriasis is assoc. to smoking

Answer 76

palmoplantar pustular

Question 77

Topical treatments for psoriasis

Answer 77

- easy and safe but less effective 1. emollients- bland with or without salicyclic acid - which breaks down desmosomes of the SC to make plaques less visible 2. Topical corticosteroids: mainstay of management, reduce thickness of plaque and reduce some scaling 3. vitamin D analogues: normalises epidermal differentiation and inhibits epidermal hyperproliferation, neutrophils 4. vitamin D analogues plus steroids

Question 78

SE of topical steroids

Answer 78

-local atrophy with telangiectasia striae systemic absorption -rebound effect

Question 79

older treatments psoriasis

Answer 79

anthralin- dithranol and tar pro- inflammatory but show anti-psoriatic activity -tar put on and then dressings and then UVB -3 to 4 week inpatient

Question 80

phototherapy two main treatments

Answer 80

UVB | PUVA

Question 81

UVB therapy

Answer 81

-shorter of the two wavelengths -accounts more for sunburn 2-3x a week for 10-15 weeks narroband UVB mostly used 311-313 works best for small plaque psoriasis especially guttate

Question 82

risks of UVB therapy

Answer 82

- sunburn | - long term increase in rate of non melanoma skin cancer

Question 83

PUVA therapy

Answer 83

psoralen and UVA - tablet taken and inert until activated by UVA - or in bathwater - only active in areas therefore that UVA can get to - hence wear glasses to block= cataracts avoid

Question 84

how does psoralen work

Answer 84

-when activated it -inhibits proliferation of both keratinocytes and any inflammatory cells present in skin also -causes mutations if the cell manages to replicate

Question 85

PUVA or UVB

Answer 85

-PUVA is more effective | but more toxic in terms of skin cancer risk of both non-melanoma (SCC) and melanoma

Question 86

systemic agents for psoriasis

Answer 86

Methotrexate ciclosporin systemic retinoids

Question 87

how does methotrexate work and SE

Answer 87

- folic acid antagonist - limits DNA synthesis - acts on immune system in psoriasis main SE - hepatic fibrosis and cirrhosis - bone marrow inhibition - teratogenicity and mutagenic on sperm - can affect response to live vaccines - increase malignancy and infection risk - nausea- so use IM

Question 88

how long do men that want to have children have to stop methotrexate and wait

Answer 88

3 months

Question 89

monitoring methotrexate

Answer 89

weekly FBC and LFT and UandE routine basis | then 3 months after 3 to 6 months

Question 90

drugs/ disease that interfer with methotrexate

Answer 90

NSAID- increase toxicity in bone marrow | renal disease impairs its excretion

Question 91

ciclosporin action and SE

Answer 91

calcineurin inhibitor blocks T cell activation short term management 3-4 months ``` SE -nephrotoxicity hypertension increase in risk of some viral cancers eg EBV, HPV and non melanoma skin cancer -hypertrichosis -gingival hyperplasia -vaccination and infection ```

Question 92

Retinoids action and SE

Answer 92

-vitamin A like actions act on nuclear receptors = ACITRETIN ``` SE -teratogenicity -elevates triglycerides -pancreatitis CVD mortality -mucosal and cutaneous dryness -hair loss -MSK pain ```

Question 93

how long do women after acitretin need to wait before conceiving children and how long for other types of retinoids

Answer 93

3 yrs 5 weeks for isotreinoin alitretinoin

Question 94

what is Isotretinoin used for

Answer 94

Acne shorter half life retinoid

Question 95

what is alitreinoin used for

Answer 95

some hand eczema | 5 weeks before pregnancy

Question 96

Biologics for psoriasis

Answer 96

1. Tumour necrosis factor inhibitor | 2. block other cytokine pathways

Question 97

TNF inhibitors psoriasis examples 3

Answer 97

-eg etanercept, infliximab, adalimumab

Question 98

ustekinumab blocks

Answer 98

IL12 23

Question 99

Ixekizumab blocks

Answer 99

IL17

Question 100

Guselkumab blocks

Answer 100

IL23

Question 101

Risks with TNF inhibitors

Answer 101

- TB | - reactivation of eg JC

Question 102

other systemic agents in psoriasis

Answer 102

fumarates mycophenolate hydroxyurea aprelimast- phosphodiesterase inhibitor

Question 103

what serious infection is assoc. to severe psoriasis

Answer 103

undx HIV

Question 104

what is acne

Answer 104

disorder of pilosebaceous unit- hair follicle and sebaceous gland

Question 105

types of comedones

Answer 105

``` whiteheads= closed blackheads= open ```

Question 106

charaterisation of acne

Answer 106

comedones, inflammatory papules, pustules and scars ``` some also get nodules forming with sinus formation and cysts (cavities lined with epithelium) and pseudocysts (inflammatory masses) ```

Question 107

pathogenic factors of acne

Answer 107

1. abnormal keratinisation of follicular epithelium - hyperkeratinisation 2. increased sebum excretion 3. infection with gram positive rod Propionibacterium acnes P. acnes

Question 108

abnormal keratinisation of the infundibulum in acne

Answer 108

- earliest change in acne is formation of microcomedones - instead of desquammation breaking up the keratinocytes- in the follicle, the keratinocytes all stick together along with sebum so form a plug towards the top of the follicle - as the plug gets larger it becomes more visible- evnetually it distends the follicle and ruptures and bursts causing an inflammatory response - get closed comedones and later open comedones

Question 109

what are open comedoens

Answer 109

Black heads filled with dead cells and sebum due to melanin makes it black

Question 110

sebum in acne

Answer 110

- sebum is necessary but not sufficient for development of acne

Question 111

how is sebum produced

Answer 111

-by cell death of sebocytes in sebaceous glands with release of lipid cell contents in the lumen of the follicle

Question 112

evidence that sebum production is under androgen control

Answer 112

teenages PCOS body builders prepubertal enuchs dont get acne as little sebum

Question 113

what is p.acne

Answer 113

propionibacterium acne - found in everyone skin - numbers are greater in those with acne with heavy colonsiation of follicular epithelium

Question 114

how does p. acne relate to acne

Answer 114

- P.acne uses sebum as a substrate and breaks down products into free fatty acids - the more sebum the more p.acnes - some fatty acids are powerfully chemotactic for polymorphonucleates and cause abnormalities of follicular keratinisations and sitimulates innate immune system so p.acne stimualates the innate immune system

Question 115

inflammatory process of acne

Answer 115

=finally ruptures due to increasing pressure and -direct release of p.acne lipases, chemotactic factors and enzymes leads to comedone rupture which results in exudation of keratin, sebum, p.acnes and cellular and vellus hair material into the surrounding dermis - this drives an inflammatory casacde with neutrophil infilitration and release of oxygen reactive species and lysosomal enzymes- t cell infiltrate

Question 116

nodulocystic acne describes

Answer 116

patents that get multiple inflammatory nodules whether there are true cysts or not

Question 117

scarring in acne

Answer 117

worse the inflammation the greater risk of scarring -different people scar to a different degree -

Question 118

types of scars

Answer 118

- Ice pick scars= narrow and deep - keloid scars= large unsightly scars also seen after surgery and trauma - also can just be shallow irregularity of skin's normal surface - hyperpigmented areas also

Question 119

why are blackheads black

Answer 119

due to melanin

Question 120

genetics of acne

Answer 120

- higher in identical twins | - sebum excretion rates under some genetic control

Question 121

diet and acne evidence

Answer 121

aka little evidence | not due to food or washing

Question 122

main types of acne 9

Answer 122

1. comedonal acne 2. papulopustular acne 3. acne fulminans 4. acne conglobata 5. acne ecxoriee- des junes filles 6. infantile acne 7. mechanical acne 8. chloracne 9. cosmetic acne

Question 123

comedonal acne

Answer 123

simple acne where comedones predominate over the inflammatory lesions of papules and pustules ie lots of blackheads/ white heads

Question 124

papulopustular acne

Answer 124

inflammatory lesions and pustules are more evident than the comedones -note comedones may not be easily visible but are still present- cant have acne without comedones

Question 125

acne fulminans

Answer 125

severe variant of acne with abrupt onset of nodular suppurating (pus producing) lesions often following a deterioration of pre-existing acne in teenage boys lesions ulcerate and result in severe scarring emergency management

Question 126

systemic features of acne fulminans

Answer 126

-joint pains -pyrexia hepatosplenomegaly osteolytic lesions high ESR leukocytosis protineuria anaemia

Question 127

acne conglobata

Answer 127

refers to severe form of nodulocystic acne with multiple painful abscesses and scarring possible extensive involvment of chest, face, back, arms, scalp and buttocks - unlike acne fulminans there are no systemic manifestations - may occur with acne inversa

Question 128

acne excoriee de jeunes filles

Answer 128

clinical picture when the acne appears fairly minimal but the patient seems to squeeze, excoriate or pick to an excessive degree the individual lesions often young women

Question 129

infantile acne

Answer 129

few months to 1 year reflects androgen activity seen in both sexes but more males in males elevated LH leads to testicular andorgen production and, in both sexes raised DHEA produced by the adrenals may be the explanation fades after one year and then re-starts with puberty seen as comedones, pustules and scarring

Question 130

mechanical acne

Answer 130

mechanical damage or frictional occlusion of the skin from headbands eg chin straps or even leaning on your hands excessively can lead to increased in number of comedones and worsening of acne

Question 131

chloracne

Answer 131

severe type of comedonal acne- usually secondary to dioxin exposure either from military campaigns, industrial accidents

Question 132

cosmetic acne

Answer 132

variety of chemicals, especially oils or tar derivatives or aromatic hydrocarbons induce comedone formation leading to acne - many are found in cosmetics - although most inducers no longer used- oils based still cause problems

Question 133

post-adolescent acne

Answer 133

- acne may persist beyond the twenties well into middle age, especially in women - areas around the jaw and mouth may be particularly affected - pre-menstrual flares are common

Question 134

Endocrine causes of acne 5 | inx

Answer 134

1. hyperandrogenism in women- change in voice, body build, androgenicalopecia and cliteromegaly - A normal menstrual cycle is strong evidence against any systemic endocrine abnormality, 2. PCOS 3. CAH congenital adrenal hyperplasia 4. androgen secreting tumours 5. androgens in body builders - evaluation should include testosterone, DHEAS and hydroxyprogesterone - steroid production adrenal and ovarian

Question 135

when to consider endocrine causes of acne

Answer 135

severe acne | age of onset in unusual- childhood or middle age

Question 136

Management options for acne approach

Answer 136

1. single topical retinoids or benzoyl peroxide 2. topical combination therapy - BPO, retinoids, abx 3. antibiotic oral or hormonal methods in females 4. systemic retinoids

Question 137

management targets for acne

Answer 137

1. reverse the keratinisation defect 2. reduce sebum production 3. kill of bacteria- p.acne

Question 138

Topical retinoids used in acne | how it works

Answer 138

eg Isotretinoin, tretinoin - vitamin A activity - topical or systemic - work by normalising follicular keratinisation - and reversing the excess adhesion of dead corneocytes in the follicle - do not affect sebum production

Question 139

SE of topical retinoids and dosing

Answer 139

- tend to promote a mild inflammatory reaction - means that they produce a slight toxic or irritant reaction like a mild sunburn -erythema, dryness, scaling - therefore use once a day or if inflamamtory response prominent then every other day

Question 140

predominant comedonal acne best treatment

Answer 140

retinoids best agent to start with

Question 141

Benzoyl peroixde BPO action on acne

Answer 141

works by reducing the levels of P.acne within the follicle | -reduction in bacteria then leads to a reduction in pro-inflammatory free fatty acids and inflammatory activation

Question 142

SE of benzoyl peroxide and dosing

Answer 142

- tend to promote a mild inflammatory reaction - means that they produce a slight toxic or irritant reaction like a mild sunburn -erythema, dryness, scaling - therefore gradually increase them

Question 143

what oral antibiotics are used in acne

Answer 143

tetracyclines eg doxycyline or erythromycin

Question 144

how long does a patient need to be on an antibiotic to see it taking an effect against acne

Answer 144

2 months

Question 145

using oral antibiotics for acne

Answer 145

-systemic antibiotics are used for 3-6 months but then withdrawn but continue with topical retinoid or BPO -may need to commence the antibiotic again but people argue increasingly for therapeutic holidays to minimise resistance

Question 146

which antibiotic can be used in pregnancy for acne

Answer 146

erythromycin

Question 147

when are tetracyclines contraindicated

Answer 147

<12 as deposits and stains teeth and in bone | pregnancy teratogenic teeth and bone effects

Question 148

which topical antibiotics are used for acne

Answer 148

erythromycin, tetracyclines, clindamycin | topical abx are commonly used with topical BPO

Question 149

when will topical antibiotics not be suitable

Answer 149

for extensive chest and back involvement

Question 150

other topical agent option for acne

Answer 150

azelaic acid- possess antibacterial, anti inflamamtory, and anti-comedonal effects

Question 151

hormonal method acne options

Answer 151

1. combined pill mainstay 2. co-cyprindiol- oestrogen and anti-androgen but not used as much and is a teratogen -in females can be used instead of oral antibiotics

Question 152

oestrogen and progesterone on acne

Answer 152

oestrogen decreases sebum | progesterone increases sebum

Question 153

how combined pill affects acne

Answer 153

- contains some oestrogen which decreases sebum | - inhibits ovulation which reduces ovarian androgen production and thus reduce sebum production

Question 154

which systemic retinoid is used for acne

Answer 154

systemic isotretinoin

Question 155

how does systemic isotretinoin work

Answer 155

potently reduces sebum excretion (rem topical retinoids do not reduce sebum excretion -does this by inducing a temporary and reversible atrophy of the sebaceous glands

Question 156

when are systemic retinoids used in acne

Answer 156

if no response to conventional treatment | acne that is causing severe acne

Question 157

how long is systemic retinoids prescribed for

Answer 157

4 months | -can be a delay before any beneficial effect is seen

Question 158

complications of systemic retinoids

Answer 158

- can precipitate acne fulminans when starting so may need to use steroids to dampen down immune response - highly teratogenic- need 2 methods of contraception

Question 159

what needs to be checked before starting isotretinoin

Answer 159

FBC LIPIDS LFT pregnancy test

Question 160

side effects of isotretinoin systemic

Answer 160

-interferes with lipogenesis not just in sebacous but also in other keratinocytes so also get chelitis, dry eyes, dry nose, nose bleeds, dry skin and eczema ? depression and mood

Question 161

what do people on systemic isotretinoin potetnially need to stop wearing

Answer 161

contact lenses

Question 162

monitoring when on on systemic retinoids

Answer 162

- blood test at start and after one month | - pregnancy test monthly and five weeks after stopping isotretinoin

Question 163

how long after isotretinoin are you not allowed to get pregnant

Answer 163

5 weeks | shorter half life then acitretin

Question 164

other treatments for acne 3

Answer 164

- potent peels (alpha hydroxy acids) - photodynamic therapy (blue light plus topical porphyrins) - comedone extraction or electrocaytery of comedones dont need to know anymore

Question 165

scarring in acne treatment

Answer 165

-scaring is irreversible- although can become less obivious RX -dermabrasion

Question 166

drug induced acne presentation

Answer 166

papulopustular eruption or folliculitis without comedones

Question 167

drugs that cause drug induced acne

Answer 167

steroids anti-epileptic medications lithium

Question 168

complication of use of tetracycline for acne

Answer 168

can develop a widespread gram negative folliculitis | -need to stop the tetracyclines

Question 169

EGF receptor inhibitors complication

Answer 169

can cause a widespread acne like pustular eruption with no comedones

Question 170

acne inversa pathology

Answer 170

- disease is centred around follicles and sebaceous glands like acne - occlusion of the follicular infundibulum and rupture of the follicle is central to its pathogenesis rupture of the follicle with dispersion of its contents into the surrounding dermis and secondary inflammation -this leads to initially

Question 171

where does acne inversa mostly affect

Answer 171

groin axillae perineum peri-anal

Question 172

presentation of acne inversa

Answer 172

- foul smelling discharge comprising of blood pus and serous exudate - pain - malaise

Question 173

complications of acne inversa

Answer 173

squamous cell carcinoma in chronic lesions | infection can contribute- not primary problem

Question 174

diff dx of acne inversa

Answer 174

often misdiagnosed as bacterial abscess

Question 175

who and when gets acne inversa

Answer 175

women and young adults | not before puberty

Question 176

treatment of acne inversa

Answer 176

- psychological important to consider as devastating disease - systemic antibiotics combinations - systemic retinoids - systemic anti androgens - systemic steroids in flare ups but response is usually poor and get recurrences - surgical: laser or excision (can be curative) - TNFalpha inhibitors can improve some patients

Question 177

cardinal lesions of urticaria

Answer 177

weal -raised dermal oedema | angioedema can also commonly be seen with urticaria

Question 178

weal vs angioedema

Answer 178

angioedema is oedema in the deep dermis or subcutis

Question 179

how long does urticaria last for

Answer 179

<24 hours

Question 180

what are urticarial dermatoses

Answer 180

``` -same morphology as urticaria but last longer than 24 hours eg urticarial vasculitis urticarial drug reactions pemphigoid ```

Question 181

pathology of formation of a weal

Answer 181

-exogenous vasoactive compounds injected into skin -eg nettle sting- dont act on mast cells or -endogenous mediators which have same effect from H1 or non H1 mediators but act on mast cells to produce this

Question 182

which proteases are found in mast cells on the skin

Answer 182

tryptase chymase determines what stimuli they react too-why the lungs and skin might react to different stimuli

Question 183

what do mast cells contain type 1

Answer 183

- mast cells contain a range of inflammatory mediators- mostly histamine but also prostaglandins, leukotrienes, cytokines, proteases and heparin - these are grouped together in granules - if the mast cells are activated they degranulate and these contents are released

Question 184

triple response weal and why get each one

Answer 184

- initial erythema-erythema close to injection site - larger flare of erythema- axon reflex in which stimulation of peripheral nerves is transmitted along sensory nerves and then back along other sensory nerves causing release of mediators leading to vasodilation= antidromic stimulation - collection of dermal oedema: due to increased permeability of post capillary venules leading to a transient increase in local oedema

Question 185

predominant symptom of urticaria

Answer 185

itch

Question 186

type 1 hypersensitivity reaction pathology and is all urticaria caused by this

Answer 186

IgE molecules are present in a sensitised individualthat binds to high affinity IgE receptors on mast cells antigen causes crosslinking of IgE receptors leading to a signalling cascade of mast cell so get urticaria -not all urticarial reactions are caused by this type 1 reaction though as some are non-immunologically mediated (dont need sensitisation) and others involve IgG or complement

Question 187

main types of urticaria

Answer 187

- acute urticaria - chronic symptomatic urticaria - contact urticaria - physical urticaria - solar urticaria - cold urticaria - cholinergic urticaria - aquagenic urticaria

Question 188

main causes of angioedema without urticaria

Answer 188

ACEi induced angioedema | C1 esterase inhibitor deficiency

Question 189

acute urticaria definition

Answer 189

Urticarial episode lasting <6 weeks

Question 190

causes of acute urticaria

Answer 190

- NSAID - recent infection - foods especially shellfish - aspirin - insect bites - antibiotics- penicillin - dyes in radiology

Question 191

inx of acute urticaria

Answer 191

-most dont need any inx beyond a detailed hx -if severe reaction refer to dermatological allergy service for inx includes - IgE testing -prick testing -biopsy only if think it is vasculitis

Question 192

length of time a weal lasts vs length of time urticaria lasts

Answer 192

-weals are the lesion of urticaria -weals last only 24 hrs -they come and go -draw around a few weals and review patient next day if weals are persisting >24 hours then consider an alternative dx such as vasculitis hence urticaria itself can last a few weeks but weals dont

Question 193

if weals persist >24 consider

Answer 193

vasculitis

Question 194

treatment of acute urticaria

Answer 194

- remove precipitant eg stop drugs - commence antihistamines non sedative- fexofenadine, cetrizine - prednisolone short course - anaphylaxis own management with adrenaline if risk of anaphylaxis give epipen

Question 195

chronic symptomatic urticaria definition

Answer 195

-urticaria lasting longer than 6 weeks

Question 196

association of chronic symptomatic urticaria

Answer 196

-autoimmune disorders | thyroid, vitiligo, rheumatoid, pernicious anaemia

Question 197

pathology of chronic symptomatic urticaria

Answer 197

most patients have IgG anti IgE antibodies or IgE antibodies to the high affinity IgE receptor on mast cells these autoantibodies cause activation and degranulation of mast cell trigger for why this autoimmune process suddenly occurs is unknown

Question 198

other cause of CSU

Answer 198

-dietary: low levels of aspirin, azo-dyes or penicillin in the diet but really there are some patients where the cause is unknown

Question 199

management of CSU

Answer 199

- exclude other causes - non sedative anti-histamines - 2nd line= trial a different non sedative anti-H rarely immunosuppression may be used eg ciclosporin, steroids -omalizumab anti IgE monoclonal biologic used if failed H1 blockade

Question 200

aspirin CSU - management

Answer 200

give leukotriene antagonists

Question 201

2 mechanisms of contact urticaria

Answer 201

1. non-immunological contact urticaria | 2. immunological contact urticaria

Question 202

non immunological contact urticaria pathology and cause

Answer 202

-either due to toxic agents from plants or animals that cause mast cell degranulation or weals directly eg jelly fish, antropod, fragrances, benzocaine, alcohol, benzoic acid

Question 203

immunological contact urticaria pathology

Answer 203

- these are usually protein products that require prior sensitisation - LATEX - examples include animal amniotic fluid exposure in vets, latex in surgical gloves and almost any foodstuff in the right individual

Question 204

physical urticarias pathology

Answer 204

- specific physical agents are able to precipitate urticaria in some individuals - mechanism linking the physical agent to the activation of mast cells is usually unclear -in some cases there is a circulating factor- IgE that can transmit the disease eg from transplant if serum given to another

Question 205

dermographism

Answer 205

-development of a weal immediately under area of skin that has had pressure applied to it

Question 206

delayed pressure urticaria and management

Answer 206

-onset several hours later can be provoked on the hands by carrying shopping or by pressure from a chair on posterior thighs -can give NSAIDs

Question 207

solar urticaria pathology | -triggers

Answer 207

- patients develop widespread urticaria under exposure to UV radiation (or even visible light) over a period of 10-15 mins - onset is usually sudden - can follow a recent infection or new drug - if over a large area can result in collapse due to generalised histamine release

Question 208

cold urticaria

Answer 208

- urticaria due to cold stress - patients can present with airway problems after eating ice cream or with generalised collapse if immerse themselves in cold water -not always related to direct contact and can occur with cold wind blowing

Question 209

cholinergic urticaria cause

Answer 209

provoked by exercise, emotional stress or heat exposure | results in many very small 1-2 mm itchy lesions

Question 210

aquagenic urticaria

Answer 210

urticaria from water contact on the skin

Question 211

angioedema definition

Answer 211

refers to deeper swelling involving the subcutis and submucosae seen in sites such as lips, eyes tongue and other body sites eg hands and face

Question 212

management of urticaria with angioedema

Answer 212

manage as urticaria

Question 213

management of angioedema without urticaria and 2 main causes

Answer 213

much more serious as dont primarily involve mast cells 1. ACE inhibitor induced angioedema 2. C1 ESTERASE inhibitor deficency

Question 214

Ace inhibitor induced angioedema pathology

Answer 214

- abnormalities of kinin metabolism eg bradykinin are central to the production of angioedema - ACEi may cause angioedema because the ACE normally breaks down kinins - can present a yr or so after starting - can rarely present with lifethreatning airway obstruction

Question 215

C1 ESTERASE inhibitor deficiency pathology

Answer 215

- C1 esterase inhibitor acts so as to inhibit a range of proteases - This action inhibits the production of bradykinin as need proteases for the production - therefore deficiency of c1 esterase= increased bradykinin

Question 216

presentation of c1 esterase inhibitor deficiency

Answer 216

- fhx of sudden death - phx of RECURRENT EPISODES of angioedema lasting several days with abdo pain, diarrhoea, upper airway obstruction NO URTICARIA

Question 217

treatment of c1 esterase inhibitor deficiency

Answer 217

-treat episodes with either c1 esterase inhibitor or subcut icatibant - bradykinin B2 receptor antagonist

Question 218

anaphylaxis presentation and pathology

Answer 218

-urticaria is often a feature but urticaria rarely progresses to anaphylaxis -widespread mast cell degranulation causes- vasodilation, hypotension, bronchoconstriction and circulatory collapse

Question 219

inx test for solar urticaria

Answer 219

monochromator

Question 220

eczema same as dermatitis commonest inflammatory skin disease pathology of eczema cardinal features...

Answer 220

- intercellular epidermal oedema- spongiosis - lymphoid infilitrate of the dermis and epidermis as the disease becomes chronic get - acanthosis- thickening of the viable epidermis - hyperkeratosis= thickening of the stratum corneum - the spongiosis can then become less apparent

Question 221

clinical features of acute eczema

Answer 221

- red - oedematous - blisters- reflect underlying spongiosis - erosions - weeping skin can stick to clothing or bed sheets

Question 222

clinical features of chronic eczema

Answer 222

- skin appears thick, rough and dry - can be fissures- narrow ulcers - with continued rubbing as a result of itch- lichenification - exaggeration of normal skin markings

Question 223

lichenification appearance

Answer 223

exaggeration of normal skin markings -from itching

Question 224

presentation of eczema

Answer 224

- can be either acute or chronic or both at the same time - many times it is hard to know how to classify an individual lesion - ITCH!!! and therefore scratch key

Question 225

two main pathological processes of eczema

Answer 225

1. immune system behaving abnormally 2. skin barrier function is in someway compromised such that noxious agents penetrate the skin and worsen inflammation, or defects in the barrier allow foreign antigens to provoke an immune response

Question 226

3 major eczema syndromes

Answer 226

1. contact allergic dermatitis 2. contact irritant dermatitis 3. atopic dermatitis - most common

Question 227

contact allergic deramtitis pathology

Answer 227

- a hapten or an antigen penetrates the skin barrier and is processed by a langerhans cell or other macrophage or APC cell in the skin - this is presented to a T cell at the regional lymph node -T cell memory for the particular antigen develops over 1-3 weeks and subsequent exposure of the individual to this antigen - anywhere on the skin's surface- results in the clinical features of eczema in 24-96 hours =type 4 hypersensitivity reaction- T cell mediated and delayed response

Question 228

contact allergic deramtitis pathology

Answer 228

- a hapten or an antigen penetrates the skin barrier and is processed by a langerhans cell or other macrophage or APC cell in the skin - this is presented to a T cell at the regional lymph node -T cell memory for the particular antigen develops over 1-3 weeks and subsequent exposure of the individual to this antigen - anywhere on the skin's surface- results in the clinical features of eczema in 24-96 hours =type 4 hypersensitivity reaction- T cell mediated and delayed response -skin barrier also plays a role to an extent as if you have a damaged skin barrier leads to greater antigen presentation so more likely to develop

Question 229

example of contact allergic dermatitis

Answer 229

nickel sensitivity 20% of the population at some point in their life when nickel placed on skin they became sensitive to it initially get acute eczema response - erythema and induration - weeping and blister - itch but if reaction is prolonged then itching and subsequent scrathing leads to acanthosis and hyperkeratosis

Question 230

why doesnt everyone have nickel sensitivity

Answer 230

some antigens like nickel only provoke a response in individuals who are genetically susceptible in terms of the way antigens are presented to the immune system -depends genetically on their propensity to recognise antigens as foreign -also reflects on society eg allergic dermatitis is rising in henna tattoos due to PPD antigenic dyes ALSO eg increase in nickel sensitivity amongst men as there is less different in men and women wearing jewellery nowadays

Question 231

clinical features of contact allergic eczema

Answer 231

- body site distibution eg glasses and watch strap, plaster - temporal pattern- better when on holidays, worse at work - occupational hx and hobbies eg cashier and nickel in coins get hand contact allergic

Question 232

examples of contact allergic eczema

Answer 232

- bricklayers and dichromates in cement= hand - nickel coins and cashier= hands - rubber bandages - medications topical - preservatives or dye in tannin leather= shoes rash - steroids - aftershave and fragrances - eye drops

Question 233

inx for contact allergic dermatitis is

Answer 233

patch testing applied to back and left for 24 hours then skin examined at 48-96 hrs after removal -know what to avoid then can get false positives or false negatives

Question 234

contact irritant dermatitis pathology

Answer 234

-it is a localised inflammatory reaction that is not initiated by the antigen specific immune system but may involve the innate immune system in response to epidermal cytotoxic damage from a range of chemicals and other stimuli

Question 235

examples of contact irritant dermatitis

Answer 235

- hand washing- breaks the barrier eg surgeon, kitchen work | - doubly incontinence

Question 236

what makes something irritant? pathology of contact irritant dermatitis

Answer 236

if they are able to emulsify or disolve lipids this will damage and overwhelm the barrier so they can pass into the epidermis, dermis and damage keratinocytes -this results in inflammation so get all the clinical and pathological hallmarks of eczema eg soaps, detergents, alcohol wipes, acids from fruit

Question 237

contact irritant dermatitis vs contact allergic

Answer 237

contact irritant -no period of sensitisation -so can have a inflamamtory response on first time exposed, and not a delayed response - dose response in contact irritant, greater the exposure to irritants the more the barrier will be damaged so greater degree of eczema - everybody in the population is to some degree sensitive to irritants whereas- for allergic it is either you are or not

Question 238

what determines susceptibility to irritant eczema?

Answer 238

-level of exposure to irritants eg gloves, hand cleaning eg healthcare workers -individual susceptibility -biggest risk factor is hx of atopic dermatitis

Question 239

latex allergy presentation

Answer 239

contact urticaria type 1 reaction so immediate (NOT eczema)

Question 240

inx for contact irritant dermatitis

Answer 240

- depends | - can do patch testing if need to exclude contact allergic eczema

Question 241

management of irritant dermatitis

Answer 241

- aim to minimise damage and treat what left - minimise exposure to soaps, detergents and other noxious agents - protecting hands with gloves in the cold and gloves for washing dishes

Question 242

atopic dermatitis most common age and clinical course

Answer 242

- 2 to 4 - often improves later during childhood but not uncommonly recurs as facial eczema in adolescence or hand dermatitis in later adulthood - in some patients severe atopic eczema is lifelong in others it clears only to return with a later relapse

Question 243

three factors in the pathology of atopic dermatitis

Answer 243

1. atopy, and the relation between IgE an altered immune system and atopic dermatitis 2. the role of an abnormal barrier in the pathogenesis of atopic dermatitis 3. the role of infection or infectious agents including the microbiome in atopic dermatitis

Question 244

atopy definition 2

Answer 244

- those individuals who have a personal or fhx of a group of disorders we have labelled as atopic- hay fever, dermatitis, asthma - individuals who have raised IgE antibodies and have a tendency to mount IgE responses to a range of common antigens eg house dust mites

Question 245

what does a RAST test measure

Answer 245

allergen specific IgE antibodies in blood

Question 246

how come IgE is raised in atopic eczema but it the rash of atopic eczema is not like urticaria another IgE response

Answer 246

positive Ige REPONSES ARE not directly causal of eczema but merely reflect an abnormal immune system - so might be a useful diagnostic marker but are not the cause of the skin rash - therefore removing the antigens from the environment of the patient will not be expected to improve the patient as the antigens are not causal

Question 247

what type of reaction is hayfever

Answer 247

type 1 hypersensitivity reaction

Question 248

do you have to have other features of atopy to have atopic eczema

Answer 248

no you can just have the cutaneous features of IgE atopic eczema but not the atopic (based on hx, fhx, ige levels or prick testing)

Question 249

what protein is implemented in the abnormal barrier seen in patients with atopic dermatitis

Answer 249

- filaggrin-filament aggregating proteins - patients with atopic eczema have an inherited skin barrier abnormality - a filaggrin deficient cornified envelope leads to a defective cytoskeletal barrier with abnormalities in lamellar bodies and the normal stratum corneum lipid barrier - these mutations occur in 10% of the population and those with a mutation in one allele are three to five times more likely to develop atopic eczema -you can develop atopic eczema without a filaggrin mutation -but probably means their is a mutation in another gene not known about

Question 250

which bacteria is found on the skin of patients with atopic eczema and why

Answer 250

- staph aureus - some products of the innate immune system such as defensins produced by keratinocytes are decreased in atopic eczema - which can contribute to an inability to deal with staph aureus on the skin -which in turn exerts an effect on the cutnaeous immune system - efficacy about treatments targeting this arent full proof

Question 251

genetics in atopic dermatitis

Answer 251

-strongly familial due to inheritance of barrier dysfunction and inherited nature of atopy

Question 252

chance of having eczema if one or both parents have it

Answer 252

20% | 50% for both

Question 253

secular changes and atopic dermatitis

Answer 253

-relates to hygiene hypothesis causing an increase in eczema in the last 40 yrs

Question 254

a baby develops an itchy rash with scaling on the face and scalp at 6-12 months of age the rash spreads involving many of the extensor surfaces itch is a prominent feature with the child scratching and rubbing the affected areas. sleep disturbance can be prominent. as the child grows older the rash appears worse in the flexures behind the knees and elbows with skin feeling weepy and sticking to the pyjamas by contrast much of the rest of skin feels rough and dry soap and detergents make it worse in the teenage years the rash subsides but facial appears intermittently and the child also develops hayfever and asthma

Answer 254

atopic dermatitis hx

Question 255

diagnosis of atopic eczema

Answer 255

- clinical features and hx -not prick testing or IgE measures (may be undertaken for assoc. type 1 clinical syndromes such as urticaria or food allergy)

Question 256

clinical feautures of atopic eczema

Answer 256

- erythema with little scale initially through to erythema with a lot of scaling -usually poorly demarcated - itchy!!-excoriations, scratching - "wet" oozy skin due to spongiosis and blisters in acute state - lichenification: in chronic form plaques of skin may be markedly thickened and rough, with an exaggeration of the normal skin folds. response to scratching - nodular prurigo is another response to scratching in which you get focal nodules in response -the skin all over may feel and look dry and feel like sandpaper - pityriasis alba - dennie morgan folds - chellitis - recurrent conjunctivitis -focal lesions measuring mm- papular eczema rather than patches or plaques measuring cm can be seen

Question 257

what is cradle cap

Answer 257

atopic dermatitis in infants | yellow crust and scale on the scalp

Question 258

what is pityriasis alba

Answer 258

white slightly scaly patches on the face and trunk of children that may be confused with vitiligo

Question 259

what is dennie morgan folds

Answer 259

double fold of skin of the lower eye lid secondary to rubbing increased peri-orbital pigmentation is also common and markedly symptomatic peri-ocular eczema

Question 260

cheilitis is

Answer 260

sometimes seen | consequent of licking of lips leads to an irritant dermatitis around the mouth

Question 261

why can patients with atopic eczema get conjunctivitis

Answer 261

due to rubbing of the eyes

Question 262

atopic dermatitis ocular assoc.

Answer 262

recurrent conjunctivitis | cataracts

Question 263

risk of applying excessive topical steroids to the eye

Answer 263

can be absorbed into the ocular mucosae

Question 264

physical signs of palms and sole eczema

Answer 264

can be different - frank blisters - lots and lots of very small vesicles - pomphyolyx eczema ie small blisters/ vesicles eczema seen first on the side of fingers - - can be marked hyperkeratosis and can mimic psoriasis so need a biopsy - hyperlinear palms- in filaggrin mutations

Question 265

secondary infections eczema

Answer 265

- can occur in all types of eczema - particularly with staphylococci - but also Herpes simplex which is a major concern and carries a risk of death = eczema herpeticum

Question 266

appearance of eczema herpeticum and risk in children

Answer 266

many ulcers that appear monomorphic and may be punched out | -herpes encephalitis

Question 267

diff dx of eczema

Answer 267

- fungal? - impetigo? - scabies? - contact allergic eczema? - ichythosis- also filaggrin mutation and get abscence of inflammation and presence of lots of scale IF there are no signs of scratching reconsider your dx of atopic eczema

Question 268

precipitants of eczema 7

Answer 268

- low ambient humidity- warm temp makes disease worse as skin dries and cracks and scale occurs and scratch increases - wool- wool is an irritant especially in the presence of sweating- use cotton instead - psychological stress- tends to increase scratching and make disease worse - exposure to water- paradoxically dries out the skin -soap and detergent exposure also worsens disease-and avoid hot and long baths - initial localised staph aureus infection of the skin can lead to generalised worsening of the disease - atopics have an increased in rate of type 1 reactions to foodstuffs-more of a problem in children in which urticaria may develop after ingesting foods leading to increased itching and scratching and resulting in worsening eczema

Question 269

Treatment of atopic dermatitis

Answer 269

1. avoidance and prevention 2. emoilients, antiseptics and bandaging 3. topical steroids or topical calcineurin inhibitors 4. new topical agents eg crisaborole - not yet licensed 5. sedative antihistamines not to target histamine but sedation reduces itch 6. phototherapy 7. systemic immunosuppressive -prednisolone, aza, ciclosporin, methotrexate

Question 270

aim of treating atopic dermatitis

Answer 270

- difficult to balance- psycho-social issues - big issue is sleep disturbance - physical signs vary over time - aim to not banish disease but reduce extent of it

Question 271

prognosis of atopic eczema

Answer 271

- uncomplicated eczema does not result in scarring or permanent damage to the skin - many children with atopic dermatitis do grow out of it -majority grow out - but more severe childhood disease the greater the chance that the disease will persist into adulthood

Question 272

avoidance and prevention advice in atopic dermatitis

Answer 272

- avoid soap and detergents and other agents that damage the barrier and make it worse - avoid wool - keep cool - bedrooms and cotton bed sheets - dont soak in a bath and not too hot - avoiding antigens- DOES NOT CAUSE THE RASH OF ECZEMA- but if the skin is broken then exposure to a type 1 antigen can provoke a type 1 response- ie urticaria which results in itching and will therefore worsen the eczema - same for food allergies and type 1 response - if a child has food allergies then they can get urticaria which causes scratching and worsening of atopic dermatitis -practically dont need to banish pets or super-clean the house

Question 273

emoilients for dermatitis

Answer 273

-first line rehydrate and restore skin barrier -range aqueous based to greasier ones

Question 274

complication of emoilients in dermatitis

Answer 274

- sometimes can get a stinging sensation immediately when applied - should switch emoilients

Question 275

antiseptics use for dermatitis examples and use in atopic dermatitis

Answer 275

- potassium permanganate or chlorhexidine can be added to bathwater - tend to help with acute atopic dermatitis as act as drying agents- -such antiseptics are also used- usually with systemic antibiotics when the skin is obviously infected as is the case when there is widespread crusting and numerous pustules

Question 276

acute eczema clinical features

Answer 276

- wet due to spongiotic oedema - breaking open - small blisters or large - red and oedematous without much scale

Question 277

chronic eczema clinical featurs

Answer 277

if a patch of dermatitis appears dry and thickened with or without lichenification it is referred to as chronic eczema -can have both acute and chronic at the same time a

Question 278

acute eczema treatment

Answer 278

- avoid ointments - use creams instead - water based ones - topical antispetics are also useful drying agents

Question 279

chronic eczema main principles of treatment-

Answer 279

dried out skin | so use ointments rather than creams

Question 280

bandaging in eczema action

Answer 280

- protects skin from damage due to scratching - reduce sensation of itch by minimising effects of external stimuli on the skin - promotes healing of broken skin

Question 281

main toxicities of steroids topical

Answer 281

- atrophy of skin- thinning, telangiectasia, striae and easy bruising - also get systemic absorption leading to cushing's- greatest in children and flexural areas

Question 282

principles of prescribing topical steroids for eczema

Answer 282

-dont combine with antibiotics- sensitisation -antiseptics can be used in combination weak

Question 283

topical calcineurin inhibitors eg tacrolimus for eczema situation and method of action

Answer 283

- useful on the face or skin creases - alternative to topical steroids-less potent but dont cause skin atrophy - worry about risk of skin cancer and herpetic infection -suppress t cell activation and reduce cytokine inflammation

Question 284

crisaborole action

Answer 284

phosphodiesterase 4 inhibitors

Question 285

how are antihistamines effective for eczema

Answer 285

- itch of all types of eczema is not mediated by histamines - so dont use topical antihistamines - can use systemic sedative antihistamines- which work by sedation of awareness of itch

Question 286

phototherapy for dermatitis

Answer 286

both UVB and PUVA have been used - UVB is safer but less effective - also more variable response to UVB in dermatitis- can get worse

Question 287

systemic immunosuppressants for eczema 6 and efficacy and how long used for and what for

Answer 287

prednisolone- only short courses and not children ciclosporin-highly efficacous but short courses methotrexate-less efficacous aza-takes a while to kick in and measure TPMT retinoids- alitretinoin for hand eczema dupilumab

Question 288

duplimumab action

Answer 288

-blocks IL4 and IL13 receptors SC every 2 weeks moderate or severe disease

Question 289

varicose eczema presentation and management

Answer 289

- legs of those with venous incompetence - target the primary problem of the venous insufficiency - however eg use of support stockings with rubber and cream can increase risk of contact allergic dermatitis

Question 290

discoid eczema presentation and treatment

Answer 290

- well demarcated annular areas , venous oedema, venous flare, varicose veins - middle aged adults - treat with steroids

Question 291

sebhorreic eczema cause and presentation

Answer 291

yeast pityrosporum treat the infection -also called cradle cap, neonate and early life then a teen peak with grease -scaly and fine

Question 292

contact allergic dermatitis main pointers in hx

Answer 292

- body site distribution eg plaster - temporal pattern - occupation and hx

Question 293

bullous disorders 3 main ones

Answer 293

1. immunobullous- pemphigoid, pemphigus and dermatitis herpetiformis 2. erythema multiforme, stevens johnson and toxic epidermal necrolysis TEN 3. staph scalded skin syndrome SSSS- young children

Question 294

pathology of forming blisters

Answer 294

- blisters reflect the accumulation of extracellular fluid either within the epidermis, between the epidermis and basement membrane or between the dermis and the basement membrane

Question 295

main cause of blister formation

Answer 295

-due to loss of adhesions between keratinocytes or between the keratinocytes and the basemement membrane or the dermis and the basement membrane

Question 296

what is epidermolysis bullosa

Answer 296

mutations in keratins - inherited disorder - blistering - often present at birth or soon after birth - some produce severe scarring

Question 297

pathology of pemphigus

Answer 297

-auto-antibodies to desmosomes-

Question 298

2 types of pemphigus and location

Answer 298

- pemphigus foliaceous- IgG antibodies attack desmoglein 1- superficial blisters - pempgius vulgaris- attack is on desmoglein 3 +/- desmoglein 1 - deeper skin

Question 299

desmoglein 1 and 3 compensation in the skin

Answer 299

- Dsg 1 is present throughout the skin but expressed most highly in superficial layers - Dsg 3 is expressed in the skin in the basal and suprabasal layers but NOT in superficial

Question 300

antibodies to desmoglein 3 only mucosa and skin expression

Answer 300

if antibodies to only Dsg3 then Dsg 1 can compensate so there is little or no blistering but will get mucosal blisters - mucosal dominant pempigus vulgaris

Question 301

antibodies to both dsg 1 and 3 mucosa and skin

Answer 301

then there is no compensation so get pemphigus vulgaris also get mucosal blisters and extensive skin disease -mucocutaneous pemphigus vulgaris

Question 302

antibodies to dsg 1 only | skin and mucosa presentation

Answer 302

get pemphigus foliaceous -superficial blisters in mucosa there will be no mucosa phenotype as little Dsg 1 expression anyway so no mucosal phenotype if foliaceous

Question 303

mucosa expression of desmogleins

Answer 303

-in the mucosae there is very little Dsg 1 expression and Dsg 3 is expressed in all layers

Question 304

who are more likely to get pempgius 2

Answer 304

middle age | certain jewish populations

Question 305

what is fogo selvagem

Answer 305

- rare variant of pemphigus foliaceous - burning pain - brazil carried by anthropods

Question 306

clinical features of pemphigus

Answer 306

- blisters- but break easily so can just have erosions and crusting - mucosal involvement only in pemphigus vulgaris which can involve the eyes mouth, pharynx, larynx oeseophagus as well as genitalia - Nikolsky sign

Question 307

where is pemphigus foliaceous rash often found

Answer 307

face chest and upper back

Question 308

what is pemphigus often misdiagnosed as

Answer 308

eczema as blisters often pop and lead crusting and erosions

Question 309

what is the nikolsky sign

Answer 309

rub apparently normal skin it causes a blister to develop or if you press a blister it spreads outwards

Question 310

diagnosis of pemphigus 3

Answer 310

- biopsy- shows acanthloysis (separation of the keratinocytes from each other) - immunofluoresence- confirms IgG intercellular staining within the epidermis - autoantibodies - indirect IF against circulating antibodies are usually present and correlate to some extent with disease activity

Question 311

treatment of pemphigus

Answer 311

- large dose of steroids - immunosuppressive sparing agents- azathioprine, mycophenolate are frequently used - IV immunoglobulin Anti CD20 antibodies or cyclophosphamide -drug treatment may be tapered off as circualting antibodies decline

Question 312

pemphigoid pathology

Answer 312

-antibodies to hemidesmosomes (anchor keratinocytes to the basement membrane

Question 313

which is more common pemphigus or pemphigoid

Answer 313

pemphigoid

Question 314

clinical features of pemphigoid

Answer 314

- itchy urticariated lesions which may precede the onset of blisters for several months - early rash can be dx as eczema

Question 315

age of onset pemphigoid

Answer 315

any age | usually >60

Question 316

pemphigus blisters vs pemphigoid

Answer 316

pemphigoid blisters are larger and more robust only 20% mucosal disease

Question 317

what is pemiphoid gestationis

Answer 317

pemphigoid seen in pregnancy result of aberrant expression of paternal MHC on placenta, and a maternal antibody response to placenta basement proteins that cross react with the target hemidesmosomal proteins in the skin

Question 318

diagnosis of pemphigoid

Answer 318

- biopsies show an eosinophil rich inflammatory infiltrate and sub-epidermal blisters - with IgG immunofluoresence staining along the basemement membrane

Question 319

TREATMENT of pemphigoid and prognosis

Answer 319

- topical steroids - systemic steroids - azathioprine as steroid sparing - IV immunoglobulins, anti CD20 antibodies or cyclophosphamide. - chronic disease so aim to use the smallest dose compatible with clinical resolution - remission will eventually occur in most patients

Question 320

dermatitis herpetiformis pathology

Answer 320

- dermatitis herpetiformis is a skin immunobullous disorder that is assoc. with GI gluten sensitivity - most have evidence of this assoc. gluten sensitive enteropathy but only a minority have clinical GI symptoms - gliaden found in gluten - gliaden is absorbed and is a substrate for a transglutaminase enzyme in the GI tract - some people with HLA groups- see this complex as foreign and T cells produce IgA antibodies to transglutaminase - transglutaminase is also found in the skin and helps to create the cornified envelope - IgA antibodies to transglutaminase bind there and causes immune complex deposition leading to recruitment of neutrophils and release of proteases - causes a neutrophil abscess

Question 321

clinical features of dermatitis herpetiformis

Answer 321

- intense itch that is described as burning - small clusters of vesicles are present most commonly on wrist, extensor aspects of elbow and knees and sacrum and buttocks - no mucosal involvement - often intense itch means cant always see intact vesicles

Question 322

diagnosis of dermatitis herpetiformis

Answer 322

-need biopsy- see small polymorph abscess in upper dermis -immunfluorescence shows IgA deposition in dermal papillae -80% will have anti endomysial antibodies -

Question 323

treatment of dermatitis herpetiformis

Answer 323

- gluten free diet | - dapsone

Question 324

side effect of dapsone

Answer 324

agranulocytosis haemolytic anaemia need close monitoring

Question 325

pemphigus immunofluoresence

Answer 325

-inter cellular staining | meshwork

Question 326

acantholysis

Answer 326

separation of keratinocytes

Question 327

age distribution pem goid and phigus

Answer 327

-pemphigoid >60 | pemphigus >50

Question 328

4 main blistering syndromes (not autoimmune ones)

Answer 328

1. Erythema multiforme 2. toxic epidermal necrolysis TEN 3. stevens johnson syndrome 4. Staph scalded skin syndrome ssss

Question 329

what is SSSS

Answer 329

scalded skin shock syndrome -due to staph toxin looks like TEN if you kill staph it goes away

Question 330

what is erythema multiforme

Answer 330

- usually a mild illness affecting the distal skin surfaces of young people possibly with mild mucosal involvement - classical clinical appearance is the "target lesion" - virtually all cases are an immunological response to an earlier infection eg herpes simplex

Question 331

what is TEN

Answer 331

toxic epidermal necrolysis - catastrophic response to a drug drug metabolism and immunological reaction -results in a large sheet of epidermal keratinocyte cell death resembling a widespread burn with mucosal involvement

Question 332

what is steven johnson syndrome

Answer 332

-milder form of TEN | overalll disease is milder but the mucosal disease predominates

Question 333

erythema multiforme clinical features

Answer 333

- target lesion- annular lesion with a red or dusky cyanotic centre and a bright erythematous outer ring separated by a slightly paler zone - haemorrhage or blistering can occur in the central lesion - lesion is initially macular and then can become raised and into bulla - lesions subside over a few weeks without any scarring -mucosal lips eyes and genitals

Question 334

where is the target lesion most commonly found

Answer 334

``` -extremities acral hands and soles face elbows knees ```

Question 335

who is erythema multiforme more common in

Answer 335

young people <40 | males more

Question 336

cause of erythema multiforme

Answer 336

- main cause of EM are infections commonly herpes simplex, or mycoplasma - other infections can cause it too - rarely drugs might precipitate EM

Question 337

18 year old male with herpes simplex then a week to two weeks later develops strange lesions on his palms which then spread to other body sites and the mucosae these lesions appeared over the course of a day and at three days are now with bullae and haemorrhages in some cases

Answer 337

erythema multiforme

Question 338

types of erythema multiforme

Answer 338

erythema major- mucosal disease more severe and fever and joint pains are a feature erythema minor: mucosal disease is milder and no systemic features

Question 339

pathology of EM and diagnosis

Answer 339

- dx is usually clinically | - can do biopsy if needed: shows widespread epidermal cell death (keratinocyte death) with some dermal inflammation

Question 340

treatment of erythema multiforme

Answer 340

- if patients develop repeated episodes it is almost certainly due to recurrent herpes simplex and can give antivirals - acute phase no treatment beyond basic skin care such as antiseptics - if clinically symptomatic then topical steroids can be used - IV fluids for severe mucosal involvement

Question 341

complication of erythema multiforme

Answer 341

-eye involvement with or without symptoms can warrant an opthalmology consult because of the potential for late scarring

Question 342

differential of target lesion

Answer 342

erythema multiforme urticaria toxic measles like drug rash

Question 343

toxic epidermal necrolysis who is it more common in 5

Answer 343

more common in elderly but can occur in children - genetics HLA - immunosuppressed - people who are slow acetylators ie drug metabolises slow

Question 344

what causes TEN and when does it tend to appear

Answer 344

- potentially fatal skin and mucosal adverse drug reaction - tends to appear 7 to 28 days after commencement of a drug - genetics HLA

Question 345

clinical presentation of TEN

Answer 345

- sudden onset of diffuse erythema with sheets of skin undergoing necrosis - wrinkling or blisters within those sheets can be seen - epidermis lifts off the basement membrane due to widespread keratinocyte death - Nikolsky positive - pyrexia, malaise, dysuria, sore eyes can precede onset of rash - mucosal involvement -lups, eyes, genitals , mouth - extrememly painful! - macular deep red/ blue areas can be seen

Question 346

where is TEN worse

Answer 346

often Trunk

Question 347

pathology of TEN

Answer 347

- full thickness epidermal death due to Fas mediated cell apoptosis - epidermis lifts off the basement membrane

Question 348

management of TEN

Answer 348

- medical EMERGENCY - stop relevant drugs ASAP -slow half lives of drug/ metabolites can be problematic - HDU/ ITU - fluid balance, analgesia - controlled pressure thermoregulated bed - aluminium sheet - skilled derma nursing - opthamology for eye

Question 349

drugs that are more likely to cause TEN

Answer 349

allopurinol carbamazepine sulphonamide

Question 350

main cause of death from TEN

Answer 350

infection | hypercatabolic state

Question 351

prognosis scoring system for TEN

Answer 351

-SCORTEN based on >5 death in 90% of cases -age, extent, HR, glucose, bicarb levels ...

Question 352

TEN mortality

Answer 352

40%

Question 353

what is steven johnson syndrome

Answer 353

best viewed as a milder form of TEN with more mucosal involvement involves <10% of the body mortality and morbidity is also lower

Question 354

SSSS pathology

Answer 354

certain subtypes of staph produce a toxin which is a serum protease that cleaves desmoglein 1 (same as pemphigus foliaceous)- so targets superficially -in SSSS it is circulating so affects all over rather than in impetigo where it will affect a certain area

Question 355

clinical features of SSSS and who gets it clinical features timeline

Answer 355

- superficial skin - no mucosal involvement (unlike TEN) - mostly children <5 but can be seen in adults with immunosuppression, renal failure - site of the staph infection is not usually the skin but nasopharynx or conjunctivae - onset is with a scarlet fever like rash, often around the mouth and nappy area, with perioral crusting and furrowing - erythema appears on the face, with or without oedema and then generalises - pyrexial but looks well initially - intense pain and separation of skin in sheets on red base - over 48 hrs widespread flaccid blisters develop and nikolsky sign can be positive

Question 356

diagnosis of SSSS

Answer 356

clinical suspicion superficial biopsy can differentiate SSSS from TEN culture swab from throat and eyes (NOT SKIN)

Question 357

management of SSSS

Answer 357

IV flucoxacillin, vancomycin- as advised by mico

Question 358

difference between ssss and TEN 3

Answer 358

SSSS - split at granular layer - children - no mucosal TEN - split full thickness epidermal- fas - older people - mucosal

Question 359

nikolsky sign

Answer 359

The Nikolsky sign is dislodgement of intact superficial epidermis by a shearing force, indicating a plane of cleavage in the skin at the dermal-epidermal junction.

Question 360

vasculitis pathogenesis

Answer 360

-most common mechanism is deposition of immune complexes in vessels walls leading to complement activation of neutrophils with resulting damage to the vessel walls and an inflammatory reaction around the vessel

Question 361

ANCA positive vasculitis pathology

Answer 361

-IgG antineutrophil cytoplasmic antibodies react with intracellular antigens on neutrophils and also activate neutrophils leading to an antibody dependent cellular cytotoxicity on endothelial walls

Question 362

main triggers of vasculitis

Answer 362

- infection - drugs - an underlying systemic inflammatory process eg SLE, RA, ANCA and positive vasculitis

Question 363

main types of vasculitis

Answer 363

``` -leucocytoplastic septic sweet's syndrome erythema nodosum pyoderma gangrenosum ```

Question 364

leucocytoplastic vasculitis pathology

Answer 364

- most common type of cutaneous vasculitis in derm - immune complex deposition leads to inflammation of the post-capillary venules - vessel wall is damaged with fibrin deposition and neutrophils move into the skin

Question 365

biopsy signs leucocytoplastic v

Answer 365

-neutrophil infiltrates -later undergo leucocytoclasis with nuclear dust - remnant of polymorph nuclei nuclear dust-

Question 366

clinical features of leucocytoplastic V

Answer 366

- palpable purpura (non blanching) - most common on the legs - early in the course can just appear as erythema - can be blistered or even pustular lesions

Question 367

main causes or assoc. of leucocyctoplastic v 5

Answer 367

- infections eg Hep ABC strep or mycobacterium - drugs - malignancies - small vessel vasculitis- wegner, churg strauss, polyarteritis nodosa - systemic disease

Question 368

what drugs are assoc. to LV 3

Answer 368

-beta blockers penicillins thiazide diuretics

Question 369

what malignancies are assoc. to LV 3

Answer 369

CLL lymphoma myeloma

Question 370

what systemic diseases are assoc. to LV

Answer 370

-IBD SLE bechet

Question 371

diagnosis LV

Answer 371

clinical | biopsy can be done

Question 372

management of LV

Answer 372

- legs usually affected so - bed rest and elevate legs and compression bandaging - topical steroids - systemic steroids - dapsone BUT BEFORE PRESCRIBING STEROIDS MAKE SURE IT IS NOT SEPTIC VASCULITIS

Question 373

prognosis of LV

Answer 373

-most resolve 2-6 weeks | in a minority it is chronic with relapses

Question 374

what type of vasculitis is henoch schonlein purpura

Answer 374

leucocystoplastic vasculitis

Question 375

septic vasculitis clinical features

Answer 375

- lesion looks similar to leucocystoplastic vasculitis- but more often pustular with necrosis and blistering - often more unwell but may not be initially - can be pyrexial - signs of other tissue damage

Question 376

main causes of septic vasculitis 2 and immunosuppressed 3

Answer 376

- gonococcus -sub acute bacterial endocarditis also -staph, meningococci, fungi eg candida (immunosuppressed)

Question 377

management of septic vasculitis

Answer 377

- FIND AND TREAT INFECTION - circulating micro-organisms - and can be immune complexes and thrombi in post-capillary venules

Question 378

other signs of sub acute bacterial endocarditis

Answer 378

osler nodes: lesions on tips of fingers and thenar and hypotheniar eminences janeway spots: superficial haemorrhages on palms

Question 379

pyoderma gangrenosum clinical feature

Answer 379

-often starts as a very small and painful lesion commonly on the legs (looks like an insect bite) -this then becomes pustular and breaks down -ulcer with red/purple edges -ulcer grows in size and get pain -can expose deep structures such as tendon and muscles -heals leaving cribiform scarring can be systemically unwell

Question 380

what is pathergy

Answer 380

-development of ULCERS eg pyoderma gangrenosum at sites of fairly minor trauma eg venous line insertion

Question 381

diseases assoc. to pyoderma g

Answer 381

- IBD - ra - ank spond - myeloma - dm - chronic active hepatitis - primary biliary cirrhosis

Question 382

pathology of pyoderma g

Answer 382

- large neutrophilic infiltrate with fibrin deposition in vessels and leucocutoclasis - can see evidence of vasculitis

Question 383

what is leucocytoclasis

Answer 383

vascular damage due to nuclear debris from infiltrating neutrophils

Question 384

dx of pyoderma g

Answer 384

clinical dx

Question 385

differential pyoderma g

Answer 385

- ulceration eg arterial and venous pathology | - tumours

Question 386

treatment pyoderma g

Answer 386

systemic steroids treat underlying assoc. disease topical steroids other immunosuppressive

Question 387

Sweet's syndrome other name

Answer 387

acute febrile neutrophilic dermatosis

Question 388

clinical features of sweet's syndrome

Answer 388

- patients present acutely with plaques or nodules that to the unintiated often look blistered due to the amount of oedema - lesions can be pustular - can be assoc. arthralgia and pyrexia

Question 389

pathology of sweet's syndrome

Answer 389

- can present as pathergy | - oedema in high dermis, prominent neutrophil infiltrates and possibly vasculitis

Question 390

diagnosis of sweet's

Answer 390

-mostly clinical

Question 391

diff dx of sweet's

Answer 391

- pyoderma g - leucocytoplastic v - erythema nodosum

Question 392

triggers of sweet's syndrome

Answer 392

- AML - infections - malignancies - gammopathies - drugs - autoimmune disorders

Question 393

treatment of sweet's syndrome

Answer 393

-prednisolone given over a few weeks

Question 394

erythema nodosum clinical features

Answer 394

- presents as a self-limiting panniculitis (inflammation of fat) - painful, red raised or indurated lesions mostly on lower legs in young adults - no ulceration and epidermis is intact - more common females - can be malaise, pyrexia arthralgia

Question 395

triggers/ asssoc. of erythema nodosum 7

Answer 395

``` drugs bacteria eg strep or mycobacterial sarcoidosis brucellosis malignancies eg lymphoma leukaemia IBD behcet ```

Question 396

2 drugs linked to erythema nodosum

Answer 396

-oral contraceptives | penicillins

Question 397

diagnosis and management of erythema nodosum

Answer 397

- over 50% patients no explanation- infection? - NSAID - compression stockings - systemic steroids

Question 398

prongosis erythema nodosum

Answer 398

most patients only have one episode

Question 399

diff dx of erythema nodosum

Answer 399

genuine nodular vasculitis- rare -can present as a similar picture -TB alpha 1 antitrypsin deficiency fat necrosis

Question 400

photosensitivity skin disorders

Answer 400

are group of disorders that are provoked by either UVR or visible light

Question 401

main photosensitivity skin disorders 5

Answer 401

- polymorphic light eruption PLE - solar urticaria - lupus erythematous - two types of porphyria - phototoxicity and drug induced photosensitivity

Question 402

body site distribution of photosensitive disorders

Answer 402

- areas of maximal sun exposure are the tops of the ears, cheeks, nose, scalp vertex if bald, face and dorsum of hands - depends also on clothing patient wears eg V neck shirts, short sleeves BUT NOT ALL FIT INTO JUST AFFECTING SUN EXPOSED SITES

Question 403

polymophric light eruption distriubtion

Answer 403

-tends to spare the face and the back of the hands

Question 404

Lupus erythematous rash distribution

Answer 404

-can appear worse on sites such as the shoulders, upper back and chest

Question 405

what does diagnostic phototesting involve

Answer 405

monochromator | -applies different wavelengths to skin to see if there is a response and at which wavelength

Question 406

problems with diagnostic phototesting 3

Answer 406

- LE will take a few weeks to respond so will be missed - some disorders need larger areas of exposure of skin to get a response - test lamps might not mimic natural exposure compleletly so false negatives can occur

Question 407

what blocks UVB

Answer 407

- glass | - sunscreen

Question 408

how common is polymorphic light eruption

Answer 408

commonest photosensitive disorder | 10-20% of the population at some time in their life

Question 409

what is polymophic light eruption often mislabelled as

Answer 409

-sun screen allergy heat rash prickly heat -so doesnt come to medical attention but for most it is mild and self -limiting

Question 410

clinical features of polymorphic light eruption

Answer 410

- called polymorphic as appears different in different people - itching and erythema several hours to days after sun exposure on sun exposed sites - symmetrical rash - papules, plaques, vesicles which may become raised with indvidual lesions that look like urticaria or large erythematous plaques - but persist for longer than urticaria - rash may last several days or longer in severe cases - can be bullours or haemorrhagic even

Question 411

where does polymorphic light eruption commonly affect

Answer 411

upper arms neck sides of face shoulder

Question 412

when is PLE most common

Answer 412

spring- spring eruption and if exposure is continued further occurrences tend to diminish till the following year the rash then usually returns

Question 413

diagnosis of PLE

Answer 413

- clinical hx and sometimes exam | - diagnostic phototesting can be used but a negative result doesnt rule it out

Question 414

diff dx of PLE and how to differentiate

Answer 414

- solar urticaria- rash comes on within 5-10 mins of exposure - LE takes 3 days to a week or more to develop rem: PLE takes several hours to days so in the middle and no scarring

Question 415

lupus erythematous diagnosis

Answer 415

biopsy and serology are needed to support a dx of LE

Question 416

management of PLE

Answer 416

1. graded early phototherapy (due to the fact that if they receive graded increase in exposure using UVB the skin appears to become less likely to develop PLE= hardening ) 2. or avoid the sun 3. short course of prednisolone if cant be avoided 4. topical steroids can be used but little efficacy 5. sedative ah1 for itch

Question 417

how long does it take for solar urticaria to develop

Answer 417

5-10 mins within exposure to UVR or visible light get widespread sheets of urticaria and itch

Question 418

how long does it take for the rash of solar urticaria to disappear

Answer 418

couple of hours

Question 419

what can trigger solar urticaria

Answer 419

drugs or infection

Question 420

pathology of urticaria

Answer 420

- mas cell degranulation with UVR or visible light as a signal - IgE probably - transimissible serum factor

Question 421

diagnosis of solar urticaria

Answer 421

- clinical dx - quick to develop whereas PLE takes 6 hours and LE days to weeks -body area also maps exposure although some sites eg face can be less sensitive

Question 422

management solar urticaria

Answer 422

``` -UVR or even visible light avoidance H1 blockade an be trialled -gradual increase in UV exposure- HARDENING -omit drug if relevant in hx -omalizumab anti IgE in severe cases ```

Question 423

porphyrias what are they

Answer 423

-rare group of inherited disorders which can affect many organs

Question 424

pathology of porphyrias and which light spectrum

Answer 424

- due to an enzymatic defect in haem biosynthesis with the result that substrate prior to the enzyme block build up - get build up of porphyrin and porphyrin precursors - some of these precursors are photosensitive so cause the cutaneous reaction - upon exposure to blue visible light (>400nm) these photosensitiers release free radicals that cause inflammation

Question 425

diagnosis of porphyrias

Answer 425

-measure porphyrins in either blood, plasma or stool

Question 426

two main types of derm porphyrias

Answer 426

- porphyria cutanea tarda PCT | - erythropoietic protoporphyria EPP

Question 427

main cause of porphyria cutanea tarda

Answer 427

usually the result of any liver damage eg alcohol viral hepatitis coupled with an inherited predisposition

Question 428

clinical features of porphyria cutanea tarda

Answer 428

- most on back of hands and on face - rash does NOT immediately follow UVR - physical signs are - erosions, blisters, crusts - milia= end result of above - hyperpigmentation and hypertrichosis- most seen on temples - hypertrichosis= excess hair growth

Question 429

diagnosis of PCT

Answer 429

-clinical biopsy porphyrins levels

Question 430

treatment PCT

Answer 430

- treat underlying liver disease - phlebotomy every 2 weeks - chloroquine is useful

Question 431

erythropoietic protoporphyria EPP when is the onset

Answer 431

usually early childhood | -can present later in life

Question 432

small child starts screaming within minutes of being placed in sunshine and then develops a rash

Answer 432

EPP

Question 433

clinical features of EPP

Answer 433

- exposure to sunshine presents with almost immediate burning pain - and erythema and oedema over several hours - waxy plaques and scarring may develop

Question 434

organ complication of EPP

Answer 434

can develop liver disease

Question 435

dx and treatment

Answer 435

- porphyrin levels - sun avoidance and sunblocks - beta carotene

Question 436

diff dx of solar urticaria

Answer 436

- PLE - LE - EPP- so check porphyrins levels

Question 437

pseudoporphyrias what is it

Answer 437

Similar clinical picture to PCT but without measurable abnormalities of porphyrins may be seen in some patients with renal failure or those on NSAID or contraceptive pill

Question 438

examples of phytodermatoses

Answer 438

- psoralen makes you more photosensitive -therefore used in careful doses in PUVA - strimmer's disease -plant sap contains photosensiters

Question 439

presentation of phototoxicity and drug induced photosensitivity

Answer 439

-sunburn like -ertyhema and scaling and peeling -blistering and then marked hyperpigmentation a few weeks later chronic over time can develop eczema or lichen planus like

Question 440

individual uses a strimmer when gardening and wears only shorts. next day he is covered by hundres of linear blisters 10-15 cm long like whipped

Answer 440

strimmer disease -strimmer has cut the plant and released their sap containing topical photosensitisers which have been deposited against the skin and then UVR exposure has caused the phototoxic rash

Question 441

drugs that induce photosensitivity

Answer 441

- quinine - ciprofloxacin - nalidixic acid - some tetracyclines

Question 442

diagnosing drug induced photosensitivity

Answer 442

- phototest patient whilst still on the drug -if reaction is abnormal then stop the drug - re-phototest some time after to confirm change in status as long as rash is not life threatening eg TEN

Question 443

what is SPF

Answer 443

sun protection factor measure of protection against UVR induced erythema eg SPF 2 means 50% of UVR is allowed through 20=5% but in real life and application usually means about 1/3 of this

Question 444

markers of chronic UVR exposure 6

Answer 444

- skin atrophy - back of the hand is thinner eg - telangiectasia- reflects collagen loss - variation in skin vascularity- weather beaten - variation in epidermal melanin pigmentation with both areas of hyper and hypopigmentation - increased fine wrinkling - focal areas of fine scaling reflecting subclinical actinic keratoses

Question 445

solar elastosis presentation and pathology

Answer 445

-alteration in collagen secondary to UVR leads to fragmentation of fibres and an apparent increase in volume yellow appearance cyst and comedones

Question 446

disorders made worse by UVR

Answer 446

- herpes simplex - rosacea - very active psoriasis UVR can provoke a rash and areas of normal sunburn can koebenerise into psoriatic plaques

Question 447

disorders improved with UVR

Answer 447

-psoriasis eczema | acne

Question 448

what is chronic actinic dermatitis

Answer 448

``` -patients are very sensitive to UVR mostly middle aged or older men rash on the nape of neck and face eczema worsened by UVR hx of other dermatitis diagnostic phototesting grossly abnormal ```

Question 449

what are the main morphological types of drug reactions6

Answer 449

- urticaria - TEN - fixed drug - AGEP - DRESS - measles like-maculopapular

Question 450

drugs causing urticaria response

Answer 450

- penicillins | - radiological contrast- but different mechanism through hyperosmolar stress causing mast cell degranulation

Question 451

what is the most common cutaneous reaction to a drug

Answer 451

maculopapular exanthema - measles like

Question 452

presentation of maculopapualr rash

Answer 452

erythematous macular in some places and papular in others sometimes itch

Question 453

how so after taking medication will a maculopapular rash appear

Answer 453

4 to 21 days after | rash seen with glandular fever and penicillin is normally quicker

Question 454

what are important drug reactions

Answer 454

-DRESS -blisters mucosal involvement target lesions of erythema multiforme necrolysis/ TENS

Question 455

TEN management

Answer 455

stop drug ASAP

Question 456

DRESS meaning

Answer 456

drug reaction with eosinophilia and systemic symptoms

Question 457

presentation of DRESS

Answer 457

-widespread rash (erythrodermic) -can be eczematous with or without facial oedema -pupura on lower legs -lymphadenopathy -pyrexia -hepatitis -nephritis

Question 458

how soon after drug does DRESS appear

Answer 458

2 weeks | so may no longer be on drug

Question 459

main precipitants of DRESS 4

Answer 459

carbamazepine phenytoin allopurinol dapsone

Question 460

pathology of DRESS

Answer 460

-much of the reaction seems to be an immunological response to reactivation of latent viral infection such as herpes and CMV

Question 461

prognosis of DRESS

Answer 461

last for several weeks or more | mortality of 10% from hepatitis

Question 462

management of DRESS

Answer 462

supportive care stop causative drug systemic steroids

Question 463

fixed drug reaction presentation and where most common and why name fixed

Answer 463

red round plaques with erythema and even blistering that resolves leaving marked hyperpigmentation rash occurs on a single or multiple body site and reoccur at same site if drug used again hence FIXED most common on genitalia, lips or acral skin

Question 464

assoc. drugs to fixed drug reaction

Answer 464

-NSAID | penicillins

Question 465

what is AGEP

Answer 465

acute generalised exanthematous pustulosis

Question 466

presentation of AGEP

Answer 466

-characterised by a fever and widespread pustular rash that resembles pustular psoriasis

Question 467

management of AGEP

Answer 467

systemic steroids

Question 468

worrying drug reactions

Answer 468

- blister - mucosal disease - TEN - DRESS

Question 469

pigmentary disorders main ones to know

Answer 469

- vitiligo - albinism - melanism

Question 470

what disorders can cause both post-inflammatory hyperpigmentation and hypopigmentation

Answer 470

eczema | DLE

Question 471

what is vitiligo

Answer 471

acquired focal loss of pigmentation due to immunological attack on melanocytes in the skin -no functional melanocytes

Question 472

genetics vitiligo

Answer 472

20% concordance in monozygotic twins | not mendelian

Question 473

clinical features of vitiligo

Answer 473

- sharply demarcated macular areas of depigmentation - symmetrical - hair may lose pigment too - sometimes limited to one or more body segments - genitalia, mouth eyes and hands are preferentially affected

Question 474

assoc. to vitiligo

Answer 474

organ specific autoimmune disorders such as pernicious anaemia and addison's

Question 475

diff dx of vitiligo

Answer 475

- piebladism- if present at birth more likely to be piebaldism which is an inherited pigmentary disorder that clinically resembles vitiligo but is due to a KIT gene mutation - LSEA and pityriasis versicolor - pityriasis alba in eczema - leprosy with loss of cutaneous sensation

Question 476

treatment of vitiligo and prognosis

Answer 476

- no treatment - some resolve spontaneously without treatment - more extensive and longer the worse prognosis - topical steroids and calcineruin inhibitors - phototherapy in dark skin - epidermal transplants - camouflage

Question 477

albinism pathology

Answer 477

autosomal recessive disorders in which the amount of melanin produced by melanocytes is reduced number of melanocytes is the same

Question 478

risks with albinism

Answer 478

- skin cancer more UVR exposure | - poor visual acuity and nystagmus as loss of pigment in retina and iris

Question 479

main gene assoc. to albinism

Answer 479

tyrosinase

Question 480

melasma /cholasma presetnation

Answer 480

appears as brown/ grey patches on the cheeks and forehead commonly seen in pregnancy and is a result of increased melanin pigmentation

Question 481

precipitants of melasma

Answer 481

pregnancy | oestrogen OCP

Question 482

treatment for melasma

Answer 482

-sunscreen azelaic acid topical retinoids

Question 483

how does rosacea differ to acne

Answer 483

- not primarily a follicular disorder | - no comedones

Question 484

clinical features of rosacea

Answer 484

-erythema telangiectasia flushing possible sensory symptoms oedema of facial skin with papules and pustules -rhinophyma= hyperplasia of sebaceous glands with fibrotic overgrowth of derms -ocular symptoms and signs NO COMEDONES

Question 485

where is rosacea most common

Answer 485

nose and cheeks

Question 486

who does rosacea affect

Answer 486

- middle age - pale skin or red hair - worse in men

Question 487

pathology of rosacea 2

Answer 487

unknown not infectious -neurovascular: with transient erythema and flushing leading to persistent erythema and telangiectasia. also get burning skin and vascular changes with oedema -inflammatory: marked perivascular and perifollicular lymphohistocytic infiltrate with sebaceous gland overgrowth and possible graunolma formation

Question 488

what is ocular rosacea and management

Answer 488

- rosacea can affect the eyes without any skin signs or with - blepharitis, keratitis, chalazia, scleritis and uveitis - untreated can lead to corneal scarring - if dont respond to antibiotics then refer to opthalmology

Question 489

what is rhinophyma and cause

Answer 489

gross sebaceous gland hyperplasia and dermal fibrous tissue leading to tissue overgrowth enlarged nose

Question 490

treatment of rosacea

Answer 490

- general skin care- avoid irritants, soaps and UVR - alcohol and spicy food tend to make telangiectasia and flushing worse - topical brimonidine tartare a selective a1a adrengeric agonist improves erythema - lasers for telangiectasia - in mild disease can use topical antibiotics- metronidazole, azelaic acid, ivermectin - if topical agents fail use systemic eg tetracyclines or metronidazole - isotretinoin systemically - rhinophyma requires surgical treatment with dermabrasion or shaving

Question 491

what should you not treat rosacea with

Answer 491

topical steroids | vasoconstriction and then gets worse

Question 492

differentials for rosacea 3

Answer 492

- acne vulgaris- comedones - sebhorreic dermatitis- scaly, nasolabial fold, dandruff -perioral dermatitis hx of steroid use

Question 493

perioral dermatitis clinical features

Answer 493

- most common young women | - presence of papules, pustules and erythema with or without small degree of scaling around the mouth

Question 494

what causes perioral dermatitis

Answer 494

-use of topical steroids on the face or steroid inhalers

Question 495

management of perioral dermatitis

Answer 495

- sudden withdrawal of steroid makes rash worse - need to gradually withdraw steroid - systemic tetracyclines as a cover whilst gradually withdraw steroid

Question 496

advice on prescribing topical steroids for face

Answer 496

DONT PRESCRIBE UNLESS SURE OF DX - make rosacea worse - cause perioral dermatitis

Question 497

sebhorreic dermatitis and dandruff cradle cap clinical features who gets it and where

Answer 497

- erythematous and scaly lesion - seen in areas of rich sebum production - young middle aged adults

Question 498

pathophysiology of seb d

Answer 498

-immunological or inflammatory response to the yeast called pityrosporum which lives and metabolises lipids on skin surface

Question 499

where is seb d commonly found

Answer 499

``` sebum areas -face nasolabial folds forehead upper chest and back ```

Question 500

who is more at risk of getting seb d

Answer 500

immunocompromised eg HIV can be more severe

Question 501

dandruff vs seb d

Answer 501

same process | dandruff is just more mild variant with less erythema on the scalp

Question 502

treatment of seb d

Answer 502

anti-yeast agents - azoles shampoo/ cream- ketoconazole sometimes topical steroids

Question 503

what does severe seb d possibly reflect

Answer 503

underlying HIV infection

Question 504

diff dx

Answer 504

- rosacea- which is red with papules and pustules - seb d is red and scaly -psoriasis- often mixed up

Question 505

lichen planus what is it

Answer 505

lichen planus is an inflammatory disorder of unknown cause characterised by intense itch and presence of violaceous polygonal plaques with frequent oral or mucosal involvement

Question 506

who gets lichen planus

Answer 506

middle age more common | hep c infection

Question 507

prognosis of lichen planus

Answer 507

-remits within 6 months to 1 yr in most but in some it persist

Question 508

clinical features of lichen planus

Answer 508

- individual lesions are violet coloured and flat topped - wickham's striae- lace like pattern diagnostic of LP - different morphological varitiers from annular to blistering - INTENSELY ITCHING

Question 509

main areas affected by lichen planus

Answer 509

wrist, forearms lower legs or feet | also get mucosal and nasal involvement

Question 510

mucosal LP CF

Answer 510

LP can affect the oral mucosa and the genitalia where ulceration or erosion can occur - see white mesh like pattern - can affect scalp and cause scarring alopecia

Question 511

nails LP

Answer 511

LP affects the nails where it may cause thinning, longitudinal ridging and a widespread pattern labelled as trachyonychia (where all the nails appear very thin with extensive shallow pits ) scarring and destruction of the nails can occur

Question 512

lichen planus pathology

Answer 512

LP seems to be a T cell mediated disease in which it appears as though the body is trying to reject or kill off many of the keratinocytes T cell infiltrate hugging the epidermis with occasional apoptosed keratinocytes called cytoid bodies features resemble some changes seen in cutaneous graft vs host disease

Question 513

diagnosis of lichen planus

Answer 513

usually clinical | histology can be helpful

Question 514

diff dx of lichen planus

Answer 514

lichenoid drug reactions -T cell hugging the epidermis

Question 515

treatment of lichen planus

Answer 515

-sedative antihistamines for itch -topical steroids -topical calcineurin inhibitors short term systemic steroids ciclosporin

Question 516

complications of lichen planus

Answer 516

-scarring alopecia- leads to total hair loss- wont regrow -severe oral disease genital disease

Question 517

two causes of scarring alopecia

Answer 517

lichen planus | LE

Question 518

systemic lupus erythematous features

Answer 518

-butterfly +/- more extensive rash | systemic on heart , kidneys ...

Question 519

what is discoid lupus erythematous CF

Answer 519

produces red scaly plaques most commonly on face and head producing and leading to scarring usually photosensitive rash so made worse by UVR exposure and if involving hair areas causes scarring alopecia post-inflammatory hypopigmentation or hyperpigmentation may occur

Question 520

diagnosis of DLE

Answer 520

clinical suspicion biopsy serology unhelpful as DNA markers often absent

Question 521

treatment DLE

Answer 521

-avoid sun use sun block topical steroids antimalarials

Question 522

sub acute lupus eythematous what is it

Answer 522

-half way house between DLE and systemic lupus -some progress to systemic more likely to have antibody serology than DLE

Question 523

presentation of sub acute lupus

Answer 523

- photosensitivity - scaly red placques over face or upper trunk which resemble psoriatic plaques or can get annular lesions with central clearing and scale often sun exposed sites eg shoulder, backs, chest and arms scarring uncommon but can get depigmentation

Question 524

diagnosis of sub acute LE

Answer 524

biopsy serology - Ro AND La are often positive phototesting clinical

Question 525

treatment of sub acute LE

Answer 525

- widespread so topical steroids less useful - antimalarials - work less well than DLE - systemic steroids

Question 526

lupus tumidus presentation

Answer 526

patients develop erythematous nodules almost resembling urticaria (which are fixed) and generally without scale -photosensitive

Question 527

lupus profundus what is it

Answer 527

deeper inflammation of sub-cutaneous tissue

Question 528

pityriasis rosea presentation

Answer 528

- very common - rash characterised by annular erythematous patch with a colarette of scale - initial lesion often on upper chest is known as herald patch consisting of a pink brown patch or plaque with a raised edge - a week to 10 days later numerous other scaly red lesions develop most commonly on trunk - chrisstmas tree - tends to be mildly itchy

Question 529

diagnosis of pityriasis rosea

Answer 529

-dont need biopsy | -

Question 530

cause of pityriasis rosea

Answer 530

response to a virus

Question 531

diff dx pityriasis rosea

Answer 531

herald patch- eczema, ringworm trunk - syphilis, psoriasis

Question 532

management pityriasis rosea

Answer 532

-none | may give topical steroids or emoilients to help

Question 533

icythoses pathology

Answer 533

-widespread scaly lesion where inflammation is not usually prominent -epidermis -mutations in proteins important for kertainocyte differentiation eg filaggrin , transglutaminase or producion of lipids eg steroid sulphatase deficiency or caused by an internal malignancy therefore -most are inherited but some are acquired

Question 534

icythosis vulgaris mutation

Answer 534

filaggrin gene

Question 535

presentation of ichythosis vulgaris

Answer 535

- diffuse polygonal scaling - tends to spare flexures - keratosis pilaris-rough and bumpy skin - hyperlinear palms

Question 536

assoc. to icthosis vulgaris

Answer 536

1/3 of patients will have atopic dermatitis as filaggrin mutations are also assoc. with atopic dermatitis (atopic dermatitis usually only have mutation on one allele whereas IV have on both)

Question 537

inherited vs acquired ichythosis

Answer 537

acquire develops in adulthood inherited either at birth or develops in childhood

Question 538

cause of acquired ichythosis

Answer 538

-underlying malignancy usually lymphoma night sweats and weight loss -drugs malnutrition

Question 539

what is keratosis pilaris

Answer 539

-in half of the population so very normal -occurs on backs of upper arm and over triceps in young people -follicular plugging with a rim of erythema around the follicle no symptomatic

Question 540

assoc. keratosis pilaris

Answer 540

ichythosis | atopic eczema

Question 541

erythroderma what is

Answer 541

refers to widespread erythema >90% involvement of body or papulosquamous rash very uncomfortable

Question 542

commonest causes of erythroderma

Answer 542

- psoriasis - atopic dermatitis or other eczema forms - drug reactions - cutaneous T cell lymphoma

Question 543

rarer cause of erythroderma

Answer 543

undlering malignancy lymphomas especially

Question 544

risks and management of erythroderma

Answer 544

- fluid loss: as thermoregulation is impaired and sweat gland duct occlusion can lead to an inability to lose heat causing hyperthermia. Or can be hypothermic due to volume of blood flowing near surface - hypothermia is often concealaed and more likely one- as patient looks hot and feels warm to touch but the core temp is reduced - rigours, shivers and malaise

Question 545

management of erythroderma

Answer 545

``` -admit skilled nursing emoilients topical steroids systemic steroids ciclosporin retinoids watchful waiting ```

Question 546

necrobiosis lipoidica presentation

Answer 546

- YELLOW or red patch with marked telangiectasia that looks like "lipid" - mainly on shins - can be raised but can be atrophic or ulcerate

Question 547

necrobiosis lipoidica condition assoc.

Answer 547

diabetes

Question 548

treatment of Necrobiosis

Answer 548

- watchful waiting can be better - topical steroids - systemic steroids

Question 549

granuloma annulare presentation

Answer 549

another necrobiotic disorder | -annular lesions made up of lots of individual papules, nodules with a smooth skin surface and no scale

Question 550

histological features of necrobiosis

Answer 550

collagen with histiocytes appearance | shows necrobiosis

Question 551

treatment of granuloma annulare

Answer 551

-most resolve no treatment -topical steroids intralesional steroids

Question 552

lichen sclerosis et atrophicus LSEA WHAT DOES it affect

Answer 552

skin or mucosa or genitals

Question 553

presentation of LSEA

Answer 553

- atrophic wrinkled skin - white - atrophy of dermis can lead to blistering and bleeding into blisters - scarring

Question 554

risk of LSEA

Answer 554

Chronic risk of LSEA on genitals is assoc, with an increased risk of SCC and may lead to narrowing of the urethral meatus and destruction of the introitus secondary to scarring

Question 555

management of LSEA

Answer 555

- topical steroids eg clobetasol propionate | - of if penile involvement extensive- circumcision

Question 556

Morphoea presentation

Answer 556

classically presents initially as a violet macule, which develops central sclerosis with a lilac ring - atrophy - can involve fascia, muscles or bones

Question 557

morphoea prongosis

Answer 557

- usually mild and spontaneously resolves | - more severe variants include muscle and bone

Question 558

treatment for morphoea

Answer 558

-topical steroids -systemic steroids PUVA

Question 559

erythema ab igne cause

Answer 559

secondary to infared damage to blood vessels due to sitting close to radiators or a fire -reticular pattern reflects normal vessel anatomy -elderly -blue red reticulated pattern that leaves permanent or semi-perm hyperpigmentation granny tartan

Question 560

keloids what are they and cause

Answer 560

-keloids occur following surgery or inflammatory processes such as acne when instead of a neat scar developing there is an overgrowth or excess producion of collagen

Question 561

where and who are keloids most common

Answer 561

-upper 1/3 body -african ancestry young people strong fhx poor surgical technique infection

Question 562

treatment of keloids

Answer 562

- intralesional steroids | - re-excision of lesion can be considered after this but can make it worse

Question 563

two clinical types of impetigo

Answer 563

bullous- less common | non-bullous- more common

Question 564

what causes impetigo 2

Answer 564

-staph aureus | beta haemolytic strep can cause non bullous

Question 565

pathology of impetigo

Answer 565

- self-inoculation of pathogenic bacteria elsewhere on skin or in the nasophraynx or sometimes following an insect bite or atrophic dermatitis induced scratching - blisters in staph impetigo are due to local toxin production against desmoglein 1 only

Question 566

clinical features of impetigo 5

Answer 566

- most commonly seen in children on face around nose and mouth - early lesions are characterised by presence of small vesicles which may be clear and rupture. subsequently blisters >1cm ,which are pus filled may then be seen - usually surrounded by scabs and characteristic golden crusted exudate - lesions may itch and scratching results in further inoculation of surrounding areas - leucocytosis is common, lymphadenopathy

Question 567

treatment of impetigo and diagnosis

Answer 567

- sample the blister or swab - crust remove with wet dressings - topical antibiotics eg mupirocin or fusidic acid if localised - topical antiseptic eg chlorhexidine - systemic anti-staph flucox or cephalosporin

Question 568

complication of impetigo

Answer 568

-glomerulonephritis

Question 569

folliculitis what is it

Answer 569

inflammation centrered around hair follicle

Question 570

cause of folliculitis

Answer 570

infective bacteria or fungi non infective mostly bacterial and self -limiting

Question 571

presentation of folliculitis

Answer 571

- inflammation around hairs-erythema - can be pain and itch - pustule looking things but not pustules as if a pustule is centered on a follicle then it is folliculitis - can also get actual pustules not centered around the follicles

Question 572

folliculitis boil presentation

Answer 572

furuncle deeper and larger and more painful focus of infective folliculitis if larger called a carbuncle - which get many boils clustered together so have multiple openings

Question 573

most common infective causes of folliculitis

Answer 573

-staph candida herpes simplex gram negative- seen in patients who have been treated with tetracyclines or other abx for acne

Question 574

non infective causes of folliculitis

Answer 574

emoilients or tar therapy

Question 575

predisposing factors for folliculitis

Answer 575

- excess sweating - occlusion and maceration - obesit and diabetes - topical or systemic steroids - oilu skin care preparations eg emoilients greasy or tar

Question 576

what is blue jean folliculitis refer to

Answer 576

refers to folliculitis that appears secondary to friction and maceration from wearing tight clothes against skin also truck drivers

Question 577

what is hot tub folliculitis and what causes it

Answer 577

-infection from pseudomonas

Question 578

treatment of folliculitis

Answer 578

- most resolve spontaneously - topical antiseptics eg chlorhexidine if needed - topical chemotherapeutic agents such as fusidic acid or mupirocin

Question 579

cellulitis what is it

Answer 579

cellulitis is inflammation of the deep dermis and subcutaneous tissue usually due to infection

Question 580

what is erysipelas

Answer 580

inflammation usually due to strep infection of the deep dermis

Question 581

erysipelas vs cellulitis

Answer 581

- erysipelas more common face - erysipelas has sharper and palpable edge but dont get too hung up in difference just call both cellulitis if in doubt

Question 582

clinical presentation of cellulitis

Answer 582

- elderly - unilateral area of erythema on the lower leg with oedema, pain and local warmth - rarely can get blisters - pyrexia and malaise - elevated WCC - negative blood culutres usually - signs of severe sepsis can be present - occasionally can be ascending painful lymphangitis and lymphadenopathy - sometimes obvious focal for bacterial entry - local wound - can affect any region - broaden antibiotics for immunosuppressed

Question 583

main causative agent of cellulitis

Answer 583

-strep or staph

Question 584

diagnosis of cellulitis

Answer 584

frequently over diagnosed | clinical dx

Question 585

treatment of cellulitis

Answer 585

- IV abx eg benzylpenicillin and flucox | - sometimes oral can be used

Question 586

diff dx of cellulitis

Answer 586

- contact allergic eczema - often on bacground of venous disease - necrotising fasciitis -erythema, malaise, collapse, crepitiations -pseudocellulitis- hypodermitis but actually represents an early stage of lipodermatosclerosis secondary to venous insufficiency usually bilateral with erythema skin thickening tightness and no systemic features - panniculitis- erythema nodosum- vasculitis - carcinomous infiltration eg breast -rare

Question 587

dermatomyophyte infections tinea clinical presentation

Answer 587

- annular erythematous scaly eruption with or without pustules - active edge-hence the phrase ringworm

Question 588

diff dx tinea

Answer 588

eczema

Question 589

management of tinea 2

Answer 589

- topical agents eg azole cream | - topical terbinafine

Question 590

when does topical azole cream not work for tinea 3

Answer 590

- scalp dermatophyte infection - dermatophyte infection of nails - tinea incognito

Question 591

dx of tinea skin disease

Answer 591

do A SCRAPING IF IN DOUBT

Question 592

scalp tinea presentation

Answer 592

``` -erythema alopecia scale pustules kerion: boggy inflammation swelling ```

Question 593

treatment of scalp tinea

Answer 593

-need also systemic treatment with oral terbinafine or systemic azoles or griseofulvin

Question 594

presentation of tinea nails

Answer 594

pitting ridging oncholysis dystrophy

Question 595

treatment of tinea nails

Answer 595

need systemic terbinafine or systemic azoles | >3 months for nails

Question 596

IMPORTANT note regarding tinea treatment

Answer 596

NEVER COMMENCE TREATMENT OF TINEA WITHOUT TAKING A SCRAPING AND GETTING A POSITIVE DX

Question 597

what is tinea incognito

Answer 597

when tinea has been misdx as eczema and topical steroids applied -initially both dr and patient think it is getting better but the steroids dampen down the immune response, resulting in spread of the fungal infection which subsequently flares with marked erythema and pustules when steroids are stopped

Question 598

candida risk factors

Answer 598

diabetes pregnancy steroids or immunosuppression occult neoplasia

Question 599

angular stomatitis / cheilitis may indicate

Answer 599

ill fitting dentures | and treat with steroid/ azole cream

Question 600

cutaneous candida location

Answer 600

favours warm moist areas such as under breasts, folds of skin due to obesity (intertriginous areas)

Question 601

presentation of cutaneous candida

Answer 601

-presents as satellite lesions well demarcated bright red areas little bit of scaling

Question 602

diff dx of candida

Answer 602

- psoriasis and eczema | - in children in nappies diff dx is irritant dermatitis secondary to ammonia

Question 603

how to differentiate candida from irritant dermatitis nappy rash

Answer 603

- candida penetrates the depths of folds | - irritant dermaitits does not permeate the skin folds as ammonia doesnt

Question 604

treatment of candida

Answer 604

azole and steroid cream

Question 605

complication of candida in men

Answer 605

can cause balantitis | sexual intercourse

Question 606

pityriasis versicolor cause

Answer 606

due to yeast infection malassezia

Question 607

when is pityriasis versicolor often noticed

Answer 607

after a summer holiday

Question 608

presentation of pityriasis versicolor

Answer 608

presents as a dull red/ light brown scaly plaques on upper chest and back which when scratched release abdundant scale but upon exposure to sun the affected area often appears paler than the surrounding area and progresses to leave pale non scaly areas which are most apparent after sun exposure

Question 609

dx of pityriasis versicolor

Answer 609

can be done using the scale and potassium hydroxide

Question 610

treatment of pityriasis versicolor

Answer 610

imidazole shampoo eg ketoconazole | can recurr

Question 611

common warts verrucae vulgaris presentation

Answer 611

- typically acral so on hands and feet in younger children - hyperkeratotic plaques or nodules - point like dermal vessles or black specks - in flexures can be more papillomatous - on feet pressure forces them inwards so can be painful

Question 612

what virus is assoc to viral warts

Answer 612

HPV

Question 613

risk factor for viral warts

Answer 613

immunosuppressed

Question 614

what are plane warts

Answer 614

also HPV infections commonly seen on back of hands or face as tiny little flat topped papules which often markedly pigment after sun exposure

Question 615

treatment of HPV warts

Answer 615

- salicylic acid - cryotherapy - curettage - electrodessication - contact sensitiers - laser

Question 616

molluscum contagiosum cause

Answer 616

due to pox virus infection spread by direct contact

Question 617

risk factors for mollscum

Answer 617

mostly in children | if in adults think immunosuppression eg HIV

Question 618

presentation of molluscum

Answer 618

- lesion, papules or nodules have a characteristic shiny white centre and central umbilication - in childhood often get eczema around and bleeding due to scratching

Question 619

management molluscum

Answer 619

leave alone | 6months should disappear

Question 620

herpes simplex presentation

Answer 620

-gingivo-stomatitis often in young children with oral ulcers and blisters can be systemic disturbance recurrent as latent herpes simplex labialis= cold sores

Question 621

signs of reactivation of simplex

Answer 621

-tingling sensation papule formation clustering or grouping of lesions blister formation

Question 622

what precipiates re-occurrence of simplex

Answer 622

- UVR exposure | - other illnesses eg fever blisters

Question 623

treatment of uncomplicated cutaneous herpes simplex

Answer 623

topical aciclovir | but needs to be early in the onset

Question 624

eczema herpeticum who gets it

Answer 624

mostly in children with atopic dermatitis

Question 625

presentation of eczema herpeticum

Answer 625

- hundreds or thousands of punched out ulcerated lesions - children become sick and pused to be fatal due to pneumonia or encephalitis - misdiagnosed as impetiginised eczema

Question 626

dx and treatment of eczema herpteicum

Answer 626

skin scrapings and PCR

Question 627

management of eczema herpeticum

Answer 627

systemic aciclovir not topical

Question 628

herpes neonatorum is

Answer 628

primary infection with herpes simplex from a HSV mother during childbirth to infant

Question 629

management of mother with active genital herpes

Answer 629

do a c-section

Question 630

herpes varicella zoster virus | how is chicken pox spread

Answer 630

via air droplets | incubates for 3 weeks

Question 631

presentation of chicken pox

Answer 631

start as red macules then form vesicles, pustules and then crust occurs in crops so different stages of evolution in different crops -itchy so get scratched off leaving scars

Question 632

where does VZV remain after chickenpox

Answer 632

in dorsal root ganglion

Question 633

why is primary varicella or chicken pox a problem in adults

Answer 633

they get a more severe illness with pyrexia malaise and potentially fatal varicella pneumonia -immunocompromised

Question 634

why is primary varicella or chickenpox an issue in pregnancy

Answer 634

in first trimester causes foetal abnormalities in third trimester can cause spontaneous abortion or premature birth also risk if close to birth the child will be born with disseminated varicella at birth

Question 635

shingles percentage

Answer 635

10-20%

Question 636

presentation of shingles

Answer 636

dermatomal pattern of vesicles on red base which then pustulate crust and may scar pain usually preceds the lesion

Question 637

complication of shingles

Answer 637

-post herpetic neuralgia- chronic pain following -trigeminal involvement ocular kertitis facial nerve palsy

Question 638

treatment of shingles

Answer 638

aciclovir can shorten course | if immunosuppresed should use IV agents

Question 639

scabies presentation and cause

Answer 639

-sarcoptes scabei mite -very itchy -worse itch at night burrows are linear structures which is where the eggs are laid- usually in palms, soles finger webs -nodules common around nipples and genitalia -excoriation

Question 640

pathology of scabies

Answer 640

produces a type 4 hypersensitivity reaction to the eggs or faeces it produces therefore cell mediated response so symptoms appear 3 weeks following infestiation

Question 641

how do you catch scabies

Answer 641

has to be close physical contact

Question 642

what is crusted scabies

Answer 642

norwegian scabies | -massively hyperkeratotic widespread crusting resembling severe psoriasis

Question 643

risk factors for crusted scabies

Answer 643

down syndrome immunosuppressed unable to scratch

Question 644

dx of scabies

Answer 644

-hx family members and itch -examine the whole patient including genitalia and interdigital folds - can push a needle into the burrow and a mite will attach to the needle and then examine under microscope - need to identify the mite as can lead to under or over treatment

Question 645

treatment of scabies

Answer 645

-permethrin or malathion commonly used- -warm bath -wash bedding and clothin in hot cycle all individuals in close contact need treating otherwise get re-cycle of infection -ivermectin for crusted scabies even carriers or asymptomatic need treatment

Question 646

perdiculosis capitis head lice cause

Answer 646

due to infestation with pediculus humanus capitis itchy scalp with secondary excoriation nits are the eggs

Question 647

treatment head lice

Answer 647

remove them these two treatments only kill off the mites but down remove the nits malathion permethrin

Question 648

pediculosis corporis body lice what is it

Answer 648

-infeciton of body itching scratching and excoriation poor hygiene

Question 649

treatment of pediculosis corporis

Answer 649

washing all clothes

Question 650

what is dermatitis artefacta

Answer 650

- skin lesions that are self -inflicted without any obvious cause - eg blue ink rash - young women using acid to bleach to needles - bizarre rashses that dont fit - level of insight varies - psychology input needed and MDT

Question 651

cutaneous dysmorphobia what is it

Answer 651

-patients presents with a mark on their skin which to all intents and purposes seems trivial but is having a sever impact on their life

Question 652

delusions of infestation- parasitophobia

Answer 652

- say they want help as various creatures living on their skin - need psychiatric input - can respond to neuroleptic pimozide

Question 653

Non accidental injury what skin diseases can be mis diagnosed as it

Answer 653

-LSEA | ehlers danlos syndrome get easy bruising and scarring as first cutaneous signs

Question 654

hyper pigmentation signs in pregnancy

Answer 654

linea nigra melasma or cholasma- which is the deep brown/ grey pigmentation of the skin most prominent on the cheeks and forehead (also seen on those on COCP) -hyperkeratosis can occur in some women on the nipples

Question 655

what happens to melanocytic nevi in pregnancy

Answer 655

increase in size darken or become more vascular

Question 656

what can happen at stretch marks

Answer 656

can get PEP or PUPP

Question 657

what can change about hair in pregnancy

Answer 657

can get hypertrichosis | and after birth telogen effluvium

Question 658

what happens to eczema in pregnancy

Answer 658

tends to get worsse

Question 659

what happens to psoriasis in pregnnacy

Answer 659

tends to get better

Question 660

pemphigoid gestationis presentation

Answer 660

blister disease in pregnancy

Question 661

diagnosis of pemphigoid gestationis

Answer 661

pathology (eosinophils and subepidermal blisters) | immunoflourosence positive c3 and IgG on basement membrane

Question 662

management of pemphigoid gestationis

Answer 662

topical steroids sedative antihistamines systemic steroids may be required

Question 663

risks of pemphigoid gestationis

Answer 663

-can be increased risk of prematurity and small for dates | greater severity greater risk

Question 664

main diff dx of pemphigoid gestationis

Answer 664

PEP

Question 665

prognosis of pemphigoid gestationis in future pregnnacies

Answer 665

if same father then rash likely to recur and be more severe in future pregnancies usually flare at time of delivery

Question 666

polymorphic eruption of pregnancy what is it

Answer 666

common | polymorphic different presentation

Question 667

presentation of PEP

Answer 667

-itchy red papules in the third trimester close to birth or just after delivery -can also see widespread erythema and small vesicles -plaques of eczema like lesions are located preferentially in striae sparing of umbilical region is characteristic rash spreads from abdomen to other parts of trunk and limbs

Question 668

pep vs pemphigoid gestationis

Answer 668

pemphigoid gestationis - doesnt favour striae - doesnt avoid the umbilicus - tends to occur earlier in the final trimester or before - biopsy for it looks like pemphigoid - pemphigoid is less common and can occur in future pregnancies

Question 669

treatment of PEP

Answer 669

-steroids and antihistamines | systemic steroids occasionally

Question 670

intrahepatic cholestasis of pregnancy presentation

Answer 670

-intense generalised pruritus usually in the late second or third trimester -no primary skin lesions just excoriations as its itchy

Question 671

inx for intrahepatic cholestasis

Answer 671

serum bile acid raised

Question 672

risks of intrahepatic cholestasis

Answer 672

can be risk of foetal loss, prematurity and foetal distress

Question 673

management of intrahepatic cholestasis

Answer 673

make sure no primary skin disease caushing itch and leave to obstetrics

Question 674

atopic eruption of pregnancy what is it

Answer 674

-most common itchy disorder of pregnancy and can either occur in those who are known to have atopic dermatitis or atopic -eczematous and papular with or without xerosis atopic dermatitis

Question 675

when does atopic eruption of pregnancy tend to occur

Answer 675

first trimester

Question 676

management of atropic eruption of pregnancy

Answer 676

as for atopic dermatitis with topical agents

Question 677

parvovirus rash is

Answer 677

slapped cheek

Question 678

risk of slapped cheek rash contact

Answer 678

-risk in pregnancy is to the foetus if the mother has no immunity foetal loss dx based on IgM obstetrics

Question 679

drugs for derm that need consideration in pregnancy

Answer 679

- systemic retinoids - methotrexate; both men and women - azathioprine- avoid in pregnancy - sedative antihistamines -chlorphenamine can be used cautiously - avoid non sedative - PUVA is not safe - UVB is safe - topical steroids can be used but may change dose and potency -discuss with obstetrics - tetracyclines dont use - use erythromycin

Question 680

hirsutism is

Answer 680

male pattern of growth of hair in females

Question 681

hypertrichosis

Answer 681

excessive hair on any part of the body -may involve lanugo, vellus or terminal hair mostly vellus hairs becoming terminal

Question 682

3 stages of hair cycle

Answer 682

anagen catagen telogen

Question 683

hirsutism conditions to consider 4

Answer 683

congenital adrenal hyperplasia adrenal tumours cushing PCOS

Question 684

inx for hirsutism

Answer 684

-hx menstrual periods, fhx other signs of virilisation- enlarged clitoris, hirsutism, acne ``` inx -testosterone sex hormone binding globulin prolactin DHEAS dehydropiandrosterone sulphate ```

Question 685

management of hirsutism

Answer 685

-non cutaneous cause refer to endo for most there is no underlying endo cause to be found -local treatment- wax, bleach, elctrolysis laser topical eflornithin an orthinine decarboxylase inhibitor endocrine give anti androgens eg finasteride or cyproterone with oestrogens

Question 686

hypertrichosis is

Answer 686

growth of hair longer and thicker and more obvious that would expect at different sites switch from vellus to terminal

Question 687

conditions that get hypertrichosis 4

Answer 687

malnutrition anorexia dermatomyositis porphyria cutanea tarda

Question 688

what is androgenic alopecia

Answer 688

male pattern baldness | reflects sensitivity to androgens resulting in a change from terminal hairs to vellus hairs and then loss of hairs

Question 689

treatments for adnrogenetic alopeccia

Answer 689

- minoxidil topical - systemic finasteride - hair transplant from posterior occiput

Question 690

telogen effluvium is

Answer 690

a clinical syndrome of hair loss several months after a major life event eg pregnancy or illness the insult causes many hairs to exit anagen simultaneously into catagen several months later they then fall out into telogen synchronously - so lots of hair fall out at once which makes it obious the hair does return when the hair cycle gets back into asynchronous

Question 691

chemotherapy induced effluvium

Answer 691

- rapid loss of hair over days seen in patients who are on chemo - cytotoxics destroy fast dividing cells eg hair follicles

Question 692

mechanism of chemo induced effluvium

Answer 692

-premature move to catagen anagen hairs falling out later telogen loss can sometimes be irreversible hair loss if hair stem cells killed by chemo

Question 693

alopecia areata is

Answer 693

characterised by sharply demarcated coin shaped areas of hair loss mostly on scalp or beard -any age common in early adulthood or childhood

Question 694

alopecia areata clinical sign

Answer 694

exclamation mark hairs- bulb of follicle becomes dot as get broken hair stumps non scarring

Question 695

prognosis of alopecia areata

Answer 695

-non scarring most it regrows normally can be white initially and then darkens can get over whole body alopecia totalis

Question 696

management of alopecia areata

Answer 696

-watch and wait -topical steroid injection induction of contact allergic sensitivity can stimulate hair growth -short burst of systemic steroids early in disease -wig in severe cases

Question 697

chronic diffuse alopecia causes

Answer 697

- most common is androgenetic hair loss - systemic malignancy - renal liver failure - hypo hyper thyroidism - iron deficiency - drugs

Question 698

drugs that can cause a chronic diffuse alopecia

Answer 698

antithyroid retinoids azathioprine

Question 699

2 main causes scarring alopecia

Answer 699

- discoid lupus | - lichen planus

Question 700

neurofibromatosis pathology

Answer 700

autosomal dominant mutations in the neurofibromin 1 NF1 or 2 gene perphieral neurofibromatosis is due to mutations in NF1

Question 701

presentation of neurofibromatosis

Answer 701

-cafe au lait spots >5 is abnormal -axillary freckling neurofibromas (soft, pressure sensation) -flexiform large sub-cutaneous neurofibromas -lisch nodules (iris hamartoma) -CNS tumours (eg gliomas) and tumours elsewhere

Question 702

pathology tuberous sclerosis

Answer 702

autosomal dominant

Question 703

presentation of tuberous sclerosis

Answer 703

- ash leaf macules, oval areas of depigmentation present at birth - connective tissue nevi, known as shagreen patches - angiofibromas, commonly seen on the face - periungal fibromas - seizures and cognitive impairment

Question 704

what is acanthosis nigricans

Answer 704

-presents as brown hyperkeratotic velvety/ warty areas in the axillae, neck and the groins and at other skin friction sites -areas develop lots of skin tags histologically resembles seb k

Question 705

what causes acanthosis nigricans 2

Answer 705

assoc. to underlying malignancies and paraneoplastic phenomenon as they produce circulating growth factors that affect the skin's frictional area - also assoc. to insulin resistance in obesity and type 2 dm

Question 706

dermatomyositis is

Answer 706

an autoimmune disorder more common in women characterised by a range of skin changes and myositis -muscle weakness

Question 707

presentation of dermatomyositis

Answer 707

-proximal muscle weakness before rash or vice versa on skin get - violet lilac rash around the eyes - erythematous rash that can appear in a photosensitive distriubtion - violaceous lichenoid rash along dorsal surface of hands and fingers= gottron's papules - painful cuticles and prominent nail fold capillaries

Question 708

cause of dermatomyositis

Answer 708

also a paraneoplastic disease with 50% having underlying malignancy

Question 709

dx of dermatomysoitis

Answer 709

-skin biopsy looks like LE -serum creatinine kinase can be raised ANA positive in 50% of cases

Question 710

management of dermatomyositis

Answer 710

- inx underlying tumour | - high dose prednisolone

Question 711

children and dermatomyositis

Answer 711

can occur in children but not a paraneoplastic disease

Question 712

hereditary haemorrhagic telangiectasia cause

Answer 712

autosomal dominant small AV malformation not telangiectasia

Question 713

where is HHT seen

Answer 713

lips oral nasal mucosae skin hands and GI

Question 714

presentation HHT

Answer 714

flat red spots nose bleeds anaemia

Question 715

what causes destruction of the nails

Answer 715

``` -psoriais lichen planus immunobullous SCC melanoma ```

Question 716

what is oncholysis

Answer 716

separation of the distal nail from nail bed

Question 717

diseases causing oncholysis

Answer 717

-psoriasis dermatophyte infection trauma thyroid rare

Question 718

what causes pitting of nails

Answer 718

psoriasis eczema lichen planus- trachyonychia alopecia areata

Question 719

what causes ridges in nails

Answer 719

psoriasis eczema fungal

Question 720

what causes horizontal ridging in nails mees lines beau reil grooves

Answer 720

cytotoxics | trauma

Question 721

what does myxoid cyst represent

Answer 721

cystic outgrowth from the distal joint gelatinous material can be expressed from cyst if ruptured pressure from cyst causes nail dystrophy due to pressure on nail matrix

Question 722

management of myxoid cyst

Answer 722

-surgery if symptomatic

Question 723

kolionychia what it is and sign of

Answer 723

sign of iron deficiency | spoon like

Question 724

what causes green nails

Answer 724

colonisation of pseudomonas aerguinosa | topical abx

Question 725

what is melanoychia

Answer 725

brown longitudinal streak in nail

Question 726

what is melanoychia a sign of

Answer 726

-common in people with dark skin | but in light skin it either reflects a benign nevus pigmentation or a melanoma - use Hutchinson's sign

Question 727

hutchinson's sign

Answer 727

pigmentation in the nail fold likely to be melanoma spread of pigmentation from a nail to the surrounding skin

Question 728

inx of melanoychia

Answer 728

exposure of dorsal matrix and biopsy | surgery if suspect melanoma

Question 729

main cause of blue black nail 2

Answer 729

haematoma- possible hx of trauma | melanoma - Hutchinson sign

Question 730

paronychia is

Answer 730

inflammation around the nail usually due to chronic infection gaining access via an abnormal cuticle eg in eczema

Question 731

main cause of acute paronychia

Answer 731

staph infection- pain swelling erythema

Question 732

who gets chronic paronychia

Answer 732

-atopic industrial exposure of hands chronic candia infection?

Question 733

management chronic paronychia

Answer 733

-topical anti candida agents with or without steroids

Question 734

erythema nodosum causes

Answer 734

``` N-not known idiopathic O- ocp, pregnancy drugs-penicillins o s-sarcoidosis u-ulcerative colitis, crohn, bechet m-microscopy-strep mycobacteiral and malignancy ```