Dermatology

** How does Cutaneous Tb- lupus vulgaris present? KEY LANGUAGE TO REMEMBER

"Apple jelly appearance" Primary inoculation into skin in someone with partial immunity

** What is scabies ?

- Scabies is a very itchy rash caused by a parasitic mite that burrows in the skin surface -may have hx od contact with symptomatic individuals -pruiritis worse at night Risks : > Poverty and overcrowding > Institutional care, such as rest homes, hospitals, prisons > Refugee camps >Individuals with immune deficiency or that are immune suppressed >Low rates of identification and proper treatment of the disease. Clinical presentation >Normally infest: web spaces between the fingers, on the palms and wrists. They may also be found on or in elbows, nipples, armpits, buttocks, penis, insteps and heels >Linear burrows ( may be tortuous) or rubbery nodules - can get secondary eczema & impetigo Pathophysiology Scabies rash is a hypersensitivity reaction that arises several weeks after initial infestation Investigations- skin scrape and extraction of the mite , view under microscope Management- Scabicide eg. permethrin/malathion Antihistamines

Atypical Mycobacteria

- mycobacteria not causing TBC or leprosy - acquired via enviornment (no interhuman transmisson, opposite to TBC) - mostly cause lung disease, lymphadenitits or affects skin - M. mariunum, M.avium, M.bovis?

Endogenous and mixed Atopic Asteatotic eczema

-Crazy-paving/ dried up riverbed pattern -Dry, red, itchy, slightly scaly, excoriated ill defined patches often with polygonal fissuring - Common condition -Males>females -Barrier dysfunction Risk Factors -Age -Low environmental humidity -Exposure to soaps, and irritants -Family history of condition

Endogenous and mixed Atopic Varicose eczema

-Lower legs -Associated with varicose veins, peripheral oedema, asteatotic and atopic eczema - Can become generalised - Scaly, itchy, dry, sometimes weepy, ill-defined erythema, may leave pigmentary changes -Prevalence 6-7% of over 50 years 20% of over 70 years Female>Male Risk Factors - Varicose veins -Pregnancy - Obesity - Immobility - Previous DVT

Endogenous and mixed Atopic Lichen Simplex

-Single or few plaques of lichenification - Due to repeated rubbing/scratching Common sites: Women : nape of neck Men : lower leg Both :anogenital ( anus and genitals0

** What is Henoch schoenlein purpura (HSP)?

-Subset of small vessel vasculitis -assoc. w. IgA -other organ involvement: affects GI, & renal system * the joints Clinical presenation -purpura on the legs Pathophysiology -antigen induces plasma cells to produce antibody -these form antigen/antibody immune complexes -these are preferentially deposited in small low flow blood vessels -leading to neutrophil activation and vessel wall damage

** What is body dysmorphic disorder?

-fixed ideation on what is perceived to be a defect -can be delusional, meaning there is no perceivable change but to them it is real -very common in patients seeking cosmetic surgery Presentation -hide away from public -overstated fixed belief -skin picking & checking skin or some choose not to look at skin -some may have ideas of reference: thinking other peoples actions are due to the fact that that person is disgusted with them -suicide Mx -pharmaco therapy -CBT -medico-legal

*What is delusional parasitises ?

-monosymtomatic hypochondriacal psychosis : focus on 1 symptom, fixed in beliefs American classification -Primary psychotic DP: delusional disorder but no other psychopathology -secondary functional DP: there is an underlying psychiatric disorder eg schizophrenia bipolar disorder, depression, anxiety state, OCD -Secondary organic DP: there is an underlying organic diagnosis physical or psychiatric: due abuse;hypothyrpidism;;cancer;CVS disease, TB, neurolofgical disorders Symptoms -some believe that they have parasites living in their skin & are fixed in this belief, some bring the parasite in a "matchbox", send it to lab to show patient you believe in them and show them that there are no results from the materials What to look for on examination? -excoriations -skin debris -nails/scalp/genitals -MSE Ix to exclude organise disease, not that necessary to do bloods MX ( treat MIND & SKIN) always exclude non-psychiatric disease eg. scabies Cant find parasites on skin on that occasion but tell patient that you know its real to them Treat with newer psychotropic drugs -Risperidone -Olanzapine -Quetiapine -NOT pimozide ( major tranquilliser, but risk of sudden death & cardiac arrhythmia) -low doses work well as minimal side effects Sometimes these patients have psychiatric com-morbid like depression so add on treatment -SSRIS WITH atypical antipsychotics : citalopram fluoxetine venlafaxine Treat skin too -emollients -abx -topical steroids -occlusion Thse patients can have a folie-a-deux meaning that their loved one believes in their fixed belief too and thinks they have a skin issue -need to treat index patient with psychotropic drugs & skin -treat skin of the others associated with them For best prognosis -patients who are abusing substances should enter rehab and stop substances so their symtoms can improve

Case study -EMERGENCY DERM **32yo 4 day hx increasingly widespread rash started on carbamezapine 2 weeks earlier to help with epilepsy o/e pyrexia & extensive skin erythema & blistering in axillae 1) ddx 2) mx/

1) >Rash with anticonvulsants can be a mild morbiliform rash through to life threatening anticonvulsant syndrome >EM/SJS -Erythema multiforme (EM) is an acute, self-limited, and sometimes recurring skin condition that is considered to be a type IV hypersensitivity reaction associated with certain infections, medications, and other various triggers. Erythema multiforme may be present within a wide spectrum of severity. -Stevens-Johnson syndrome (SJS) is a rare, serious disorder of the skin and mucous membranes. It's usually a reaction to medication that starts with flu-like symptoms, followed by a painful rash that spreads and blisters. Then the top layer of affected skin dies, sheds and begins to heal after several days >TEN Toxic epidermal necrolysis (TEN) is a type of severe skin reaction. Together with Stevens-Johnson syndrome (SJS) it forms a spectrum of disease, with TEN being more severe. Early symptoms include fever and flu-like symptoms. A few days later the skin begins to blister and peel forming painful raw areas. >Anticonvulsant hypersensitivity syndrome 2)Stop drug Assess for other organ involvement Supportive measures for skin

Case study ** 76yo noticed lump on his ear several months at least recently become larger and more painful , uncomfortable to lie on, occasionally bleeds 1) Ddx? 2) Referral?

1) BCC ( months-years) SCC ( painful, weeks- months) Chondrodermatitis nodularis (Winkler disease) - inflammatory condition on ears commonly as people lie 1 sided on ear, mistaken for skin cancer 2) Dermatology 2ww referral

Case study ** 34 yo man comes to casualty with sudden exacerbation of longstanding atopic dermatitis usual uses potent topical steroid & Diprobase (emollient) no other meds feels shivery & unwell face severely affected 1) causes of sudden exacerbation of atopic dermatitis ? 2) initial mx?

1) Herpes simplex virus infection --> Eczema herpeticum Staph. Aureus infection Contact dermatitis 2) Sepsis screen Swab for bacteria and viruses Aciclovir +/- flucloxacillin Analgesia Consider suspending topical steroid

Case study ** 25 yo with severe hand dermatitis. Difficult to control despite potent topical steroid creams eczema in babyhood, no problems in skin until recently went back to work as hairdresser 6 months after maternity leave 1)Which factors in the history are relevant, and why? 2)What investigations would you do? 3)List 6 things you would advise this patient to do in order to look after her hands.

1) History of atopy- reduced barrier function Frequent hand washing with new baby Occupational exposure to irritants and potential allergens -hairdressers -nurses Nickel jewelry ! 2)patch testing 3) Avoid soap Use soap substitute Can someone else wash hair at work? Change nappies at home? Wear gloves Apply emollients Apply topical steroids Continue with hand protection measures even when hands better

Case study -EMERGENCY DERM ** 45yo develops nausea & malaise right lower leg painful red & swollen blisters on foot from a few days earlier 1)ddx 2)signs o/e? 3) ix ? 4)Mx?

1) Soft tissue infection/cellulitis DVT Bullous disorder 2) BP, Temp, oxygen saturation, mental state, state of skin (necrosis, crepitus, rapid progression may suggest necrotising fasciitis) 3)Ix FBC, U&E, LFTs, lactate, glucose, INR Blood cultures, skin swab 3) mx Oxygen IV antibiotics Fluid therapy Reassess for SEVERE SEPSIS with hourly observations

Case study ** 54 yo man with 25 y hx of plaque psoriasis in 30s x3 hospital admissions psoriasis controlled on topical calipotriol & tar preparations until last 12 months, he has more extensive troublesome psoriasis 1)What factors do you think may have contributed to the deterioration of his psoriasis? 2)Formulate three treatment plans with >PROS= relatively safe, effective, no monitoring required, self administered >CONs time consuming, may make unstable psoriasis worse,

1) Stress Time for self care 2) Phototherapy >PROs: relatively safe, effective >CON: time consuming, might not be practical ,risk of burning, UV damage, Systemic therapy >PROs: effective, less time commitment than phototherapy >CONs: need for monitoring, potential for side effects,

Case study ** 62yo morbidly obese female chronic back pain,wheelchair ulceration on both lower legs over last 3 years more painful and exuding more fluid over last 3 weeks practice nurse is dressing the ulcers with an absorbent dressing and using Diprobase as an emollient. The ulcers are superficial but large, involving anterior and posterior surfaces of both lower legs. 1) ddx for lower limb ulceration 2) factors in hx contributing to lads leg ulcers 3) causes of deterioration in longstanding leg ulcers? 4) most effective treatment for this type of leg ulcer

1) Venous Arterial Traumatic/pressure/neuropathic Infection- acute, chronic Diabetic- mixed aetiology Hypertension- Martorell ulcer Malignancy Pyoderma gangrenosum Drugs- Nicorandil, hydroxyurea, anticoagulants Vasculitis Coagulopathies 2) Obesity Leg dependency Immobility 3) Infection Arterial insufficiency Diabetes VTE 4) Compression Elevation

Case study **87 yo 6m history of itchy rash -thought to be eczematous difficult to control with moderate potency steroids large tense blisters on lower legs 1) diagnosis 2) Ix to make diagnosis 3) mx 4) side effects of treatment with systemic steroids & how to monitor this ? 5) what causes blistering in the skin?

1) Very typical for BULLOUS PEMPHIGOID - acquired blistering condition that is common in elderly 2) Clinical picture & skin biopsy for histology and immunofluorescence ( look for autoantibodies) 3) Very potent topical steroids Doxycycline Oral corticosteroids 4)SEs >Diabetes or poor control in known diabetics >Hypertension > Weight gain >Fluid retention, may cause fluid overload >Psychological disturbance 5)Causes: >Coeliac disease -->blisters: igA response >Insect bites-->blistering -->Phytophoto dermatosis: sap of plants -->phototic reaction-->burn-->blister

1)How does diabetes affect skin?

1) Yeast infection due to candida organism -affects moist regions of body especially corner or inside mouth giving candida stomatitis (white patches on tongue), groin ( candida vulvitis) ,under breast, genitalia ( candida balantitis in males produces erythema, scaling, papulues & pustules affecting the foreskin & glans penis NB. characteristic satellite lesions from main body of rash, this distinguishes from other rashes like psoriasis

** When you are suspicious of skin cancer in a patient what further investigations/staging is needed? High RFs for metastasis ?

1) BCC -none 2) SCC because they do metastasise to lymph nodes important to assess to reduce this risk High RFs for metastasis - >2cm breadth>4mm depth -poorly/mod differentiation -not on sun exposed sites -Arising in Bowen's, chronic ulcer or scar -located on Lip or ear pinna : high lightlihood of metastasising -is patient immunosupressed

** What specific diseases arise when Desmoglein 1 ( a type of desmosome ) is targeted by a bacterial infection (rather than genetic mutation or autoantibodies )

1) Bullous Impetigo Bacterial infection: Staph Aureus Staphylococcal toxins can directly weaken and cleave Desmoglein 1 ( a type of desmosome) to form blisters 2) Staphylcoccal Scalded Skin Syndrome(SSSS) Description ● circulating epidermolytic toxin from phage groupII, benzylpenicillin-resistant (coagulase positive) staphylococci ( Staph Aureus) , this bacterial toxin leads to Clevage of Desmoglein 1 ●Commonly seen in infancy and early childhood Clinical presentation ● Develops within a few hours to a few days, and may be worse over the face, neck, axillae or groins ●SSSS usually starts with fever, irritability and widespread redness of the skin. Within 24-48 hours fluid-filled blisters form. These rupture easily, leaving an area that looks like burn ● A scald-like skin appearance is followed by large flaccid bulla ● Perioral crusting is typica ● There is intraepidermal blistering in this condition ● Lesions are very painful ● Sometimes the eruption is more localised ● Recovery is usually within 5-7 days Mx ● Antibiotics (e.g. a systemic penicillinase-resistant penicillin, fusidic acid, erythromycin or appropriate cephalosporin) ● Analgesia

2 main patterns of photosensitivity in skin ?

1) Polymorphic light eruption (PLE) -reaction to UV not heat -pts develop itchy erythamaotus eruption on sun exposed skin, hours or days after going in sun. Goes after a few days in shade -can take several appearances: papulovesicular 2) Drug photosensitivity or chronic actinic dermatitis( -in absence of drug , requires immunisupression & strict light avoidance) -severe erythema & swelling,,sharp cut off from sun exposed and sun sparing areas -drugs with a polycyclic structure: tetracycline, phenylthyzine, amiodorone

Case study ** 32 yo presents with changing mole -Longstanding mole on lowerleg -changed over period of 3-6 months-->bigger and darker -no symtoms -on OCP, fit & well 1) What do you ask in hx? 2) is she at high risk of skin cancer? 3)O/e mole of her leg ABCDE approach 4) Assessment and diagnosis 5) Histology reports a malignant melanoma with Breslow thickness of 1.4 mm with no ulceration What Stage is she? 6) How do you Mx her?

1) Risk factors >age 32 >sun exposure: sunburn badly on 3 occasions in childhood -no sun beds -no excessive occ or recreational sun exposure >Lived in south africa till 14 >skin type 2 >few clinically typical melanocytes naevi >No fhx of MM >no personalty hc of MM >regularly uses high factor suncreen >no hx of immunosuppression of HIV 2) living in SA & Skin type 2 & history of sunburns 3) A- asymmetrical B-irregular borders C- light bits and dark bits, arranged asymmetrically D-bigger than 6mm, 12mm E-evolving yes -scores 5/4 SO enough features in Hx & o/e to be concerned Ugly duckling sign- when one particular lesions thing stands out on the skin ` Scores 3 major + 1 motor =7/10 on Glasgow checklist 4) Dermoscopy ( LED light lens); supports diagnosis of melanoma General skin examination is otherwise unremarkable and there is no palpable lymphadenopathy MX For urgent surgery excision body under LA within 2-mm Margins ( nano margins) Specimen sent for histology 5) Stage 1B Breslow >1-2 mm without ulceration 6) Mx >Check Vitamin D levels -said if they are low, worse prognosis >Staging CT CAP >Offer sentinel lymph node biopsy -same as for breast cancer -take out 1st lymph node that the area drains too, as idea is that is where the cancer would metastases to first -doesnt confer any survival benefit >1cm wider local excision based on breslin thickness >Follow up in secondary care Her results >Vit D: borderline low >no evidence of metastatic melanoma on CT CAP >Negative sentinel lymph node biosy ( SLNB) >1cm wider local excision at the same time as SLNB >follow up in secondary care

** FUNGAL infections 1)What is tinea corporis ? aka ring worm 2) Tinea capitals

1) Tinea corporis is a superficial dermatophyte ( such as Trichophyton rubrum) infection characterized by either inflammatory or noninflammatory lesions on the glabrous skin (ie, skin regions other than the scalp, groin, palms, and soles). Clinical presentation ring of erythematous plaque corporis-affects body 2) tinea capitis ( ringworm of scal-.head) wapitis=head more inflammatory kerion, condition Microsporum canis= common organism

Benign skin tumours **1)What lesions can arise from each layer of the skin? 2) From a pt hx what clues can help you differentiate from benign vs malignancy ?

1) see image 2) multiple lesions--> benign rapid hx-->malignancy

** 1)overall structure of skin? 2) function of each cell type in the epidermis? -composition of each of the 4 layers in the epidermis ? -Pathology of epidermis? 3) cell types in the dermis and function? 4) a)Hair, b)nails c)sebaceous glands d)sweat glands

1)-epidermis follows by dermis overly subcut tissue -skin appendages are structured formed by skin-derived cells like hair, nails, sebaceous glands & sweat glands 2)Epidermis 1)Keratinocytes: Produce keratin as a protective barrier 2)Langerhans' cells:Present antigens and activate T-lymphocytes for immune protection 3)Melanocytes: Produce melanin, which gives pigment to the skin and protects the cell nuclei from ultraviolet (UV) radiation-induced DNA damage =THEY ARE DENDRITIC CELLS IN THE BASAL CELL LAYER OF THE SKIN -melanocytes make melanosomes -melanosomes are packaged and inserted into keratinocytes via dendritic processes -form cap over nucleus of keratinocyte to protect DNA from UV damage -epidermal thickening occurs as a direct consequence of UV exposure to protect DNA from UV damage 4)Merkel cells :Contain specialised nerve endings for sensation Layers of the epidermis 1)stratum corneum ( horny layer): layer of keratin, most superficial layer 2)sstratum granulosum (granular cell layer): so-called because cells lose their nuclei and contain granules of keratohyaline. They secrete lipid into the intercellular spaces. 3)Stratum spinosum(prickle cell layer):differentiating cells 4)Stratum basale ( basal cell layer): actively dividing cells, deepest layer -basement membrane -dermis NB. in areas of thick skin like the sole of the foot there is an extralayer called stratum lucidum beneath the stratum corneum Epidermis pathology: a) changes in epidermal turnover time - e.g. psoriasis (reduced epidermal turnover time) b) changes in the surface of the skin or loss of epidermis - e.g. scales, crusting, exudate, ulcer c) changes in pigmentation of the skin - e.g. hypo- or hyper-pigmented skin 3) Dermis cell types 1) Collagen (mainly) 2)elastin 3) glycosaminoglycans:made by fibroblasts Collective functions of these cells: provide the dermis with strength and elasticity. 4)immune cells 5) nerves, +skin appendages & lymphatic and blood vessels. Dermis Pathology: a) changes in the contour of the skin or loss of dermis e.g. formation of Hair papules, nodules, skin atrophy and ulcers b) disorders of skin appendages e.g. disorders of hair, acne (disorder of sebaceous glands) c) changes related to lymphatic and blood vessels e.g. erythema (vasodilatation), urticaria (increased permeability of capillaries and small venules), purpura (capillary leakage) 4) a) Hair types: 1)lanugo hair (fine long hair in fetus) also present in anorexia nervosa 2) vellus hair (fine short hair on all body surfaces) 3) terminal hair (coarse long hair on the scalp, eyebrows, eyelashes and pubic areas) • Each hair consists of modified keratin and is divided into the hair shaft (a keratinized tube) and hair bulb (actively dividing cells, and melanocytes which give pigment to the hair). • Each hair follicle enters its own growth cycle. This occurs in 3 main phases: 1) anagen (long growing phase) 2) catagen (short regressing phase) 3) telogen (resting/shedding phase) Hair pathology a) reduced or absent melanin pigment production e.g. grey or white hair b) changes in duration of the growth cycle e.g. hair loss (premature entry of hair follicles into the telogen phase) c) shaft abnormalities b)Nails made up of: -a nail plate (hard keratin) which arises from the nail matrix at the posterior nail fold, and rests on the nail bed. • The nail bed contains blood capillaries which gives the pink colour of the nails. Nail Pathology a) abnormalities of the nail matrix e.g. pits and ridges b) abnormalities of the nail bed e.g. splinter haemorrhage c) abnormalities of the nail plate e.g. discoloured nails, thickening of nails c)Sebaceous glands • Sebaceous glands produce sebum via hair follicles (collectively called a pilosebaceous unit). Function: secrete sebum onto the skin surface which lubricates and waterproofs the skin. • Sebaceous glands are stimulated by the conversion of androgens to dihydrotestosterone and therefore become active at puberty. Sebaceous glandsPathology a) increased sebum production and bacterial colonisation e.g. acne b) sebaceous gland hyperplasia d)Sweat glands Function: regulate body temperature and are innervated by the sympathetic nervous system. • 2 types: 1)eccrine sweat glands -universally distributed in the skin. 2) apocrine sweat glands.(PUBERTY!) -found in the axillae, areolae, genitalia and anus, and modified glands are found in the external auditory canal. -function from puberty onwards and action of bacteria on the sweat produces body odour. Sweat glands pathology a) inflammation/infection of apocrine glands e.g. hidradenitis suppurativa b) overactivity of eccrine glands e.g. hyperhidrosis

Case study -EMERGENCY DERM **25yo female NURSE has a fruit salad in restauance feels very unwell develops itchy raised rash(urticaria) tightness in throat & difficulty breathng Her friends call her an ambulance 1)What should her first line management be? 2)What factors in the history may be relevant? What additional questions would you ask? 3)What investigations could be performed?

1)ABCDE > Place the person in a comfortable position. -May prefer to sit up as this will make breathing easier - Lying flat with or without leg elevation is helpful for people with low blood pressure. -If the person feels faint, do not sit or stand them up as this can cause cardiac arrest -Place people who are breathing and unconscious on their side (recovery position) -Pregnant women should lie on their left side to prevent caval compression -Give (IM) adrenaline 1:1000 -anterolateral aspect of the middle third of the thigh (ideally) -Assess the response to treatment after 5 minutes, and repeat IM adrenaline at 5 minute intervals until there has been an adequate response. -Remove the trigger if possible e.g. remove stinger after a bee sting. -After food-induced anaphylaxis, attempts to make the person vomit are not recommended. 2) Known allergies Sudden onset, severity, airway involvement Restaurants should be able to provide allergy guidance, but unintentional exposure to known allergens is less likely in self prepared food 3)IgE, RAST or prick testing

Case study **16yp with no history of skin problems, except for scaly scalp presents with sudden onset of widespread rash on trunk & limbs You diagnose it as guttate psoriasis She is due to go on holidays to Greece in 3 weeks time 1) Ddx? 2)exacerbating factors ? 3) Ix ? 4) Mx for guttate psoriasis

1)DDx Seborrhoeic dermatitis Discoid eczema Pityriasis rosea? Pityriasis lichenoides ? Secondary syphilis Cutaneous T-cell lymphoma 2)Preceding sore throat ? this can exacerbate rash 3) Throat swab, but no good evidence that anti streptococcal antibiotics help 4)Mx >Wait- she is going on a sunny holiday >Emollients >Potent topical steroid/ Vitamin D analogue

**Wound healing (MDEMO LINK) 1) What are the 4 phases of wound healing?

1)Haemostasis ● Vasoconstriction and platelet aggregation ● Clot formation 2)Inflammation ● Vasodilatation ● Migration of neutrophils and macrophages ● Phagocytosis of cellular debris and invading bacteria 3)Proliferation ● Granulation tissue formation (synthesised by fibroblasts) and angiogenesis ● Re-epithelialisation (epidermal cell proliferation and migration) 4)Remodelling ● Collagen fibre re-organisation ● Scar maturation

Case study **87yo man presents with a lesion on the right ear Thinking about lifetime sun exposure and sun damage and other RFs for increased carcinogenesis 1)What will you ask in hx? He tells you: -been there for 18m, weepy and blues but not painful -no past or family hx of skin cancer -skin type 1-2 -stationed in Egypt on national service -o/e has some other crusted areas on head, neck and back of hands **think ACTINIC/SOLAR KERATOSES 2) what helps you differentiate what type of skin cancer this is? 3) he has no cervical lymphandenopahty o/e but has a pearly papule like skin lesion on right ear What diagnosis does this eliminate ? 4) In primary care When do you refer a skin lesion to secondary care? 5) MX?

1)Hx Occupation Lived or worked abroad skin cancer before? family history? genetic predisposition 2) significant sun exposure fair skin Actinic keratoses on backs of hands ( see image), pre-cancerous some dont notice the crusty bits on hand until they bleed 18m significant as SCC: appears over weeks-->months( grows faster) BCC: appears over months-->years Sounds like non-melanoma skin cancer 18m hx is a bit long for an SSC, but appearances could represent SCC 3)SKIN LESION ON EAR -nodular type of BCC( most common), pearly papule -->BCC tend not to grow into lymphomas, it grows locally whereas SCC more lily to metastases into lymph nodes and around body SO reassuring to not feel lymph nodes sounds most like a bCC 4) Skin lesion on ear looked quite severe so refer to secondary care. 2WW 5) Mx is guided by -anticoagulants -immunospuression of pt -general health patient choice The patients is on aspirin and would prefer surgery under LA- day case Excision Case ends: Histology reported as a nodular BCC completely excision Patient is discharged back to primary care Once site of surgery has healed he asks for treatment for the actinic keratoses on his hands -not logical to treat each keratoses -patients dont need treatment tend to be asymptomatic -however there are some topical options

Vascular: common tumours 1)Cherry Angioma 2) Pyogenic Granuloma

1)Multiple small red papular vascular lesions Common in older adults 2) Rapidly developing over 2-3 weeks Red or weepy crusted nodule Trauma induced Young adults and children

Case study ** 35 yo female sudden onset of painful pustules on sole of right foot dry up to leave red brown macule but then another crop appears no meds fungal scrapings negative 1) Diagnosis ? 2)She has been given a tube of Clobestasol Propionate (Dermovate) Ointment by a doctor at a previous consultation but is not sure how to use it. How are you going to advise her? 3)'They also mentioned tablet treatment, which sounds much easier than creams.' What do you think?

1)Palmoplantar pustulosis -Might occur on palms and soles -More common in smokers - Chronic remitting and relaspsing 2) Once daily to any affected areas, consider using under polythene occlusion to feet 3) Consider pros and cons of systemic treatments Acitretin, ciclosporin, methotrexate

Pigment change in skin 1) depigmentation 2)hypopigmentation 2)hyperpigmentation normal skin colour is due to a mixture of melanin, oxyhemoglobin in blood vessels and carotene in stratum corner and subcut fat

1)complete loss of coloure 2) -scarring -post-inflammatroy e.g. pityriasis versicolor ( overgrowth of skin yeast, infection gone but left with areas of hypopigmentation) 3) -localised:usually post inflammatory;occasionaly drugs ( AMIODERONE) -gerneralised: rare, usually serious

** How do you manage acne?

1. Topical treatments, i.e. those that are applied directly to the skin 2. Oral antibiotics -Lymecycline ( tetracycline antibiotic) 3. Oral contraceptive pills - discuss changing OCP to Dianette -contains a combination of drugs that is used to reduce androgens and regulate hormones in women. Cyproterone is an anti-androgen which prevents overproduction of sebum and excessive hair growth in women. Ethinylestradiol is a synthetic version of oestrogen, a naturally occurring sex hormone. Dianette is often prescribed for women who are experiencing the symptoms of Polycystic Ovarian Syndrome (PCOS) such as acne or excessive facial hair as it can help with regulating periods too. 4. Isotretinoin capsules ( secondary care) -work after 7-10 days, great outcome -4 weeks of 0.5mg/kg/day then 16 weeks of 1mg/kg/day -a repeat LFTs and lipids after a month of treatment and is seen every 4 weeks for a pregnancy test -blood test before you start taking: Baseline LFT & fasting lipids !!SIDE EFFECTS: -skin may become very dry and sensitive to sunlight during treatment. Using lip balm and moisturisers will help. -important not to become pregnant while using isotretinoin capsules and for at least 1 month after stopping. This is because isotretinoin can harm an unborn baby. -change in mood/depression -liver or kidney problems (jaundice) !!MED INRERACTIONS -don't take with :supplements that contain vitamin A - dont take with :tetracycline antibiotics such as doxycycline, oxytetracycline, minocycline, and lymecycline - other acne medicines (using both together may make skin irritation worse) -can drink alcohol but not excessively 5. Other treatments Prognosis: -oral retinoids CAN potential of inducing remission of disease

2) How does diabetes affect the skin?

2) Granuloma annulare -small dermal papules -Lesions are asymptomatic -develop over joints, knuckles, elbows, ankles

MELANOCYTES >Benign melanocytic naevi aka moles( most common skin lesions)

3 classes 1) Junctional naevus -flat mole, melanocyte proliferation confined to base of epidermis 2) Compound naevus -melanocyte components in dermis and epidermis 3) Intradermal naevus Melanocytes proliferate in dermis only -some have very little pigment, variable in colour Malignant melanoma can arise in de novo moles or prexisting moles

**How do you manage eczema/dermatitis? Complications ?

3 principles: 1. Avoid triggering factors -diet in young children 2. Maintain or repair epidermal barrier 3. Dampen down the inflammatory response Acute Remove or treat cause If weeping -> 0.01% potassium permanganate soaks Corticosteroid cream or aqueous lotion Systemic antibiotic Wet dressing Systemic steroid Chronic Remove/ treat cause Emollient e.g. Diprobase Topical corticosteroid cream Paste bandages Tar Lichenification -> Salicylic acid 2nd: UV, immunosuppressant This can be achieved by: LIFESTYLE >Bathing- Reduce how often you bathe or shower, using lukewarm water. Showers are better. Replace standard soap with a substitute such as a mild detergent soap-free cleanser: your chemist or dermatologist can advise you. > Clothing- Wear soft smooth cool clothes; coarse fibres (wool or synthetic) are best avoided (microfine merino wool may be suitable) >Irritants- Protect your skin from incontinence, dust, water, solvents, detergents, injury. TOPICALS >Emollients- Apply an emollient liberally and often, particularly after bathing, and when itchy, and avoid perfumed products when possible. 1)bland white cream eg Cetraben, Diprobase, -watery, lighter, more cosmetic for patients 2)greasy ointment eg Hydromol ointment, Epaderm ointment -frequently and generously all over 2-3 times per day -heavy, may not be acceptable to patient better to give them a lighter treatment which they'll use than a heavier emollient >Topical steroids- mild eg 1% hydrocortisone ointment once or bd to all red, itchy areas -Tailor strength of steroid to severity of condition use least potent that is likely to be effective **know principles of topical steroid strength e.g. very potent ( dermovate) to penetrate hard skin like hand and foot eczema. Use least potent that is likely to be effective. -Steroid atrophy can be avoided by lack of continous use -Used for flare-ups. - Apply a topical steroid cream or ointment to the itchy patches for a 5 to 15-day course. >Topical immunomodulators (e.g. tacrolimus, pimecrolimus) -can be used as steroid-sparing agent. Pimecrolimus - is a new non-steroidal anti-inflammatory cream shown to be very effective for atopic dermatitis, with fewer side effects than topical steroids. >Antihistamines- Symptomatic relief as it reduces irritation. Consider sedating antihistamine eg chlorphenamine nocte -helpful to sedate patients ands top itching but not actually good at treating eczema Other treatments: can be used for severe cases > Phototherapy > Immunosuppressants * oral prednisolone SEs: Weight gain, indigestion, hypertension, diabetes, osteoporosis *azathioprine SEs:Nausea, vomiting, liver abnormalities, cytopaenias, probably ok in pregnancy *ciclosporin SEs:Hypertension, renal impairment, headaches, paraesthesia, probably ok in pregnancy -blood test and blood pressure monitoring *methotrexate SEs:Nausea, liver abnormalities, cytopaenias, not advised during pregnancy *Dupilumab SEs:Severe dry eyes, eczema herpeticum, only if benefits outlay risks in pregnancy

3) How does diabetes affect the skin ?

3) Necrobiosis lipoidica more severe, less common develops on shins in smal lproprotion of diabetics atrophic yellow look in centre of lesion & active red edge Typically waxy, yellow, hairless atrophic plaques with ref edge Probably a microvascular disease, or immune complex composition Can ulcerate, sometimes painful NB.Diabetes damages small & large blood vessels

BLOOD VESSELS aka red lesions >Angioma ( Campbell de Morgan spots)

>Angioma ( Campbell de Morgan spots) \ -acquired,increase with age -fairly common -asymptomatic -Mx: can be lasered off for cosmetic reasons

**What is Mycosis Fungoides (cutaneous T-cell lymphoma)?

>CD4 T cell neoplasm ( lymphoma ) of the skin >Patches, plaques, tumours of skin >skin lesions are scaly, erythematous, atrophic skin+/- dyspigmentatoin and alopecia >SPautrier's microabscesses >majority of patients have normal life expectancy >usually diagnosis is delayed as it is mistaken for eczema or psoriasis >Early diagnosis doesn't make much different to long-term outcome >looks like "autumn leaves" >staged according to degree of skin and lymph node and haematological involment Mx >early disease managed with moisturisers, topical steroids & phototherapy >more extensive/advanced disease may need radiotherapy of chemotherapy

BLOOD VESSELS aka red lesions >Capillary haemangioma

>Capillary haemangioma ( strawberry naevus) -commonest benign tumours of infancy -higher in preterm infants -develop in first few days of life and grow for up to 1 year, nearly all resolve after several years -if in an awkward area can affect underlying structures

FIBROBLASTS- In connective tissue, cells that secrete the proteins of the fibers. >Dermatofibroma ( Fibrous Histiocytoma)

>Dermatofibroma ( Fibrous Histiocytoma) -firm nodule in dermis -variable pigment ( pink to brown) -located particularly on legs -most commonly occur after insect bite -mx: no treatment required but if diagnosis is uncertain, an excision can be performed

**What common viral rashes do children get ?

>Fifth disease(erythema infectiosum_aka slapped cheek syndrome -caused by the human parvovirus. This common community-acquired disease does not usually require treatment, but respiratory isolation is recommended for 7 days following the onset of symptoms. The initial stage of the disease presents as red cheeks that appear to be "slapped" or "slapped cheeks" with circumoral pallor Hand, foot and mouth disease -Caused by RNA Virus: Coxsackievirus -->type of Coxsackievirusvirus syndrome -resolves after 7 days -The first signs of hand, foot and mouth disease can be: a sore throat a high temperature, above 38C not wanting to eat -->painful red blisters in the throat and n the tongue, gums, hard palate, inside of cheeks, palms and soles of the feet >More on coxackie virus (picornavirus family) -causes symptoms that affect different body parts: 1_)Hand, foot & mouth disease -more common in young children -causes fever ( febrile convulsion), blanching papular rash 2)Herpangina (fever, mouth blisters) an infection of the throat, causes red-ringed blisters and ulcers on the tonsils and soft palate, the fleshy back portion of the roof of the mouth. 3)Haemgorragic conjunctivitis an infection that affects the whites of the eyes, usually begins as eye pain, followed quickly by red, watery eyes with swelling, light sensitivity, and blurred vision. More serious 4)Viral meningitis/enecphalitis 5) Myocarditis Gianotti- Crosti syndrome -rare childhood skin condition characterized by a papular rash with blisters on the skin of the legs, buttocks, and arms. It typically affects children between 9 months and 9 years of age. Kawasaki disease mainly affects children under the age of 5. It's also known as mucocutaneous lymph node syndrome. The characteristic symptoms are a high temperature that lasts for 5 days or more, with: a rash. swollen glands in the neck.

FIBROBLASTS- In connective tissue, cells that secrete the proteins of the fibers. >Keloid scar

>Keloid scar -fibrous tissue overgrowth beyond site of trauma -hypertrophic scar is different as this remains confined to the original defect/wound -upper trunk most vulnerable -more common in afro-Carri beans Mx -Silicone-sheet/gel -Steroid-cream/tape/injection

FAT >Lipoma

>Lipoma -subcutaneous nodules -single or multiple -very common -shoulders, neck, trunk or arms most common, but can grow anywhere on body where there is fat -family hx Mx: surgically removed through small incision via LA

NERVES >Neuroma >Neurofibroma

>Neuroma -benign nerve tumour >Neurofibroma -benign nerve sheet tumour in the peripheral nervous system -if multiple are present then individuals usually will have neurofibromatosis type 1 (NF1): autosomal dominant neurocutaneous disorder characterised by multiple neurofibromas on the skin + 6> café-au-lait macules. NF1 Associated with non-cutaneous complications

BLOOD VESSELS aka red lesions >Pyogenic granuloma

>Pyogenic granuloma -name=misnomer, as it doesn't relate to infection -lobular proliferation of blood vessel -localised trauma can trigger -head & neck & extremities especially fingers& hands -most occur before 5yo, but can be found in adults and during pregnancy -mx:surgical removal via curettage & Cautery -sample must go to histology as appearance mimics amelanoytic(non-pigmented) melanoma ( difficult to distinguish, see image)

Sebaceous glands (oil glands) >Sebaceous gland Hyperplasia >Sebaceous Adenoma

>Sebaceous gland Hyperplasia -common in middle aged, elderly or immunosuppressed patients -soft yellow dome papules on face & cheeks , have a characteristic central dimple( can be mistaken for BCC) -MX: no treatment, can be flattened with gentle cautery >Sebaceous Adenoma -benign growth of sebaceous glands, present as firm yellowish papules -may be a marker for an underlying cancer prone genetic syndrome aka Muir Torre Syndrome. Syndrome associated with solid tumours especially GI & Genito-urinary tract tumours

BLOOD VESSELS aka red lesions >Telangiectasia -dilated blood vessels ( left pic) -Spider naevus has central arteriole, surrounding capillary network ( right picture) -spider naevus most common in children, can occur in pregnancy & liver disease -mx: many resolve spontaneously after years, can be lasered off for cosmetic reasons

>Telangiectasia -dilated blood vessels ( left pic) -Spider naevus has central arteriole, surrounding capillary network ( right picture) -spider naevus most common in children, can occur in pregnancy & liver disease -mx: many resolve spontaneously after years, can be lasered off for cosmetic reasons

HAIR FOLLICLE-CYSTS used to be called sebaceous cysts (wrong origin) >epidermoid cyst ( stratified squamous epithelial cysts) >Trichilemmal (pilar) cyst [stratified squamous cell cyst, keratin filled cyst]

>epidermoid cyst ( stratified squamous epithelial cysts) -come epidermal cells that line top of hair follicle aka infundibulum -small, pea-sized, but can grow -commonly develop on neck face chest and upper back , can develop anywhere -common in young & middle-aged adults -have a punctum (illustrated by arrow) -may accompany acne vulgaris -can become painful if they have a secondary infection, usually only removed for cosmetic reasons (removed by small incision via LA) >Trichilemmal (pilar) cyst [stratified squamous cell cyst, keratin filled cyst] -originates from outer hair root sheath, bottom of hair follicle -occur mostly in scalp -common in middle-aged women

** what is impetigo ?

A common and highly contagious skin infection that mainly affects infants and children. Impetigo usually appears as red sores on the face, especially around a child's nose and mouth, and on hands and feet. The sores burst and develop honey-coloured crusts. • Impetigo is due to localised, superficial and non-follicular infection with Staphylococcus aureus &/or Streptococcus pyogenes • Staphylococcal impetigo is characterised by surface honey-yellow crusting or blisters. It tends to be itchy. • Bullous impetigo is specifically due to S. aureus that produces an exfoliative exotoxin, exfoliatin. This cleaves desmoglein 1 complex and produces a split between stratum granulosum and stratum spinosum within the epidermis. • Ecthyma is a more serious and deeper infection but caused by the same organisms. • Ecthyma results in scabs covering full skin thickness ulceration. These deeper infections may be painful • Risks : > Climatic conditions (humidity, occlusive clothing) >Underlying skin disease (atopic dermatitis, hidradenitis suppurativa) >Iron deficiency >Diabetes mellitus > Defective neutrophil function (treated with oral vitamin C) > Immunodeficiency, including hypogammaglobulinaemia and HIV infection Mx • Staphylococcal infections are contagious, requiring careful attention to hygiene. -Wash hands frequently -Use antiseptics for bathing -Hot wash clothing, bedding, towels -Avoid sharing clothing and towels • Localised staphylococcal infections may be managed using meticulous wound care and antiseptics (povidone iodine, chlorhexidine, triclosan and others) as local application and cleanser. DONT USE topical antibiotics (particularly fusidic acid and mupirocin) because of increasing prevalence of topical antibiotic-specific and methicillin-resistant strains of staphylococci. • Oral antibiotics may be prescribed for more extensive or recurrent infections but should not be prescribed for trivial reasons. 1st line treatment : flucloxacillin or dicloxacillin. In penicillin-allergic patients, erythromycin may be used but there is a higher rate of resistance. Complications -cellulitis - erysipelas

**How do you assess pigmented lesions? What checklist can you use

ABCDE approach -more commonly ysed Asymmetry Border Colour Diameter >6mm Enlargeing/Evolving Checklist GLASGOW 7point checklist for pigmented lesions -not be all and end all -benign lesion can still have all 7 of these lesions >Major features 1)change in size 2)irregular shape -3)rregular colour >Minor features 4)Diameter >7mm 5) Inflammation 6)oozing 7) Change in sensation

Endogenous and mixed -Atopic Atopic Dermatitis (Eczema) genetic factors? triggering factors?

AD is thought to be associated with dysfunctional skin barrier and Th2 cell adaptive immune responses to common environmental allergens It is a disease with complex genetic and environmental susceptibility factors Filaggrin gene mutations - Prevalence of childhood AD 15-30%, adult AD 2-10% in industrialised countries - Frequent associated with other atopic conditions food allergy, rhinitis, asthma -80% have raised IgE -May have itch with very little rash other than scratch marks - Sensitive, often dry skin Presentations Onset in infanc: on the face Later childhood: often elbow and knee flexures In adults :face, trunk and hands common 60% remission during childhood May relapse with trigger factors Triggering factors -Infection - Irritants e.g. Soap, detergents -Allergies e.g. House dust mite, pets, foods, grass -Stress -Others Complications - Growth retardation - Steroid side effects e.g. striae -Depression -Infection Widespread - Herpes Simplex - Eczema herpeticum -Usually Staphylococcus aureus - Sometimes Streptococcus pyogenes

Mycobacteria

Acid Fast; fever, night sweats, wt loss, hemoptysis M. tuberculosis: TB, M. kansasii: TB-like sx M. avium-intracellulare: AIDS prophyl: Azithromycin

**Retinoids: Acitrerin & Isotreinoin

Acitrerin used in -psoriasis (limited use) -congenital ichtyoses -discoid lupus erythematosus -prohpylaxis against skin cancer in high risk patients Dose -slow onset of action ->50mg daily Can be used long term Isotrerinon Used in -Acne vulgaris (very Effective) BUT possible link with depression/suicide, not clear if drug-related Side effects -hair thinning etc. -NOT GOOD FOR PREGNANCY & can stay in blood for 2 years, avoid in women of child bearing age

**different types of acne?

Acne vulgaris= most common

** Urticaria classification clinical presentation ? see image

Aetiology/ Classifications Allergic (IgE) or non-allergic mechanisms leads to mast cell degranulation 1)Acute urticaria - episodes over period of <6 weeks, often gone within hours to days, tends to have clearer trigger (if allergic cause, may develop into anaphylaxis) • Idiopathic • Acute infection - URTI, viral hepatitis, sinusitis • Food allergy - milk, egg, peanut, shellfish • Drug allergy - antibiotics commonly • Drug-induced urticaria - aspirin, NSAIDs, opiates, radiocontrast, ACE-i • Vaccination • Bee/ wasp sting hypersensitivity • Localised contact - latex, pollen, nettles 2)Chronic urticaria - repeated near daily episodes for >6 weeks, less clear aetiolog • Mainly idiopathic (autoimmune tends to have more protracted course than idiopathic) • Autoimmune associations - SLE, thyroid disease • Autoimmune causes - urticarial vasculitis, acquired angioedema Inducible spontaneous urticaria (aka Physical urticaria) subtypes: • Symptomatic dermographism - stroking skin, towel drying or tight clothing triggers • Cold urticaria - cold air, water or ice triggers • Heat urticaria - hot drink triggers • Cholinergic urticaria - triggered by sweat hypersensitivity or emotional upset. LOOKS like 'multiple pin point lesions' on the skin. • Vibration - ie. Jackhammer trigger • Solar urticaria - sun exposed areas • Aquagenic urticaria - water on skin trigger (can still drink) • Delayed pressure - pressure on skin (several hours later) from bag, seat belt etc 3)Angioedema without urticaria [more unusual, do further investigations] • Drug-induced o ACE-inhibitors recognised cause of this, should be discontinued o NSAIDs and antibiotics can also be a cause • Complement pathway defects: o Hereditary angioedema is a rare autosomal dominant condition - C1 esterase inhibitor deficiency or dysfunction allows complement activation to go unchecked o Acquired angioedema due to consumption or inactivation of C1 esterase inhibitor - associated with malignancy in older population

**What disease do Tick Bites cause and what is the bacterial organism which causes it?

Allows transfer of Borrelia burgdorferi(spirochaete) causing: Lyme disease Sign: Spreading annular erythema around bite is Erythema Chronicum Migrans

** What is alopecia? " I'm losing my hair" Scarring vs non-scarring?

Alopecia= hair loss Scarring vs Non-scarring >Scarring -can be primary or secondary -permanent , irreversible , hair cant grow again even after underlying cause of hair loss is treated -rate >Non scarring - temporary, potential for hair to grow again through treatment Different types of non-scarring alopecia ●Androgenetic alopecia Aka male and female pattern baldness, this is the most frequent cause of hair loss. As you get older, your body will produce more androgens. These hormones, including testosterone, will cause baldness, usually in a very specific pattern. For men, it typically begins along the hairline. Women usually experience thinning hair across the crown. Hair loss often progresses over time. ●Alopecia areata an autoimmune disorder in which your own body attacks your hair follicles. This condition causes telltale round or oval patches of baldness. Fortunately, in most cases, hair will grow back on its own. ●Telogen effluvium a temporary form of hair loss. It usually results from another health condition or a medication, such as chemotherapy. Hair follicles follow a cycle of rest and growth. If you develop telogen effluvium, an unusual number of follicles enter the resting stages. Due to the excessive shedding of resting or telogen hair after some shock to the system. New hair continues to grow. Telogen hair is also known as a club hair due to the shape of the root. ●Traumatic alopecia occurs because of damage to the scalp. Often, these injuries can be the result of straightening, tight braids, dyes, and other hair treatments. If scars have not yet formed, this type of alopecia is reversible. ●Trichotillomania severe stress and anxiety causes you to pull out your hair. Cognitive and emotional therapy are vital for this condition. Often, with proper psychological care, your hair will grow back Although hair may not always grow back if damage is great and scars have formed.. Key questions to determine diagnosis ● Increased hair shedding or reduction of hair density? o Hair shedding - coming out by roots --> Telogen effluvium: o Breaking near the scalp--> Acute alopecia areata o Breaking near the ends --> Hair shaft abnormalities ● Diffuse, patchy or patterned? o Diffuse --> acute or postpartum telogen effluvium, alopecia areata o Patchy --> >Alopecia areata ( see above) >tinea capitis: infection of the scalp with a dermatophyte fungus. Although common in children, tinea capitis is less frequently seen in adults. Hair can be infected with Trichophyton (abbreviated as "T".) and Microsporum ("M".) fungi. >lichen planus: Lichen planus is a T cell-mediated autoimmune disorder, in which inflammatory cells attack an unknown protein within the skin and mucosal keratinocytes. ● Redness or scaling? ● Any scarring? ● Hair shafts normal? ● Women o Ask about changes with periods ● Associated symptoms? >Scarring 1. Scalp Infection ● Fungi ● Pyogenic bacteria ● Syphilis 2. Traumatic Alopecia Can be non-scarring if in early stages ● Burns, accidents ● Excessive bleaching ● Trichotillomania (psych condition) ● Corn roads, braids 3. Dermatosis ● Psoriasis and eczema - Usually causes hair loss related to the degree of inflammation and there is seldom scarring ● Discoid lupus erythematous -Scarring cause of hair loss - Treatment needs to be aggressive to get control early otherwise there is irreversible hair loss ● Lichen Planus -Scarring scalp condition - Requires aggressive therapy to prevent irreversible hair loss 4. Congenital ● Monilethrix aka beaded hair (condition that affects hair growth. Its most characteristic feature is that individual strands of hair have a beaded appearance like the beads of a necklace.) The name beaded hair reflects hair shafts with narrowed segments between "nodes" of normal thickness. It is also called monilethrix. The scalp is most commonly involved. The affected hair shafts appear beaded a few months after birth. They break off leaving patches of the scalp with abnormally short hairs. The scalp may also have a rough appearance because of a build-up of keratin around the hair follicle. Monilethrix is inherited as an autosomal dominant characteristic. This means an affected individual has a 50% chance of passing it on to each of their male and female children. It is caused by changes in the keratin gene cluster at chromosome12 (gene map locus 12q13, OMIM ID #158000). ● Menke's disease ( affects copper levels in body, different to wilson's disease which is assoicated with liver and brain) ● Hair shaft abnormalities A hair shaft defect is any structural abnormality of the hair shaft. Some hair shaft defects are easily diagnosed with the naked eye, others may require microscopic examination. Hair shaft defects may result in: No visible hair abnormality >Hair loss (alopecia) >Coarse or frizzy hair >Uncombable hair - when disordered hair bundles grow in all directions and cannot be arranged by combing >Fragile hair - hair shafts with reduced tensile strength. A gentle pull of several hair shafts will help determine if the hair is abnormally fragile.

Reactive viral exanthemata

An exanthem is a rash, usually of viral origin, accompanied by systemic symptoms such as fever, headache and malaise. Symptoms can be secondary to a reaction to toxin produced by the organism, damage to the skin by the organism or an immune response.

Connective tissue Shagreen patch

Areas of rough, leathery, orange peel-like skin typically seen on the lower back or nape of the neck in tuberous sclerosis

** What is Actinic/Solar Keratoses? worth treating?

Background >PREMALIGNANT-Can progress to SCC >If patient affected by multiple, AK lesions, it is suggested that the annual risk of developing invasive cutaneous SCC lies between 0.15% -80% ( uncertain) >· Occur on sun exposed sites eg. Tips of ears of men, bald sites, backs of hands >Not particularly painful, can bleed, patients usually asymptomatic >not indulated - no nodular change like with SCC >not changing rapidly unlike SCC >AK--> Bowen's (SCC in situ) Risk factors · Fair skin · Outdoor occupation · Sunny climates · Old age Mx >none-not worth treating >hats for bald men >cryotherapy: kills off dysplastic skin cells >topical FLUOROURACIL( 5-FU) +/- salicylic acid - very effective, very safe -leaves normal tissue alone >topical imiquimod >topical ingemol mebutate >PDT(photodynamic therapy) >curettage/shave >excision if SCC

** What is Herpes Simplex virus ( HSV)? what about HSV in pregnancy ? ** What serious disease does Herpes Simplex virus infection lead to ?

Background 2 herpes simplex virus strains that cause skin infection · HHV1-Herpes Simplex Virus Type 1 ( non genital herpes aka 'cold sores') · HHV2- Herpes Simplex Virus Type 2 ( genital herpes) · They can be transferred from person to person by direct skin to skin contact with the affected place when enough virus is present. This is often a lesion or sore but transmission may also occur at other times, perhaps when there is only an itch or tingle in the area. · Most people are only infected in one area and are unlikely to transfer the infection to other parts of their bodies. · Infection may be followed by symptoms, such as sores or blisters, within a few days but some people will not notice anything for months or years. Others are carriers who never have symptoms. · The virus remains dormant in the sensory nerves close to the place of original infection. · Reactivation may result in more genital herpes nearby, on skin that is served by the same nerves (dermatome). · The frequency of recurrences varies from person to person. For some people symptoms appear several times a year, in others rarely or never. · Herpes cannot be caught from towels, swimming pools, saunas or from toilet seats. However, it can be passed on through sharing sex toys, or other intimate items such as razors, when there is an active lesion. Clinical presentation >Coalescing polygonal vesicles then crusting · 1st infection: The very first infection is often unnoticed as it may only produce a short-lived redness of the skin. Sometimes, however, a first infection can make a person feel very unwell with a temperature, swollen lymph glands and soreness and blisters in the mouth, on the lips or elsewhere on the skin. · Reoccurrence: The virus may lie dormant in the nerve endings for some time but when it becomes active again, the first symptom is a burning or stinging pain at the affected site, followed by pink bumps and small blisters. The blisters quickly dry and crust over, and the areas usually heal within a few days. Symptoms may recur at the same place or nearby. · In the eye: If herpes simplex virus infects the eye, it causes pain, discharge and sensitivity to light, and can cause scarring. Diagnosis: · Usually the clinical appearance of the skin affected by herpes simplex is enough to make a diagnosis. · A surface swab can be taken to confirm the diagnosis. · If the patient has herpes of the genital area, it's important that they attend a Genito-Urinary Medicine (GUM) or Sexual Health clinic. This is because other sexually transmitted diseases may be present and should be tested for as well. Reactivation and Flare-ups: · Symptoms clear in 7-10 days, with or without treatment · However, the virus will remain in a dormant state in the body. · In most patients, recurrent symptoms are mild and infrequent, or do not happen at all. · For a minority, troublesome recurrences can usually be prevented by using oral anti-viral drugs or adopting lifestyle changes. Factors that contribute to flare-up's: · Other infections, such as colds or 'flu'. · Getting tired and run down · Sunlight on the affected area · A skin injury, such as an operation or a graze, at the place where the virus shows itself at the surface Mx > Antiviral oral tablets can help to lessen the severity of the outbreak and/or shorten it: aciclovir, famciclovir or valaciclovir · Aciclovir and famciclovir are also available as creams, but these do not work as well as the tablets HSV In pregnancy A baby may become infected with herpes during childbirth if it comes into contact with a lesion when the mother is newly infected. For mothers with recurrent symptoms, infection risk is low and a vaginal birth is normally recommended. Antiviral medication can be taken by the mother to prevent an outbreak at the time of delivery. SERIOUS DISEASES CASUSED BY HSV simplex Eczema herpeticum ( Kaposis varicelliform eruption) Definition Widespread eruption, serious complication of atopic eczema or less commonly other conditions Cause Herpes simplex virus infection Clinical presentation ( see images) >Extensive crusted papupes,BLISTERS & erosions -coalescing polygonal vesicles then crusting >Systemically unwell w. fever & malaise Mx >Antivirals e.g. aciclovir >Antibiotics for bacterial secondary infection Complications >Herpes hepatitis >enecephalisits >Disseminated intravascular coagulation (DIC) >(Death)

EMERGENCY DERM **What is Stevens-Johnson syndrome? What is Toxic Epidermal Necrolysis ( TEN)?

Background >characterised by mucocutaneous necrosis with at least 2 mucosal sites involved. >Skin involvement may be limited or extensive. >Drugs or combinations of infections or drugs are the main associations. >Epithelial necrosis with few inflammatory cells is seen on histopathology. >prodromal illness. >responds to symptomatic treatment over 2 week >more localised, can spread to the mouth **The extensive necrosis distinguishes Stevens- Johnson syndrome from erythema multiforme. Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are now believed to be variants of the same condition, distinct from erythema multiforme. SJS/TEN is a rare, acute, serious, and potentially fatal skin reaction in which there are sheet-like skin and mucosal loss. - it is nearly always caused by medications. overlapping symptoms: prodromal illness. TEN Background - usually drug-induced, is an acute severe similar disease characterised by extensive skin and mucosal necrosis accompanied by systemic toxicity. - On histopathology there is full thickness epidermal necrosis with subepidermal detachment. Clinical presentation of both Fever > 39 C Sore throat, difficulty swallowing Runny nose and cough Sore red eyes, conjunctivitis General aches and pains. Mx ● Early recognition and call for help ● Full supportive care to maintain haemodynamic equilibrium Complications ● Mortality rates are 5-12% with SJS and >30% with TEN with death often due to sepsis, electrolyte imbalance or multi-system organ failure

** What are Keratocanthomas?

Background Epithelial tumors which resemble SCC ( SCC variant) Grow very quickly Progress to typical dome with central crater containing keratinous material Usually with regress spontaneously Sun exposed sites, late middle age Difficult to differentiate from early SCC so treated in same way

Epidermis BENIGN condition **What is SEBORRHOEIC KERATOSiS? aka seborrhoeic warts, and as basal cell papillomas.

Background Seborrhoeic keratoses (SK) are also known as seborrhoeic warts, and as basal cell papillomas. They are benign growths due to a build-up of skin cells. SK are very common, harmless, often pigmented, growths on the skin. nothing to do with sebaceous glands or viral warts. Basal cell papilloma- proliferation of basal cell keratinocytes Clinical presentation >Brown- so often present as potential melanoma skin cancer >Very common in older adults affects 80-100% of those over 50 years >Male=Female >Associated with skin tags >Typically- grey or yellow brown, Stuck on appearance, matt warty surface >Usually multiple harmless warty spot, looks like a mole due to brown colour but is NOT melanocytic)

***What is bullous pemphigoid? What is epitope spreading ( EP)? Mx?

Background- acquired blistering disorder -A blistering skin disorder which usually affects the elderly -autoimmune disease with antibodies which attack a component of the hemidesmosome -Assocaited with neurological disease & MALIGNANCY -associated with epitope spreading -sitagliptin ( T2D drug) linked to it Cause -Autoantibodies against antigens between the epidermis and demis causing a sub-epidermal split in the skin *Autoantibodies against these different proteins disrupt the integrity of the dermal-epidermal junction and give rise to different autoimmune blistering skin diseases depending on which protein is targeted by the autoantibodies. CLINICAL PRESENTATION -tense fluid filled blisters on an erythematous base -large tense haemhoragic blisters -lesions often itchy -may be preceded by non-specific itchy rash -usually affects trunk & limbs ( mucosal involvement less common) -usually presents in pts over 70y Management >General measures -wound dressings where required, monitor for signs of infection **The majority of treatment involves immunosuppression. >Principally with corticosteroids - topically in select cases when disease is localised often -systemically, when disease is widespread >Oral therapy for Bemph: tetracycline & nicotamdide( B3 supplement) -Steroids and oral therapies can be used in conjunction with steroid-sparing immunosuppressive agents such as azathioprine, mycophenolate mofetil or IV gamma globulin. Epitope spreading & autoimmune acquired disease >Epitope =the part of an antigen molecule to which an antibody attaches itself. >Spreading: a primary autoimmune or inflammatory process may cause tissue damage in such a manner that certain protein components that are immunologically "hidden" from the immune system become "revealed" and evoke a secondary autoimmune response.

skin function?

Barrier to physical agents Protects against mechanical injury Barrier to fluid loss Barrier to infection/ immune surveillance Thermoregulation Sensory organ Vitamin D production Reduces penetration of UV radiation Cosmetic association

Why can you still get burnt on a cloudy day ?

Because visible light is only a surrogate marker for UV

Fat lipoma

Benign tumours of fat Present as soft masses in subcutaneous tissue Often multiple Sometimes painful

Benign skin tumours vs malignant

Benign: -Haemangioma (aka strawberry spot, collection of small blood vessels that form a lump under the skin. - seborrhoeic keratosis(harmless warty spot, looks like a mole due to brown colour but is NOT melanocytic) -melanocytic naevi ( pigmented moles) Malignant-3 most common 1) Basal cell carcinoma (BCC) 2)Squamous cell carcinoma (SCC) 3)Malignant melanoma (MM)

**POTENT STEROIDS

Betamethasone valerate

** What is a blister? What are the different types ? -Vesicle -Bulla

Blister - a raised, clear fluid filled lesion - Only a few conditions blister, as such it is important to identify blistering skin disease. - Diagnosis is relatively straightforward if the patient gives a clear history of blisters or shows signs. - It is important to consider whether the blisters have ruptured, in which case the examination may only reveal superficial erosion, exudation and crusting.

What conditions does xanthelasma (fatty deposit in eyelids) present it?

Can indicate Hyperlipidaemia -but only 50% cases have raised circulating lipids

** NON -Melanoma SKIN CANCER Pathophysiology behind carcinogenesis process types of skin cancer

Carcinogenesis Skin is exposed to environmental UV radiation -->Radiation damages DNA-->DNA repair mechanisms are necessary to prevent cancer-->skin cells try to protect themselves from radiation damage-->accumulated damage, genetic predisposition, failure of repair mechanisms , iatrogenic immunosuppresion-->development of skin cancer Types of skin cancer 1)Basal cell carcinoma (BCC) aka non-melanoma Background -origin cell uncertain: ketaniocyte, hair follicle cell -rarely metastasises -most common malignant skin tumour -local concern but can be extremely destructive -development of BCC: months to years RFs ●history of frequent or severe sunburn in childhood ●skin type I (always burns, never tans) [develops in up to 30% of Caucasians] ● fair skin: red hair, freckling, blue/green eyes ●increasing age ●arsenic exposure ● Gorlin's syndrome (nevoid basal cell carcinoma syndrome, is a condition that affects many areas of the body and increases the risk of developing various cancerous and noncancerous tumors happens in teens & 20s.) ●male sex ●immunosuppression ● previous hx of skin cancer ●genetic predisposition Clinical presentation NB.Development is complex, can occur on non sun-exposed areas like scrotal and vulval skin Subtypes a)nodular -most common -surface telangiectasia. shiny " pearly rolled edge" "pearly papule" -lesion may have a necrotic or ulcerated centre aka rodent ulcer -most common over visor region ( face & eye) + neck region b) superficial: confined to surface layers of skin -occurs on back and trunks - patients can have multiple, sometimes 20+ -topical therapy ideal Mx for this type of tumour -translucent look still present -development of SCC: weeks to months ( grow faster) RFs ●childhood UV exposure ● radiotherapy to spine for lymphoma c)infiltrative -harder to diagnose -scar like changes -goes far beyond changes in skin you can visibly see, making harder to treat 2)Squamous Cell carcinoma (SCC) aka non-melanoma -cell or origin, where mutation occurs: keratonocytes -higher chance of metastasising than BCC -2nd commonest after BCC RFs (same as for Solar Keratoses) ● excessive UV exposure ● pre-malignant skin conditions (e.g. actinic keratoses) ● chronic inflammation (e.g. leg ulcers, wound scars) ● immunosuppression ● genetic predisposition Clinical presentation -keratotic ( contain keratin) scaly crusty Subtypes a) Premalignant actinic keratoses -dysplastic ( cells not behaving in normal way, but not malignant yet) b) Carcinoma in situ/Bowens disease -skin patches on lower legs in elderly people Ddx for BCC & SCC Chondrodermatitis nodularis (Winkler disease) - inflammatory condition on ears commonly as people lie 1 sided on ear, mistaken for skin cancer -harmless

** What different locations within the layers of the skin can blisters occur in ? What are they called? What 2 layers of skin should you pay attention to RE blisters - what is the pathophysiology ?

Causes >Trauma -burns >Infections -Insect bites -Herpes simplex infection -Impetigo (Bullous Impetigo) -acute contact dermatitis -Herpes zoster infection ( SHINGLES) >Drugs >Acquired autoimmune - pompholyx (vesicular eczema of the hands and feet) >Genetic disease Pathophysiology: different locations blistering develops in !!The fragility of blisters depends on the level of split within the skin - an intra- epidermal split (a split within the epidermis) causes blisters to rupture easily; whereas a sub-epidermal split (a split between the epidermis and dermis) causes blisters to be less fragile. 1) Blisters which occur in epidermis-->intra-epidermal blisters -fragile roof breaks easily, flaccid-->EROSION -Within the epidermis, a 'brick wall' like structure that represents our skin barrier. The keratinocytes, the individual cells (the bricks) of the skin are held together by intercellular cement and there are a number of skin diseases in which the epidermis can be broken down, involving a breakdown of the epidermal 'brick wall' or 'cement' like structures that hold the keratinocytes together. The main structures that hold the keratinocytes together (the cement) are desmosomes. - Blisters occurring within the epidermis are classified intra-epidermal blisters - Intra-epidermal blisters break easily so often clinical presentation will be superficial erosions, NOT blisters e.g. ●Pemphis Vulgaris ● Friction ( break desmodomes mechanically) ● Eczema ● Infection: o Viral (HSV, HZV) : weaken desmosomes o Bacterial (bullous impetigo and SSSS): toxins weaken desmosomes ● Toxic epidermal necrolysis o Usually severe drug reaction in adults 2)Blisters occur at DEJ--> sub-epidermal blisters (tough, tense roof - often intact -The junction between the epidermis and the dermis, known as the dermal-epidermal junction(DEJ), where the adhesion between these 2 layers occur and are maintained by an intricate network of proteins (hemidesmosomes) and attachment structures. - Blisters occurring at the DEJ are classified sub-epidermal blisters - Sub-epidermal blisters are tough with a tense roof as the epidermis lies above them, subsequently the patient will often have intact blisters Eg. ● Bullous Pemphigoid ● Burns ● Dermatitis herpetiformis ● Erythema multiforme ● Insect bites ● Porphyria cutanea tarda ● Epidermolysis Bullosa 3) At Dermis -->Subdermal blister e.g. blood blister

Inflammatory skin conditions Rosacea Causes? Types?

Chronic skin disorder of the face with red inflamed areas appearing mostly on the nose and cheeks Causes -being outside in the heat, sun, wind, or cold doing very active sports, such as running drinking alcohol eating spicy foods -drinking hot coffee or tea -feeling stressed or upset Background 165 per 100 000 population Female> Males 80% diagnosed after age of 30 years Chronic disorder of pilosebaceous units coupled with a tendency for flushing and NO comedones Types >Vascular/telangiectatic >Papulopustular >Rhinopyhma >Rosacea fulminans (pyoderma faciale) >Ocular (blepharitis, rosacea keratitis) 20% have ocular manifestations Dry eyes Irritation Redness Crusting Itching Burning Recurrent Infections

** What is cutaneous small vessel vasculitis ? How is it different to HSP?

Clinical presentation -tender palpable non blanching purpura -variable amount of tissue damage from sparse non ulcerated purpuric lesions, to confluent superficial ulceration or skin necrosis Background -inflammation in small blood vessels -immunocomplex deposition -40-70 years Associations -single self limiting episodes with no other organ involvement are mainly idiopathic or drug related -if patient presents with the skin changes then investigate for systemic involvement as it may be HSP, if there is no involvement then it can be called cutaneous smalll vessel vasculitis

** Complications of eczema?

Complications ->Staph aureus or Step pyogenes infection, present transiently on healthy skin, often colonises causing impetiginisation of lesions. May need oral abx- flucloxacillin. >Eczema herpeticum: (see image) DERM EMERGENCY primary HSV infection in atopic dermatitis. Clinical pres -Umbilicated vesicles over eczema areas, fever, LAD. Can be life threatening in infants. -extensive crusted papule, blisters & erosions Tx- acyclovir. Complications -herpes hepatitis -encephalitis -DIC -(Death) > Molluscum contagiosum: viral infection with pearly vesicles. May require antivirals.

**What are pressure sores? Risk factors? Pathogenesis? classification?

DEFINITION >Pressure ulcers, also known as bedsores, are localized damage to the skin and/or underlying tissue that usually occur over a bony prominence as a result of usually long-term pressure, or pressure in combination with shear or friction >The most common sites are the skin overlying the sacrum, coccyx, heels, and hips, though other sites can be affected, such as the elbows, knees, ankles, back of shoulders, or the back of the cranium. -->occurs mainly in patients over 70, patients with fractured femurs RISK Factors 1. The most important risk factor and prerequisite for pressure sore development is immobility. Mobility is commonly impaired because of pain (arthritis, fracture), reduced consciousness (sedatives, cerebrovascular disease) or paralysis. 2. Other important risk factors include incontinence, reduced sensation, hypotension, oedema, dehydration, septicaemia, dementia, acute confusion, Diabetes mellitus, peripheral vascular disease and nutritional deficiency. 3. Lab tests indicating risk include anaemia and low albumin. 4. Age making skin more susceptible to damage. These changes include a reduction in the number of dermal blood vessels, decreased elasticity, flattening of the dermo-epidermal junction and increased skin permeability. PATHOGENESIS > Most serious pressure sores originate from damage that occurs in deep tissues, which are particularly susceptible to pressure and shearing forces. Superficial tissues are more liable to damage from friction and moisture. CLASSIFICATION •Grade 1 Erythema only • Grade 2 Erythema, blistering, shallow ulceration • Grade 3 Ulceration extends to subcutaneous tissues • Grade 4 Lesion extends into deep fascia & destruction of muscle and facial pain extension DIAGNOSIS • Review the skin in its totality . • This often involves rolling a patient and examining back, bottom and heels. • If you admit a patient with a bandage, it is very important to take down the bandage to review the skin underneath. • Also examine a patient's pulse, BP, temp etc. • Ensure that you are aware of any broken areas e.g. sacrum/leg ulcers etc. as these patients are likely to need additional protein supplements/vitamins/zinc/vit c • Since skin is a major organ acting as a barrier to infection, small breaks can introduce bacteria and cause sepsis. COMPLICATIONS • Sores may contain a necrotic core which can harbour high concentrations of bacteria: Proteus, E Coli, Klebsiella, Pseudomonas, Staph Aureus, Group A streptococci, enterococci, bacteroides • These necrotic sores will require debridement and antibiotics • Cellulitis, septicaemia and osteomyelitis are serious complications for which antibiotics are clearly indicated. • Osteomyelitis may be the cause of a non-healing ulcer PREVENTION ( reduces cases by 50%) - identification of risk, approaches to reduce pressure, repositioning plan, moisture reduction and nutritional support. • Identification of high-risk patients is routine on admission and throughout hospital stay and in the community with the use of risk assessment tools such as the Norton Scale or Waterlow score. • It has been said that two hourly turning of ill patients is enough to prevent pressure sores. (but is time consuming for nursing staff and can be painful for the patient) • Pillows and rubber rings enhance not reduce pressure. • The NHS mattress is a block of foam with poor pressure relieving features and inadequate ventilation. • Alternating pressure air mattresses (APAM) are an alternative approach.

** What other specific diseases can occur when desmosomal proteins are targeted by gene mutations or acquired auto antibodies

DIAGRAM EXPLAINED Centrally, highlighted in colour are a number of different types of desmosomal proteins. ( don't need to remember names) To the left, the inherited disease consequences that result because of gene mutations in those different desmosomal proteins. Many of these cause: - Blisters - Cutaneous abnormalities such as hypotrychosis (reduction in hair), keratoderma (thickening of the palms/soles) - Other abnormalities, particularly cardiomyopathy (desmosomes are not just expressed in skin but also in myocardium, meninges and the cortex of lymph nodes) On the right, the clinical consequences of autoantibodies against the same desmosomal proteins. Many of these conditions are associated with: - Intra-epidermal blistering, which we refer to as pemphigus when autoantibodies target specific desmoglein (a desmosomal protein) molecules.

**What assessments can you do with eczema to assess severity ?

DLQI -Dermatology Life Quality Index EASI - Eczema Area and Severity Index (EASI) is a validated scoring system that grades the physical signs of atopic dermatitis/eczema POEM-Patient Oriented Eczema Measure (POEM) is a tool used for monitoring atopic eczema severity. It focuses on the illness as experienced by the patient. 1. Over the last week, on how many days has your skin been itchy because of your eczema? No days 1-2 days 3-4 days 5-6 days Every day 2. Over the last week, on how many nights has your sleep been disturbed because of your eczema? 3. Over the last week, on how many days has your skin been bleeding because of your eczema? 4. Over the last week, on how many days has your skin been weeping or oozing clear fluid because of your eczema? 5. Over the last week, on how many days has your skin been cracked because of your eczema? 6. Over the last week, on how many days has your skin been flaking off because of your eczema? 7. Over the last week, on how many days has your skin felt dry or rough because of your eczema?

Purpura/Ecchymosis in skin reasons why ?

Defined as: multiple pinpoint hemorrhages and accumulation of blood under the skin-bruising Why: old age: loss of supporting collagen in dermis associated with old age. steroid treatment of ANY TYPE

Inflammatory skin conditions **Eczema/dematitis Features in acute vs chronic? Common presentations?

Definition Dermatitis =group of inflammatory conditions affecting the epidermis ( outer layer of skin), often used interchangeably with eczrma Eczema (or dermatitis) is a chronic inflammatory non-infective skin condition, characterized by papules and vesicles on an erythematous base, with Xerosis (dryness) and Pruritic skin (itchiness). Pathophysiology Not fully understood, but a positive family history of atopy (i.e. eczema, asthma, allergic rhinitis) is often present. A primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin) appears to underlie atopic eczema. Exacerbating factors such as infections, allergens (e.g. chemicals, food, dust, pet fur), sweating, heat and severe stress. Clinical presentation >More common on the face and extensor aspects of limbs in infants, and the flexor aspects in children and adults. >A child has had 'cradle cap' since the age of 4 weeks and has now developed generally dry skin. His mother complains that he never sleeps and sometimes scratches until he bleeds. He has been on soya milk for the last 6-weeks, with no change in his skin condition. Hx >Family history of atopy > Failure to thrive/ GI symptoms- is baby putting weight on? Any d & v? -if failure to thrive, change milk to hypoallergenic milk ? Environment/potential triggers eg pets >Treatments tried > Bathing routine- bubble bath? Detergents can be irritants Types Acute: refers to a rapidly evolving red rash which may be blistered and swollen -eyrethamatous(Redness), swelling, usually ill defined Papules, vesicles, weepy (exudate), crusting Scaling Subacute: Refers to a long-standing irritable area -appear red, dry, and scaly. An in-between stage between acute and chronic. Chronic -Thickened, scaling, pigmented Fissured Lichenification -Chronic scratching/rubbing can lead to excoriations and lichenification -appears less red -. May show nail pitting and ridging of the nails. Types of dermatitis/DDx When classifying: 1)Cause 2)Clinical pattern 3)Body site Endogenous and mixed: >Atopic( most common ) -particularly prevalent in children: 60% remission in childhood may relapse with trigger factors : • Infection • Irritants e.g. Soap, detergents • Allergies e.g. House dust mite, pets, foods, grass • Stress • Others - associated with dysfunctional skin barrier and Th2 cell adaptive immune responses to common environmental allergens It is a disease with complex genetic and environmental susceptibility factors -inherited factors seem important, as there is nearly always a family history of dermatitis or asthma. •Filaggrin gene mutations -Frequent associated with other atopic conditions food allergy, rhinitis, asthma 80% have raised IgE clinical presentation -May have itch with very little rash other than scratch marks Sensitive, often dry skin •Onset in infancy on the face • Later childhood often elbow and knee flexures • In adults face trunk and hands common Complications • Growth retardation • Steroid side effects e.g. striae • Depression • Infection • Widespread Herpes Simplex- Eczema herpeticum Usually Staphylococcus aureus, sometimes Streptocoocus pyogenes >Seborrhoeic dermatitis & dandruff: are due to irritation from toxic substances produced by Malassezia yeasts that live on the scalp, face and sometimes elsewhere. >Nummular dermatitis/Discoid eczema -may be set off initially by an injury to the skin: scattered coin-shaped irritable patches persist for a few months >Infective dermatitis seems to be provoked by impetigo (bacterial infection) or fungal infection. Gravitational dermatitis arises on the lower legs of the elderly, due to swelling and poorly functioning leg veins. >Otitis externa - dermatitis affecting the external ear canal >Meyerson naevus - dermatitis affecting melanocytic naevi (moles). > Pompholyx/dyshidrotic eczema) -type of eczema that causes tiny blisters to develop across the fingers, palms of the hands and sometimes the soles of the feet. It can affect people of any age, but it's most often seen in adults under 40. >Asteatotic eczema/xerotic eczema or eczema craquelé -form of eczema that occurs when the skin becomes abnormally dry, itchy and cracked. It is often found in elderly people, though it is not uncommon for people in their 20s. >Venous/Gravitational eczema - long-term skin condition that affects the lower legs. It's common in people with varicose veins. Varicose eczema tends to be a long-term problem. However, treatments are available to help keep it under control. > Lichen Simplex - response to the skin being repeatedly scratched or rubbed over a long period of time (also called lichen simplex chronicus). A single or multiple plaque (thickened area of skin) of rough skin forms, with increased markings and sometimes little bumps around the hair follicles. Lichen simplex can affect any age group, but is most common in adults and is unusual in children. Exogenous >irritant contact -provoked by body fluids, handling water, detergents, solvents or harsh chemicals, and by friction. Irritants cause more trouble in those who have a tendency to atopic dermatitis >allergic contact -due to skin contact with substances that most people don't react to, most commonly nickel, perfume, rubber, hair dye or preservatives. A dermatologist may identify the responsible agent by patch testing >Photoaggravated dermatitis/photodermatitis >food-induced atopic eczema:: > Ask about itch or redness after certain foods (immediately or hours later), diarrhoea, vomiting, and/or poor weight gain. -Milk, egg, wheat, soy, and peanut account for about 75% of the cases of food-induced atopic eczema. > Consider asking the person to keep a food diary over 4-6 weeks. >In infants, also ask about feeding history (weaning, breastfeeding, or bottle feeding). >Suspect food allergy in children with atopic eczema who have reacted previously to a food, with immediate symptoms, or in infants and young children with moderate or severe atopic eczema that has not been controlled by optimum management, particularly if associated with gut dysmotility (colic, vomiting, altered bowel habit) or failure to thrive.

** What is lichen planus?

Definition Lichen planus is a T cell-mediated autoimmune disorder, in which inflammatory cells attack an unknown protein within the skin and mucosal keratinocytes. a chronic inflammatory skin condition affecting the skin and mucosal surfaces. Contributing factors to lichen planus may include: ●Genetic predisposition ●Physical and emotional stress ●Injury to the skin; lichen planus often appears where the skin has been scratched or after surgery — this is called the isomorphic response (koebnerisation) ●Localised skin disease such as herpes zoster—isotopic response ●Systemic viral infection, such as hepatitis C (which might modify self-antigens on the surface of basal keratinocytes) Contact allergy, such as to metal fillings in oral lichen planus (rare) ●Drugs--> lichenoid rash. -gold - quinine -quinidine ● Hypertrophic lichen planus may resemble squamous cell carcinoma. However, rarely, longstanding erosive lichen planus can result in true squamous cell carcinoma, most often in the mouth (oral cancer) or on the vulva (vulval cancer) or penis (penile cancer). Clinical presentation ●Skin +/- mucosal surfaces ●Grouped firm polygonal violaceous plaques on wrists, shins, lower back ●Lacy white streaks on the oral mucosa and skin lesions (Wickham's striae) ●Painful erosions on tongue, vulva, vagina, penis NB. Can present as oral, cutaneous, nails, vulval or penis, scalp or on face. Can look like SSC so need to do biopsy. If chronic inflammation in specific sites can increase risk of carcinoma. Typical features include: ●Irregularly thickened epidermis ●Degenerative skin cells ●Liquefaction degeneration of the basal layer of the epidermis ●Band of inflammatory cells just beneath the epidermis ●Melanin (pigment) beneath the epidermis Ix Biopsy confirmatory Mx -Treatment is not always necessary. ●Local treatments for the symptomatic cutaneous or mucosal disease are: -Potent topical steroids -Topical calcineurin inhibitors, tacrolimus ointment and pimecrolimus cream -Topical retinoids -Intralesional steroid injections

**Psoriasis risk factors? Genetics? types?

Definition chronic inflammatory skin condition characterised by clearly defined, red and scaly plaques (thickened skin). It is classified into several subtypes and is caused by the hyperproliferation of keratinocytes and inflammatory cell infiltration. Epi -Psoriasis affects 1.5-3% western populations, -Male =Female -Two peaks of onset second/third and sixth decade Aetiology -1/3 of patients with psoriasis will have family members with psoriasis Risk Factors- - Streptococcal tonsillitis and other infections - Injuries such as cuts, abrasions, sunburn (koebnerised psoriasis aka koebner phenomenen aka a linear eruption arising at a site of trauma ) - Sun exposure in 10% (sun exposure is more often beneficial) - Obesity -Smoking - Excessive alcohol - Stressful event - Medications such as lithium, beta-blockers, antimalarials, nonsteroidal anti-inflammatories and others - Stopping oral steroids or strong topical corticosteroids. Pathophys - Psoriasis is multifactorial. It is classified as an immune-mediated inflammatory disease (IMID), which can be induced by trauma such as infection, drugs, alcohol. -Genetics: histocompatibility complex HLA-C*06:02 =risk alllele(previously known as HLA-Cw6) is associated with early-onset psoriasis and guttate psoriasis. This major histocompatibility complex is not associated with arthritis, nail dystrophy or late-onset psoriasis. -immune factors and inflammatory cytokines (messenger proteins) such as IL1β and TNFα are responsible for the clinical features of psoriasis -. Current theories are exploring the TH17 pathway and release of the cytokine IL17A. Presentation = variable - chronic plaque form with well demarcated erythematous plaques topped by silvery scale affecting -commonest sites: scalp, elbows, knees &sacrum -plaques shiniest in skin folds -Lesions can sometimes be itchy, burning or painful. -Auspitz sign present (scratch and gentle removal of scales cause capillary bleeding) - 50% have associated nail changes (e.g. pitting, onycholysis). -5-8% suffer from associated psoriatic arthropathy - symmetrical polyarthritis, asymmetrical oligomonoarthritis, lone distal interphalangeal disease, psoriatic spondylosis, and arthritis mutilans (flexion deformity of distal interphalangeal joints) - When psoriatic plaques clear up, they may leave brown or pale marks that can be expected to fade over several months Types >Guttate >Flexural >Palmoplantar pustulosis >Generalised pustular psoriasis >Erythroderma Affects nails & joints Nails - Pitting discolouration, onycholysis JOINTS:Inflammatory arthritis "psoriatic arthritis" and spondyloarthropathy - occurs in up to 40% of patients with early-onset chronic plaque psoriasis -Distal IP joints affected, Seronegative rheumatoid-like factor - Sacroiliitis -Monoarthropathy -Arthritis mutilans=severe inflammation damaging the joints of the hands and feet, and resulting in deformation and problems with moving the affected areas; Associations ~ Inflammatory bowel disease (Crohn disease and ulcerative colitis) ~ Uveitis (inflammation of the eye) ~ Coeliac disease ~ Metabolic syndrome: obesity, hypertension, hyperlipidaemia, gout, cardiovascular disease, type 2 diabetes Diagnosis -Clinical but can be supported with skin biopsy Management ( see other sldes for specifics) ● General measures - avoid known precipitating factors, emollients to reduce scales ● Topical therapies (for localised and mild psoriasis) - vitamin D analogues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics and scalp preparations ● Phototherapy (for extensive disease) - phototherapy ● Oral therapies (for extensive and severe psoriasis, or psoriasis with systemic involvement) - methotrexate, retinoids(acitretin), ciclosporin, mycophenolate mofetil, fumaric acid esters and biological agents (e.g.infliximab, etanercept, efalizumab) Systemic corticosteroids are best avoided due to a risk of severe withdrawal flare of psoriasis and adverse effects. COMPLICATION-->DERM EMERGENCY >Erythroderma( red skin) Description -exfoliative dermatitis involving at least 90% of skin surface Causes -precipitated by previous skin disease (psoriasis , eczema) -lymphoma -drugs: (e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol, captopril) - idiopathic Clinical presentation -skin appears inflamed, oedematous scaly - systemically unwell with lymphadenopathy and malaise Mx -treat underlying skin condition , -emollients & wet-wraps to maintain skin moisture -topical steroids may relieve inflammation Complications of erythroderma: -Secondary infection, fluid loss & electrolyte imbalance -hypoethermia -high output cardiac failyre -capillare leak syndrome most severe)

**What is acne?

Definition: • Tagline: "An inflammatory disease of the pilosebaceous follicle" • Acne is a very common skin condition characterised by comedones (open = blackheads and closed =whiteheads) & pus-filled spots (pustules). It usually starts at puberty and varies in severity from a few spots on the face, neck, back and chest, which most adolescents will have at some time, to a more significant problem that may cause scarring and impact on self-confidence. For the majority it tends to resolve by the late teens or early twenties, but it can persist for longer in some people. Epidemiology: • Over 80% of teenagers aged 13- 18 years • Acne can develop for the first time in people in their late twenties or even the thirties. It occasionally occurs in young children as blackheads and/or pustules on the cheeks or nose. Risk factors • 12-24 years • Genetic predisposition • Greasy skin type • Precipitating drugs (androgens, corticosteroids (topical, oral, or injected), antiepileptic medications, isoniazid, lithium, and adrenocorticotropic hormone.) Pathophysiology ( see image) Diagnosed: • Usually no testing is necessary but free testosterone is most sensitive to establish presence of hyperandogenism. • Acne is easily recognised by the appearance of the spots and by their distribution on the face, neck, chest or back. However, there are several varieties of acne and, type can be determined from examination. • The most common type is 'acne vulgaris' Complications • Post-inflammatory hyperpigmentation • Scarring • Deformity • psychological and social effects. DDxRosacea-no presence of comodomes

EMERGENCY DERM **What is erythema nodosum?

Description A hypersensitivity response to a variety of stimuli Panniculitis= inflammation of subcutaneous fat peak incidence 18-34y, females >males Occurs without obvious cause but in western countries sarcoidosis can be a cause esp young women w Mylar lymphandeonopathy Causes >Group A beta-haemolytic streptococcus >Primary TB >Pregnancy >Malignancy >Sarcoidosis >IBD >Chlamydia >Leprosy >COCP Clinical presentation >Discrete tender nodules which may become confluent due to inflammation in s/c fat >Lesions continue to appear for 1-2 weeks and leave bruise-like discolouration as they resolve >Lesions do not ulcerate and resolve without atrophy or scarring >Shins=most common site

** What is necrotising fascitis?

Description A rapidly spreading infection of the deep fascia with secondary tissue necrosis Causes Group A Haemolytic streprococcus, or a mixture of anaerobic bacteria RFs >Abdominal surgery >Medica co-morbidities -diabetes -cancer NB. 50% of cases occur in previously healthy individuals Clinical presentation >severe pain >erythematous, blistering & necrotic skin >systemically unwell with fever and tachycardia >Presence of crepitus ( subcutaneous emphysema)-bubble wrap >x-ray may show soft tissue gas ( absence should not exclude the diagnosis ) Mx >Urgent referral for extensive surgical debridement >IV abc Prognosis Mortality up to 76%

Inflammatory skin conditions **Acne "I've got spots" Features? Variants?

Description ·An inflammatory disease of pilosebaceous units · Acne is a very common skin condition characterised by comedones (open = blackheads and closed =whiteheads) & pus-filled spots (pustules). It usually starts at puberty and varies in severity from a few spots on the face, neck, back and chest, which most adolescents will have at some time, to a more significant problem that may cause scarring and impact on self-confidence. For the majority it tends to resolve by the late teens or early twenties, but it can persist for longer in some people. Risk factors · 12-24 years · Genetic predisposition · Greasy skin type · Precipitating drugs (androgens, corticosteroids (topical, oral, or injected), antiepileptic medications, isoniazid, lithium, and adrenocorticotropic hormone.) Aetiology · Hereditary?- Acne can run in families, but most cases are sporadic and occur for unknown reasons. · The sebaceous (oil-producing) glands of people who get acne are particularly sensitive to normal blood levels of androgen hormones, which are present in both men and women. · These hormones cause the glands to produce an 1)excess of oil. · 2)Simultaneously, the dead skin cells lining the pores are not shed properly and clog up the follicles ( hyperkeratosis) · These 2 effects result in a build-up of oil, producing blackheads (where a darkened plug of oil and dead skin is visible) and whiteheads aka comedomes · The acne bacterium (known as Propionibacterium acnes) lives on everyone's skin, usually causing no problems. · But in those prone to acne, the build-up of oil creates an ideal environment in which these bacteria can multiplyàinflammation and the formation of red or pus-filled spots. · Some acne can be caused by medication given for other conditions or by certain contraceptive injections or pills. Some tablets taken by body-builders contain hormones that trigger acne and other problems. · Acne can be associated with hormonal changes. · FYI developing unusual hair growth or hair loss, irregular periods or other changes to your body, should be mentioned to doctor in case it is relevant. (?PCOS) Clinical presentation Seborrhoea - greasy skin Hyperkeratosis in duct forms microcomedones Colonisation with P.acnes · Typical appearance of acne is a mixture of: oily skin(seborrhoea), blackheads and whiteheads, red spots, yellow pus-filled pimples, and scars. · Occasionally, large tender spots or cysts may develop that can eventually burst and discharge their contents or may heal up without bursting. · Commonly affects the face, chest and upper back · The affected skin may feel hot, painful and be tender to touch. 1)Non-inflammatory lesions (mild acne) - open and closed comedones (blackheads and whiteheads) 2)Inflammatory lesions (moderate and severe acne) - papules, pustules, nodules, and cysts NB. nodulocystic acne is extreme end of Acne Vulgaris >Grading • Mild - comedones, few scattered papules & pustules • Moderate - more papules, pustules & nodules • Severe - multiple papules, pustules, nodules & cystic lesions Additional qs to ask in Hx Hirsuitism, androgenetic alopecia, regularity of periods, severe or treatment resistant acne Quality of life Family history Presence of scarring Variants of Acne >Acne Fulminans -Context of vulgaris, nodula cystic acutely and systemic unwell with it JOINT PAIN& FEVER >Acne Conglobata -extreme of Nodulocystic acne within Acne vulgaris > Acne excoriee -Those with Acne Vulgaris who due to psychological reasons (OCD cross-over) who pick and scratch their acne lesions. >Pomade/ Cosmetic Acne -physical blocking of pores due to makeup, cosmetics etc, not part of physiological problem >Mechanical >Industrial (Chloracne) >Drug-induced -see above Others >Gram-negative >Infantile:Often get acne as teenagers transplacental androgen why lasts for 5 years

Blistering skin disorders ** What is Pemphigus Vulgaris (PV)? Cause Presentation MX

Description -An ACQUIRED blistering skin disorder which usually affects middle-aged -INTRA-EPIDERMAL blisters form Cause -Autoantibodies against antigens within the epidermis causing an intra-epidermal split in the skin Pathophysiology -Intercellular adhesion is maintained by desmosome cell-cell junctions -They are similar to hemidesmosomes, desmosomes are protein chains holding structures together. -Desmosomes bridge from one keratinocyte to the next binding to the cell cytoskeleton forming a stable structure. -Intra-epidermal blisters occur in 2 ways: 1) the desmosomal proteins can be targeted by gene mutations giving rise to inherited blistering skin diseases.aka NOT Pemphis Vulgaris 2) the same desmosome proteins can be targeted as acquired abnormalities with autoantibodies giving rise to acquired . Autoantibody binding to the desmosomal proteins in the epidermis causes the desmosome to break apart and the epidermis to become disrupted and easily friable. Presentation -Flaccid, easily rupture blisters ( forming erosions and crusts) -Lesions are often painful -Usually affects the mucosal areas ( can precede skin involvement) Management >General measures -wound dressing ( where required, monitor for signs of infection , good oral care ( if oral mucosa is invovled) >Oral therapies -high dose oral steroids -immunosuppressive agents eg. azathioprine, mycopheneolate mofetil methotrexate & other

EMERGENCY DERM ** What is Erythema multiforme? signs ?

Description -often unknown cause, infections and drugs like penicillin can cause it -acute self-limiting inflammatory condition -herpes simplex virus (HSV)= main precipitating factor -mucosal involvement tis absent or limited to only one mucosal surface Clinical presentation Symmetrical eruption of discoid plaques on back of hands some plaques blister in middle Variable in appearance Characteristically affects body peripheries (hands+feet) sometimes face reaction pattern 2-3 weeks Mx ● Early recognition and call for help ● Full supportive care to maintain haemodynamic equilibrium Complications ● Mortality rates are 5-12% with SJS and >30% with TEN with death often due to sepsis, electrolyte imbalance or multi-system organ failure

EMERGENCY DERM ** What is acute meningococcaemia?

Description ● A serious communicable infection transmitted via respiratory secretions; bacteria get into the circulating blood Cause ● Gram negative diplococcus Neisseria meningitides Clinical presentation ● Features of meningitis (e.g. headache, fever, neck stiffness), septicaemia (e.g. hypotension, fever, myalgia) and a typical rash ● Non-blanching purpuric rash on the trunk and extremities, which may be preceded by a blanching maculopapular rash, and can rapidly progress to ecchymoses, haemorrhagic bullae and tissue necrosis Mx ● Antibiotics (e.g. benzylpenicillin) ● Prophylactic antibiotics (e.g. rifampicin) for close contacts (ideally within 14 days of exposure) ● Septicaemic shock, disseminated intravascular coagulation, multi- organ failure and death

**What is cellulitis & Erysipelas ?

Description ● Spreading bacterial infection of the skin >Cellulitis involves the deep subcutaneous tissue >Erysipelas an acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue Causes ● Streptococcus pyogenes -->· ERYSIPELAS ● Staphylococcus aureus >Erysipelas is usually caused by streptococci. >Cellulitis is also often caused by streptococci, but many other bacteria may be involved, such as staphylococci. Risk factors ●immunosuppression ● wounds ● leg ulcers ●toeweb intertrigo minor skin injury Presentation ● Most common in the lower limbs ● Local signs of inflammation - swelling (tumor), -erythema (rubor) -warmth (calor -pain (dolor) ●may be associated with lymphangitis (Inflammation of lymph channels secondary to an infection near said channel) ● Systemically unwell with fever, malaise or rigors, particularly with erysipelas >Cellulitis -An area of redness develops and enlarges, often slowly with an ill-defined edge in cellulitis -This can happen over the course of a few hours to a few days -As the blister top comes off, a raw area of skin can be seen. In severe cases, areas of skin may turn purple or black. There may be red streaks in the skin above the affected area -most common on the lower leg >Erisipelas -An area of redness develops and enlarges and more suddenly with a sharp edge in erysipelas, -a well-defined, red raised border -This can happen over the course of a few hours to a few days -As the blister top comes off, a raw area of skin can be seen. In severe cases, areas of skin may turn purple or black. There may be red streaks in the skin above the affected area · This can happen over the course of a few hours to a few days -most common in legs and face, but any area of skin can be affected Diagnosis · Cellulitis and erysipelas are diagnosed by the typical appearance and symptoms. ·A skin swab or blood tests may be taken to try to identify the bacteria in the laboratory; however, identification of the bacteria is rarely possible. · Erysipelas is usually caused by streptococci. Cellulitis is also often caused by streptococci, but many other bacteria may be involved, such as staphylococci. Mx ● Antibiotics (e.g. flucloxacillin or benzylpenicillin) ● Supportive care including rest, leg elevation, sterile dressings and analgesia Complications · The severity can range from mild to severe. This will depend on how large the red area is, which part of the body is affected (erysipelas of the face is more serious) and if there are any other health problems such as an impaired immune system or poorly controlled diabetes. -Septicaemia -Infection spreading to deeper tissues, like the muscle or bone -Long-term swelling of the affected site due to lymphatic vessel damage -Increased likelihood of further cellulitis or erysipelas at the same site -Kidney damage following streptococcal infection -Meningitis following facial erysipelas -Local necrosis

Commensal organisms that can cause infection What does corynebacteria cause?

Diphtheria is an infection caused by the bacterium Corynebacterium diphtheriae. Diphtheria causes a thick covering in the back of the throat

***HIV skin manifestations? sometimes seroconversion rash NB. (when HIV-specific antibodies develop) is often accompanied by a mononucleosis-like syndrome that may be mistaken for the flu. These symptoms, called acute HIV infection, generally occur 2 to 4 weeks after initial infection and last for 1 to 2 weeks.

Dry skin, seborrhoeic dermatitis 'Ordinary' skin infections Infections with more extreme presentations

What skin changes happen with pre-tibial myxoedema?

Due to deposition of mural polysaccharides (hylaluronic acid) in dermis and subcutaneous tissues of pre-tibial skin Probably due to over activity of fibroblasts >Associations: Deveops years after autoimmune Graves thyroid disease -LOOK FOR: exophthalmic eyes & goitre NB> this picture is end stage acute PTM looks like a red rash on your shins

What kind of inflammatory skin conditions exist?

Eczema Acne Psoriasis

EPIDERMIS >Seborrheic keratosis/basal cell papilloma/sebborhoeic warts

Epidemiology -Occurs post 40 -family hx Presentation -Asymptomatic -raised surface -most common on trunk -vary in colour

**Benign lumps and bumps throughout the layers of the skin these can all proliferate

Epidermis Seborrhoeic keratosis Dermis Dermatofibroma- proliferation of histiocytes and fibroblasts Vascular Cherry angioma Pyogenic Granuloma Nerve Neurofibromas Connective tissue Shagreen patch Melanocytes Benign melanocytic naevi Fat Lipoma Lymphatic Lymphangioma circumscriptum

Endogenous and mixed- Atopic Discoid eczema

Fairly well defined round patches eczema Often secondarily infected with Staph Aureus Cause unknown Can be seen in other types of eczema

*** What is Fish tank granuloma? What is it caused by ?

Fish tank granuloma? Atypical mycobacterial infection Inoculation into skin then sporotrichoid spread through lymphatics leading to other lesions **mycobacterium marinum -ulceration or abscess with a line of nodules along lymph drainage -expose abraided skin to contamination, 2-3 wk later solitary nodule or pustule, then breakdown into crusted ulcer, abscess or verrucous nodules -confirm with culture -lacks significant lymphadenopathy -rifampicin, clarithromycin, septra, tetracyclines for 6 weeks with ID consult Ddx: Cat-scratch fever Primary inoculation tuberculosis Inoculation leishmaniasis Sporotrichosis Other mycobacterial infections Deep fungal infections

Commensal organisms that can cause infection What does Strep pyogenes( Lancefield Group B beta haemolytic streptococci) cause?

GROUP B STREP INFECTION MCC all throat infections, lymphangitis, impetigo, necrotizing fascitis, erysipelas, scarlet fever 2nd MCC: all other skin infections

**Terminology in examination findings General 1)Pruititis 2)Lesion 3) Rash 4) Naevus 5) Comedome Distribution ( the pattern of spread of lesions) is it symmetrical or unilateral? 1) generalised 2) widespread 3) localised 4) flexural 5) extensor 6) pressure areas 7)dematome 8)photosensitive 9) Koebner phenomena Configuration: the patter or shape of grouped lesions 1) Discrete 2)Confluent 3) Linear 4) target 5) annular 6)dsicoid 7) nummular Colour 1) Erythema 2) purpura 3) hypo-pignmentation 4) de-pigmentation Morphology-structure of a (primary) lesion 1)Macule 2) patch 3)papule 4)nodule 5)plaque 6)vesicle 7)bulla 8)pustule 9)abscess 10) w(h)eal 11)boil/furuncle 12) carbuncle Morphology-structure of a (secondary) lesion 1)excoriation 2)lichenification 3)scales 4)crust 5)scar 6)ulcer 7)fissure 8)striae Hair 1)alopecia 2)hirsuitism 3)hypertrichosis Nails 1)clubbing 2)kolionychia 3)onycholysis 4)pitting

Genreral 1) Itching 2) An area of altered skin 3) An eruption 4) A localised malformation of tissue structures eg. pigmented melanocytic naevus (mole) 5)A plug in a sebaceous( oily) follicle containing altered sebum, bacteria and cellular debris, can present as either open ( blackhead) or closed ( whitehead) Distribution 1) all over the body 2) extensive 3) restricted to one area of the skin only 4) body filed: groin, neck, behind ears, popliteal and antecubital fossa 5)knees, elbows , shins 6) sacrum, but, ankles and heels 7) an area of skin supplied by a single spinal nerve 8) affects sun exposed areas : face, neck and back of the hands 9)a linear eruption arising at a site of trauma Configuration: the patter or shape of grouped lesions 1) individual lesions separated from eachother 2)lesions merging togetehr 3) in aline 4) concentric rings ( like a dartboard) present in erythema multiforme 5)like a circle or ring like in tinea corporis (ringworm) 6) a coin shaped/round lesion like in discoid ecxema Colour 1) Redness ( due to inflammation and vasodilation ) which glances on pressure eg. palmar erythema 2)red or purple colour ( due to bleeding into the skin or mucous membrane) which does not blanch on pressure- petechiae( small pinpoint macules_ ecchymoses ( larger bruise like patches) eg. Henoch-Schönlein purpura (palpable small vessel vasculitis) 3) areas of paler skin eg. piyriasis versicol: superficial fun cat infection 4) white skin due to abs)white skint due to abscess of melanin e.g. vitiligo ( loss of skin melanocytes) 5)darker skin which may due to various causes -. post inflammatory eg.. melasma ( increased melanin pigmentation) Morphology-structure of a (primary) lesion 1)flat area of altered skin eg.freckles aka lentigines 2_larger flat area of altered colour or texture e.g. vascular malformation like naevus flammeus/port wine stain 3)solid raised lesion <0.5cm in diameter eg. xanthomata 4)solid raised lesion >0.5 cm in diameter with a deeper component eg. pyogenic granuloma ( granuloma telangiectaticum) 5)palpale scaling rated lesion >0.5cm e.g. psoriasis 6)small blister, raised, clear fluid-filled lesion <0.5 cm in diameter e.g. acute hand eczema (pompholyx) 7)large blister, raised, clear fluid-filled lesion >0.5 cm e.g. reaction to insect bites or a burn 8)pus containing lesion <0.5 cm e.g. acne 9)localised accumulation of pus in the dermis or subcutaneous tissue eg.periungual absences ( acute paronychia) 10(transient raised lesion due to dermal oedema e.g. urticaria & TB test 11)staph infection around or within hair follicle 12)staph infection of adjacent hair follicles-multiple boils/furuncles, a collection of furuncles Morphology-structure of a (secondary) lesion 1)loss of epidermis following trauma eg.g.. excoriations in eczema 2)well defined roughening of skin with accentuation of skin markings e.g. lichecnification due to chronic rubbing in eczema 3)Flakes of stratum corner e.g. psoriasis: silvery scales 4)rough surface consisting of dried serum, blood, bacteria and cellular debris that exuded through an eroded epidermis (from a burst blister) e.g. impetigo 5)new fibrous tissue which occurs post-wound healing and may be atrophic(thinning) hypertrophic )(hyper proliferation within wound boundary) or keloids ( hyperprolifarion beyond wound boundary) 6)loss of epidermis and dermis (heals with scarring) e.g. leg ulcers 7)an epidermal crack often due to excess dryness. eg. eczema 8)linear areas which progress from purple to pink to white, with the histopathological appearance of a scar ( associated with excessive steroid usage and glucocorticoid production, growth spurts and pregnancy) Hair 1)loss of hair e.g. alopecia areata(well-defined patch of complete hair loss) 2)androgen-dependent hair growth in a female 3)non-androgen dependent pattern of excessive hair growth eg. dairy ear Nails 1)loss of angle b/w the posterior nail fold and nail plate assoc w. suppurative lung disease, cyanotic heart disease, IBD & idiopathic 2) spoon-shaped depression in the nail plate.. assoc. w. Fe deficiency anaemia congenital & idiopathic 3)separation of the distal end of the nail plate from nail bed associated w. trauma, psoriasis, fungal nail infection & hyperthyroidism 4)punctuate depressions of the nail plate associated w. psoriasis, eczema & alopecia areata

**How many strains of human herpes viruses are there? What are their names

HHV1-Herpes Simplex Virus Type 1 HHV2- Herpes Simplex Virus Type 2 HHV3- Varicella zoster virus ( chickenpox, shingles) HHV4- EpsteinBarrVirus -->glandular fever HHV5- Cytomegalovirus HHV6- Roseola virus HHV7- ?pityriasis rosea HHV8- Kaposi's sarcoma

** Mx of high risk BCC vs low risk types **How do you identify high risk BCC? Complications of BCC? MX or incomplete excision & follow up?

HIGH RISK >occurring on eyes, nose, lips, nasolabial folds, ears >Tumours >2cm diameter >ill-defined >Patient immunosupressived >Infiltrative, microdocular >basisquamous >perineural invasion (see image) >recurrent or incompletely excised Complications of BCC >perineural invasion (see image), when BCC tumour invades intro cranium ( rare cause of death). >●Local tissue invasion and destruction Prognosis ●Depends on tumour size, site, type, growth pattern/histological subtype, failure of previous treatment/recurrence, and immunosuppression Mx of high risk >Surgical excision: treatment of choice as it allows histological examination of the tumour and margins -excision to clear deep surgical pain &4mm margin -But if tumours >2mm then 6mm margin is needed rather than 4 >Mohs micrographic surgery(excision of the lesion and tissue borders are progressively excised until specimens are microscopically free of tumour) - considered if tumour & site of tumour are high risk or recurrent >Radiotherapy -when surgery is not appropriate -not good for younger population -frail or elderly -palliation >Curettage & Cautery is avoided EXCEPT for -small nodular types of BCC -palliation (3 cycles) >Cryotherapy avoided except for small nodular types -2 30 second freeze thaw cycles >Topical therapy (Aldara & imiquimod cream),topical PDT is avoided except for superficial low risk disease LOW RISK >Surgical excision to clear deep surgical plane & 4mm margin >Curettage & Cautery useful in small & superficial tumours -AVOID in disease of lower legs >Cryotherapy useful in small & superficial tumours -AVOID in disease of lower legs >Topical therapy(Imiquimod) -small nodular & superficial disease >Mohs rarely appropriate even in recurrent disease MX oF INCOMPLETE EXCISION & FOLLOW UP >Tumors that are incompletely excised at the deep margins-->managed as high-risk tumours >Incomplete lateral margins on low risk sites can be treated less aggressively >low risk tumours need not be followed up routinely >multiple tumours, complex repairs or close excision margins may benefit from review

** Mx of high risk SCC vs low risk types **How do you identify high risk SCC? Complications of SCC? MX or incomplete excision ? SCC follow up?

HIGH RISK SCC >Sun-exposed sites -lip -ear -scalp -eyelids >Non sun exposed sites arising in areas of chronic injury & radiation -sacrum -perineum sole of foot > >2cm in diameter, M4mm in depth >Extending down to deep dermis S/C fat >Poor differentiation, -ill defined >Perineural invasion >If patient is immnosuppresed or has recurrent tumours >Incomplete excision of tumour HIGH RISK SCC MX >Surgical excision: 1st line -clear deep surgical plane & 4mm margin (if tumours >2cm diameter then 6mm margin) >Mohs micrographic surgery -recurrence of tumour -where margins may be technically difficult to ace or are indistinct >Radiotherapy -used as an adjunct for tumour in lip, nasal vestibule & ear -used if patients will not tolerate surgery >Curettage & cautery -avoid except for palliation LOW RISK SCC MX >Surgical excision: 1st line -clear deep surgical plane & 4mm margin >Curettage & cautery -useful in small (<1cm) tumours -superficial tumours particularly early in situ disease >Cryotherapy --useful in small (<1cm) tumours -superfical tumours particularly early in situ disease >Radiotherapy -frail or elderly Prognosis ● Depends on tumour size, site, histological pattern, depth of invasion, perineural involvement, and immunosuppression ●worse prognosis compared to BCC SCC FOLLOW UP >Check scar >Check at risk sites & LNs >Low risk tumours followed up at 3 months & discharged if no signs of recurrence >High risk yours followed where practical for 2 years at 3 month intervals >Patients on immunosuppression follows dup for 5 years >All cases should be discussed at an MDT

Background on hair growth?

Hair growth Hair grows in cycles, -with the growing phase (anagen) lasting about 1000 days on the scalp - catagen phase, cuts off from blood supply and nutrient -before the follicle enters the resting phase (100 days of telogen) during which the hair is shed - a new cycle of hair growth (exogen) begins. Why doe areas of hair become thin? The growing phase is becoming shorter and the shedding phase longer Normal person loses about 100 hairs a day Types of hair: ● Lanugo - fetal ( this type of hair grows in anorexia nervosa as an adaption) ● Vellus - cheeks etc ● Terminal - pubes and head

** How does varicella-zoster virus lead to Herpes zoster aka shingles and lead to blistering on the skin? What is the complication postherpetic neuralgia?

Herpes zoster (shingles) infection: VZV varicella zoster virus · HHV3 ( part of herpes virus family) Background ·varicella zoster virus also causes chickenpox ·The virus is called herpes zoster when it causes shingles and herpes varicella when it causes chickenpox. They were named before it was known that a single virus was responsible for both conditions. · More common in older people Pathophysiology · It is a painful blistering rash caused by the reactivation of the varicella zoster virus that causes chickenpox · After a person has had chickenpox, the virus lies inactive in the nervous system within the dorsal root ganglion. When the virus reactivates it multiplies and moves along the nerve fibres to the area of skin supplied by those particular nerves aka dermatomal distribution; shingles then appears in this area. · Shingles can appear anywhere on the body. · Shingles is not caught from someone who has shingles or from someone who has chickenpox. ·It develops when the inactive herpes zoster virus awakens, for example when a person's immune defences are weaker than normal. ·However, a person affected by shingles can give chickenpox to someone who has never previously had chickenpox. ·A person with shingles is infectious from the point of the first blister until the blisters crust over (approximately 7 days) · 1 person in 5 will develop shingles at some time. Most outbreaks of shingles occur for no obvious reason, but are more likely if the individual: is elderly, is experiencing physical or emotional stress, has an illness that weakens the immune system, such as leukaemia, lymphoma (e.g. Hodgkin's disease) or HIV infection, imunnosupressed Clinical presentation -development of painful, inflamed blisters that follow the nerve routes, dermatomal distribution >Symptoms · Before the blisters appear, the first obvious symptom is pain in the area where the virus is reactivating. · However, it is important to note that not all people affected by shingles will experience pain. · For example, many young people will only experience an itching or mild burning sensation in the affected area. · For those who do experience pain, it is usually in one small area. The pain can range from mild to severe and could be a constant dull, tingling, aching or burning pain/sensation. · The rash usually appears a day or two after the onset of pain, and a fever and/or a headache may develop >Signs: · Shingles appears as a group of red spots on a pink-red background which quickly turn into small fluid-filled blisters. · Some of the blisters burst, others fill with blood or pus. The area then slowly dries, crusts and scabs form. · The scabs will fall off over the next two to three weeks. · The rash usually covers a well-defined area of skin on one side of the body only (right or left) and will not cross to the other side of the body. · The position and shape of the rash will depend on which nerves are involved. · Shingles can affect any area, but the most common areas include the body or down an arm or leg. · Less commonly, shingles can affect one side of the face, and occasionally can cause complications affecting one eye eg. ophthalmic division of Cranial Nerve V ( trigemnial nerve) -EXAMINE THE EYE !. Diagnosis: · Clinically based on apperance · If there are doubts, a skin scrape can be taken Mx · Shingles usually resolves on its own within a few weeks. · Oral antiviral treatment may help clear the rash sooner and can reduce its unpleasant effects. · Usually Acyclovir, but ONLY EFFECTIVE IF GIVEN WITHIN THE FIRST 3 DAYS OF SYMPTOM ONSET Complications: · Shingles affecting the face (forehead and nose) may spread to the eye leading to inflammation and ulceration in the eye, and later to scarring, which if untreated could lead to vision problems or blindness. Blisters coming up on the side of the nose will alert your doctor to this risk, and you should also get urgent advice from an eye specialist (ophthalmologist). · Muscles in the area affected by shingles occasionally become weak and there may be temporary facial paralysis on the shingles-affected side of the face. · The pain caused by shingles may persist long after the rash has cleared, particularly in the elderly. This is called postherpetic neuralgia and may persist for a long time. Mx · Using an anaesthetic ointment (lidocaine 5%) before applying a topical analgesic cream (capsaicin cream) may help with Postherpetic Neuralgia pain. · A vaccine is licensed to prevent shingles in people who are 70 to 79 years old.

** PC :itchy skin hx? Ddx Mx What is an itchy eruption ??

Hx"Important questions to ask: · Is the itch localised or generalised? · What is the severity of the itch? Are you able to concentrate /sleep? · What is its distribution? · Is there a primary rash or not? · Erosions, crusting, bruising and infection can be due to excoriation and are of no help diagnostically. · PMH and general health? · Do you think there is anything causing the itch? Ddx >Very itchy skin with a localised rash ●Contact dermatitis ●Head lice ●Insect bites ●Lichen planus ●Eczema ●Venous eczema >Mildly itchy skin with a localised rash ●Venous eczema ●Psoriasis ●Eczema (seborrhoeic) >Very itchy skin with a generalised rash ●Bullous pemphigoid ●Eczema atopic ●Erythroderma ●Lichen planus ●T cell lymphoma ●Urticaria ●Scabies ●Nodular prurigo ●Neurodermatitis >Mildly itchy skin with a generalised rash ●Psoriasis - can get urticaria around psoriatic plaque ●Xerotic eczema - general dry skin >Localised itchy skin without rash ●Neuropathic/neurogenic >Generalised itchy skin without rash ●Pruritus/prurigo of pregnancy ●Chronic renal insufficiency ●Cholestasis ●Iron deficiency ●Polycythaemia vera ●Hyperthyroidism ●Lymphoma ●Diabetic neuropathy ●Drug-induced (eg, opioid, chloroquine, vancomycin flushing) ●Chronic pruritus of unknown origin Mx antihistamines help reduce itchiness symptom but you nee to treat cause if it is from an infection or an inflammatory cause Itchy eruption An itchy (pruritic) eruption can be caused by an inflammatory condition (e.g. eczema), infection (e.g. varicella), infestation (e.g. scabies), allergic reaction (e.g. some cases of urticaria) or an unknown cause, possibly autoimmune (e.g. lichen planus). Eczema hx - Personal or family history of atopy - Exacerbating factors (e.g. allergens, irritants) Common sites - Variable (e.g. flexor aspects in children and adults with atopic eczema) Lesion - Dry, erythematous patches - Acute eczema is erythematous, vesicular and exudative Associated features - Secondary bacterial or viral infections Possible Ix - Patch testing Serum IgE levels - Skin swab Mx - Emollients - Corticosteroids - Immunomodulators - Antihistamines Scabies hx - May have history of contact with symptomatic individuals - Pruritus worse at night Common sites Lesion - Sides of fingers, finger webs, wrists, elbows, ankles, feet, nipples and genitals Lesion - Linear burrows (may be tortuous) or rubbery nodules Associated features - Secondary eczema and impetigo Possible Ix -Skin scrape, extraction of mite and view under microscope Mx - Scabicide (e.g. permethrin or malathion) - Antihistamines Urticaria hx - Precipitating factors (e.g. food, contact, drugs) Common sites - No specific tendency Lesion - Pink wheals (transient) -May be round, annular, or polycyclic Associated features May be associated with angioedema or anaphylaxis Possible Ix - Bloods and urinalysis to exclude a systemic cause Mx - Antihistamines - Corticosteroids Lichen planus hx - Family history in 10% of cases - May be drug-induced Common sites - Forearms, wrists, and legs - Always examine the oral mucosa Lesion - Violaceous (lilac) flat-topped papules - Symmetrical distribution Associated features -Nail changes and hair loss - Lacy white streaks on the oral mucosa and skin lesions (Wickham's striae) Possible Ix Skin biopsy: differentiate from SCC Mx -Corticosteroids - Antihistamines

FITZPATRICK Skin types

I Always burns, never tans II Always burns, sometimes tans III Sometimes burns, always tans IVNever burns, always tans V-Brown skin VI-Black skin sunscreen UVB- factor 30 UVA- 5 stars

1)What are the acute consequences of excessive sun exposure? 2) what are the chronic effects of excessive sun exposure?

Image shows someone with skin ageing to one side of the face RHS. Could be a lorry driver who had UVA sunlight coming through via the window-->wrinkling 1)SUBNURN -erythema develops 2-12 hours -eyrthema settles over 2-3 days -Desquamation (peeling, skin shedding due to damaged keratinocytes) -resollution RISK: episodes of sunburn increase risk of skin cancer 2) Depends on >Skin type >genetic predisposition eg. Gorlin's syndrome (nevoid basal cell carcinoma syndrome, is a condition that affects many areas of the body and increases the risk of developing various cancerous and noncancerous tumors happens in teens & 20s.) >sun exposure Consequences: SKIN TYPE +Genetic predisposition + sun exposure( natural or UV) >Accumulated DNA damage -Actinic /solar keratosis (pre-cancerous SCC condition, dysplastic keratinocytes). NB. solar/actinic mean sunlight, keratosis =scaly increases risk of skin cancer -->bald men, head & neck -Skin cancer: BCC/SCC >Degradation of connective tissues -sun ageing/weathering -solar elastosis: puckered chicken effect -wrinkling -telangectasia >Solar lentigines (freckles)

What kind of skin infections exist?

Impetigo, cellulitis, VZV, HSV, tinea pedis, syphilis

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

In-situ SCC: Bowen's disease Clinical features >1 or more , slowly enlarging erythematous scaly plaques. >Habitually sun-exposed or covered sites. Mx > on the face:photodynamic therapy, but such lesions are commonly managed by cryotherapy, 5-fluorouracil cream, imiquimod cream and surgery.

**investigations & management of urticaria? prognosis ?

Investigations >Underlying triggers (if any) best identified through careful history and examination >Not indicated unless chronic or atypical lesions > Following done often to exclude systemic conditions presenting with urticaria • FBC • LFTs • Antinuclear antibodies • Anti-IgE receptor antibodies • CRP • ESR • Urinalysis Management > Acute urticaria +- angioedema -1st line - trigger identification & avoidance -Plus - H1 receptor antagonists (mainstay of therapy) (non-sedating preferred) • Loratadine • Cetirizine • Fexofenadine Plus - oral prednisolone if severe (If airway involvement ABCDE approach and utilise adrenaline) Chronic urticaria +- angioedema 1st line - trigger identification & avoidance (psychosocial stress thought to play key role) >Plus - treatment of underlying illness >Plus - H1 receptor antagonists (same as acute) (best taken prophylactically than reactively) >Adjunct - H2 receptor antagonists i.e. Ranitidine >Adjunct - systemic corticosteroids for flare-ups but not long-term 2nd line - immunomodulating agents i.e. Omalizumab or Ciclosporin Hereditary angioedema C1 inhibitor - Ecallantide Prognosis Acute - mostly self-limiting and short lived Chronic - well managed with antihistamines Angioedema alone - complex but well managed

** Causes of alopecia aka different types of alopecia ? Scarring vs non-scarring clinical presentation Ddx MX

Ix Assess psychological impact TFTs Ferritin Signs of androgen excess What treatment would you consider, if investigations prove to be normal? No treatment, hairstyling, hair pieces OTC topical minoxidil- not prescribable on NHS Causes 1)Male pattern baldness aka androgenic alopecia ● This androgen dependent trait causes the conversion of scalp terminal hairs into miniaturised vellus hairs ● Frequency and severity increases with age -. 80% of men and 50% of women by 70 Ddx >Other non scarring hair disease: ● Alopecia areata ● telogen effluvium > If Early onset in women ● concern for hyperandrogenism -->test Mx > Male o Minoxidil (k+ channel opener) and finasteride( treat an enlarged prostate or hair loss in men.) o Hair transplantation and scalp reduction >Female o Minoxidil o Oral contraceptive can be helpful 2)Diffuse alopecia >Hair changes with menstrual pattern is a useful indicator ●Heavy periods: iron deficiency ●Irregular periods, amenorrhoea or menorrhagia, o long standing and gaining weight --> Polycystic ovary syndrome --> thyroid disease o Short term and masculinisation: -->adrenal tumour 3)Telogen Effluvium > Acutely increased shedding. IF definable precipitating event, hair loss begins approximately 3 months after the event >Caused by medication or systemic disease: ● Drugs o Antimitotic: A type of drug that blocks cell growth by stopping mitosis (cell division). They are used to treat cancer. -cyclophosphamide vincristine o Anticoagulants o Thiouracils (anti thyroid) ● Endocrine o Cushing o thyroid o ovarian o CAH ( congenital adrenal hyperplasia ) o Post-menopausal -Women are often androgenised by menopause ● Idiopathic o Similar to men 4)Alopecia areata ● These are autoimmune disorders that are related to inherited factors ● Can be split into three classes: 1) Alopecia areata - small areas of hair loss scattered around the scalp 2)Alopecia totalis - Scalp is totally bald 3) Alopecia universalis - All body hair is lost ● Increased risk of other autoimmune disorders Mx > Topical steroids > Topical irritants (Azelaic acid) >Topical minoxidil

** Mx of acne?

Ix · Usually no testing is necessary but free testosterone is most sensitive to establish presence of hyperandogenism. · Acne is easily recognised by the appearance of the spots and by their distribution on the face, neck, chest or back. However, there are several variants of acne and, type can be determined from examination. · The most common type is 'acne vulgaris'. Mx · Currently there is no 'cure' for acne, although the available treatments can be very effective in preventing the formation of new spots and scarring. · Make patient aware most treatments take 2 or 4 months to show max effect, no quick-fix · no specific food has been identified to cause acne >Grading • Mild - comedones, few scattered papules & pustules • Moderate - more papules, pustules & nodules • Severe - multiple papules, pustules, nodules & cystic lesions Acne treatments fall into the following categories: 1)Topical treatments, i.e. those that are applied directly to the skin 1st line: -topical retinoids: anti-inflammatory -benxoyl peroxide :Anti-Comedogenic: treat comedonal element of acne -antibiotics:antibiotic & anti-inflammatory -->Rx at least 8-12 weeks -->MODERATE ACNE 2)Oral antibiotics, i.e. tablets taken by mouth -oral tetracyclines:1st line -erythromycin -trimethoprim --> Rx at least 8-12 weeks --> Exrtensice or every acne 3)Oral contraceptive pills e.g. - Dianette (Cyproterone acetate&Ethinylestradiol) -think about risks /benefits of using COCP -reduces the amount of oil the skin produces. It usually takes at least 3 - 4 months for the benefits to show. Although they may not be taken for this reason, the pills also help to prevent conception. As they prevent ovulation, they may be less suitable in young teenage girls where ovulation is not well established. Risks: -increase the risk of blood clots which can be dangerous. -greater risk for people who smoke, are overweight or have others in the family who have had blood clots. 4)Oral retinoids -isotretinoin capsules aka roaccutane -->1mg/kg for 4 months -->highly effective -->potential for remission -->teratogenic, dont take if planning on conceiving a child and getting prganct -->Take if : >Severe Nodular/cystic acne or >Failed 2 x courses of oral abc or >Evidence of scarring 5)Other treatments e.g. ?Spironolactone Treatment depends on severity of acne >If patient presents with nodulocystic acne and has had no treatment besides OTC preparations -consider Severity, assess presence of scarring, consideration of psychosocial factors Mx -Topical treatment: BPO,( benzyl peroxide) retinoid, antibiotic or combination -Consider referral for isotretinoin Prognosis -oral retinoids CAN potential of inducing remission of disease Complications · Post-inflammatory hyperpigmentation · Scarring · Deformity · psychological and social effects Mx of acne scarring -NHS treatment treats active acne disease e.g. with isoretinoin >Hypetrophic itchy keloid scarring ( beyond site of original location) If symptomatic can inject steroid, doesn't get rid of appearance but gets rid of symtoms CO2 lasers >Atrophic scarring Derm abrasion, microneedling, laser Topical retinoids can be helpful

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Keratoacanthoma Clinical features >Difficult clinically and histologically to distinguish from invasive SCC >Typically presents as a rapidly growing dome-shaped nodule with a keratinous core. >May resolve spontaneously within a few months. Mx Surgical excision should be arranged in case the lesion is an invasive squamous cell carcinoma. Sometimes, shave, curette and cautery is adequate.

** Where does blistering occur within the dermal epidermal junction? What is the weakest part of this junction called?

LAMINA LUCIDA= weakest part of DEJ

** How can blistering be classified ?

LEFT images -blistering in DEJ: sub epidermal blisters ( intact roof) e.g. -BURN -Pemphigoid RIGHT images -inraepidermal blistes -no roof intact -eroision

**Limitations of Vit d analogues, coal tar & Dthranol

Limitations are very similar: Irritate the skin and they are not suitable for the more inflammatory forms of psoriasis. Their use should be suspended during an inflammatory phase of psoriasis. The efficacy and the irritancy of each substance varies between patients. If a substance irritates significantly, it should be stopped, or the concentration reduced; if it is tolerated, its effects should be assessed after 4 to 6 weeks and treatment continued if it is effective.

***How do you manage pressure sores?

MANAGEMENT • Careful documentation is required of the site, size and number. • Patients should be transferred to a better pressure relieving surface and regimen of repositioning. • Attention should be paid to other factors such as incontinence, nutritional status, medications (analgesics, sedatives, hypnotics), sepsis and confusional states. • Micronutritional deficiencies are common as is a catabolic state. • Multivitamins Vitamin C, zinc and protein intake are among the most important nutritional factors to be considered but RCTs in this area are lacking. Grades 1-2 may heal within a fortnight but in Grades 3-4 healing frequently takes months. 1. Debridement of the sore will often aid healing but can cause a transient bacteraemia (NB prophylaxis vs SBE). This can be achieved surgically (cutting away the necrotic tissue) or medically through the use of topical enzymatic agents (e.g. streptokinase) or more simply by covering the sore with a occlusive/semi-occlusive dressing allowing the wound and the body's own enzymes to digest the material in the wound. The latter approach should not be used if there is a lot of infected material in the sore-this needs to be removed by surgery or manual irrigation of the wound with normal saline. Topical enzymatic agents are powerful (care must be taken to avoid damaging surrounding skin and healing tissue once the sore is clean). 2. A moist environment has been shown to promote healing. This is usually achieved by putting a hydrocolloid gel within or on the ulcer (e.g. Granuflex). This will need to be changed every 3-5 days. Granulation tissue will develop and the edges of the ulcer will epithelialis and bridge the gap. Topical antibiotics are rarely indicated but may have a role where there is persistent foul odour or purulent discharge. Antiseptics are virtually never indicated. 3. If healing by secondary intention fails skin grafts may be considered. Failure of healing may indicate that the diagnosis is incorrect e.g. ischaemic ulcers, vasculitides and skin maligna

**Ciclosporin pregnancy fine !

Mode of action : -inhibits NFAT-dependent cytokine production aka Nuclear factor of activated T cells -anti-t cell Used for: -psoriasis -atopic dermatitis -pyoderma gangrenosum -other inflammatory skin conditions Can be used in pregnancy Dose 3-5mg/kg -rapid onset of action, clinical response 4-8weeks Good for short-term treatment as long-term renal toxicity risk increases Side effects -renal impairment -Risk factors, elderly and thees with pre HTN & renal impairment -increase risk of SSC esp phototherapy pts

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Morphoeic or sclerosing basal cell carcinoma. Clinical features >Presents as 1 or more, slowly growing, scar-like indurated plaques. >Usually located on face or scalp. Margins are poorly defined and frequently underestimated. Mx >wide excision > Mohs microscopically controlled surgery is appropriate in recurrent lesions or where clinical margins are difficult to determine, especially on mid-facial sites.

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Multiple superficial basal cell carcinoma Clinical features >Presents as one or more, slowly growing ,irregularly shaped erythematous plaques. >Most often located on the trunk and limbs. >Lesions may be scaly and frequently have a shiny slightly elevated edge. >May be difficult to distinguish from in situ SCC(Bowen's disease). Mx >excision, superficial surgery (shave, curette and electrosurgery), photodynamic therapy, cryotherapy (double freeze thaw technique) and imiquimod cream.

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Nodular basal cell carcinoma (BCC) Clinical features >Presents as a slowly growing , pearly nodule or plaque with prominent arborizing( tree-like)vasculature. >Most often located on the head and neck ( sun-exposed areas) >Ulceration is common, hence alternative name, rodent ulcer. Mx >Excision biopsy is recommended with a 3 to 4 mm margin >. Mohs microscopically controlled surgery is indicated for recurrent, ill-defined and large tumours of the mid-face.

Exogenous inflammatory skin conditions Photoaggravated dermatitis

Note sparing of photo protected areas Think about: Allergic contact dermatitis to airborne allergen -Photosensitive drug reaction -Phytophotodermatosis: also known as berloque dermatitis or margarita photodermatitis, is a cutaneous phototoxic inflammatory reaction resulting from contact with a light-sensitizing botanical agent followed by exposure to ultraviolet light (from the sun, for instance).

EMOLLIENTS- a moisturiser which helps rehydrate skin, forms layer on epidermis protects skin from water loss Types? Ointment vs cream vs lotion

Ointment: highest oil content good for dry skin (night) Cream: less oil content, lighter & easier to leave on skin lotion -lease oil content and least effective for dry skin Dose: 500g-1000g/week children :250-500 g/week

What skin signs do you get in the condition Porphyria cutanea tarda? What

On hand 1) Blisters 2) erosions PTD:abnormality of haem biosynthesis , enzyme deficiency leads to the build up of precursors, activated by sunlight leading to skin fragility and blistering -exacervated by alchohol

**What is Pityriasis Versicolor (Tinea Versicolor)? What is it caused by?

Over growth of commensal yeast Malassezia furfur Also common cause of dandruff and seborrhoeic dermatitis

**Scoring system for psoriasis ?

PASI: & of body affecting by psoriasis -used in specialist settings https://dermnetnz.org/topics/pasi-score/ BSA ( boddy surface are) classified as: -Mild psoriasis: < 5% of BSA -Moderate psoriasis: 5%-10% of BSA -Severe psoriasis: > 10% of BSA.

EMERGENCY DERM **what is urticaria ( hives)?

PC: I am itchy Definition -Characterised by eruption of wheals or angioedema or both -Wheal = superficial pale swelling surrounded by erythema (very itchy) -Angioedema = deeper swelling of dermis (subnormal) and subcutaneous tissues -Transient <24hrs and blanching Pruritic in most instances Risk Factors • Atopy/ Parental history of atopy • Exposure to triggers/ allergens Ddx • Atopic dermatitis - tends to last much longer and be more visibly dry • Urticarial vasculitis - autoimmune, atypical lesions • Toxic erythema of new-born - benign Epidemiology >1 in 5 have an episode of acute urticaria in their lifetime >Acute more common in <18 years old, chronic more common in adults >Chronic spontaneous urticaria affects 0.5-2% of the population Pathophysiology (see image) Mast cells are primary effector cells in urticaria, rapidly. releasing histamine, leukotriene C4 and prostaglandin D2 Causes vasodilatation and increased vascular permeability, leading to extravascular leakage of plasma Delayed second release of other cytokines causes inflammatory cell infiltrate and longer lasting lesions. >Autoimmune cause of chronic urticaria thought to be due to IgG autoantibodies to high affinity IgE receptors or thyroid antibodies

Pyoderma gangrenosum

PG causes rapidly progressive painful ulcer with a purulent base and BLUE borders. necrophilic dermatosisis More than 50% of patients have associated systemic disease -IBD -RA -Haematological disease: leukaemia, monoclonal gammopathy Tx: local or systemic CORTICOSTEROIDs

ORF

POX virus infection from infected SHEEP Or from infected sheef-->eryethema multiforme

**What is dermatitis artefacta?

Patterns of signs -excoriations -linear tears -bruising -nails/hair Patients dont tend to tell you about the problem, different to self-harm (different group of pts). They dont know how the patterns happened MX -exclude other skin disease -never confront ( this skin problem is self-induced) dont collude ( you have an organic skin disorder) Treat -the ulcerations -any skin disease -counselling

** What is Darier's disease?

Photo aggravated inherited, autosomal dominant widespread seborrhoea and/or photo-exposed flexural rash consisting of crusty papules rare defect in keratin-desmosome filament complex CLINICAL PRESENTATION can present after episode of sunburn sudden eruption of small crusty papules, Seborrhoeic distribution higher risk of staph infection, can be crusty & uncomfortable intraoral lesions Nail changes, V SHAPED NOTCH in nails , alternating red & white bands "candy cane" Neuropshyciatric symptoms

Phototherapy

Phototherapy can use UVA & UBVB: >UVB- TL-01 phototherapy >PUVA(Psoralen + UVA) Phototherapu-UVB -Flares significantly after 2 weeks of treatment -Requires course of oral prednisolone -patients can find it difficult to take time off work to have it done - Still relying on potent topical steroids to maintain any control USE Psoriasis Eczema PLE Vitiligo Cutaneous T cell lymphoma Risk -skin cancer

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Porokeratosis. If solitary, it is known as porokeratosis of Mibelli Clinical features >Stable asymptomatic, round or polycyclic, skin coloured or pink plaque >Elevated keratotic rim (cornoid lamella) encircling a smooth dry centre Mx The lesion is harmless, so no treatment is necessary. The lesion might clear with cryotherapy or fluorouracil cream, or spontaneously in time.

What skin changes does addison's disease present with ?

Presents with: -non specific symtoms like fatigue & weight loss Pathology primary adrenal insufficiency and hypocortisolism, is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones. Skin -generallised hyperpigmentation due to pituitary production of ACTH & MSH which stimulates pigment production in skin Can be assoc. with vitiligo: due to auto immune destruction of skin melanocytes due to autoimmune destruction of the adrenal glands

What virus causes chickenpox?

Primary infection with Varicella Zoster Virus (HHV3)

PSYCHOCUTANEOUS MEDICINE What primary psychaitric disease presents as skin deisacse to dermatologists/psyhcaitrists? What primary dermatological disease presents with psycho-social morbidity ?

Primary psych disease presenting as skin disease 1) Delusional parasitosis 2) body dysmorphic disorder 3) Dermatitis arteacta 4)Neurotic excoriation 5) OCD spectrum disorders: tricholtillomania (lulling hair) skin damage from repeated handwashing Primary dermatology disease with psych-social issues -patients with acne & psoriasis can develop disorders of affect: depression, anxiety

**What is the aetiology of acne? What is the acne bacterium that lives on everyone's skin known as ?

Propionibacterium acnes

1)Vasculitis skin changes?

Proximal nail fold blister interrupted blood supply, damage to epidermis uncommon presentation

Problems within the epidermis & dermis **What is epidermolysis bullosa? Mx

REMINDER Layers of the epidermis 1)stratum corneum ( horny layer): layer of keratin, most superficial layer -->fungal infections usually confined to this layer [stratum lucidum] 2)stratum granulosum (granular cell layer): so-called because cells lose their nuclei and contain granules of keratohyaline. They secrete lipid into the intercellular spaces. 3)Stratum spinosum(prickle cell layer):differentiating cells 4)Stratum basale ( basal cell layer): actively dividing cells, deepest layer -basement membrane -dermis hemidesmosomes attach skin cells onto basement membrane desmosomes -links b/w keratinocytes Scarring depends on how deep the split is in your skin , if it is superficial you are less likely to scar Epidermolysis bullosa(EB)- Genetic -A group of inherited genetic diseases that are characterised by blistering lesions on the skin and mucous membranes. These may occur anywhere on the body but most commonly appear at sites of friction and minor trauma such as the feet and hands. In some subtypes, blisters may also occur on internal organs, such as the oesophagus, stomach and respiratory tract, without any apparent friction. -mutations in the genes coding for structures in the hemidesmosome -often present with blistering in neonatal period -SUB EPIDERMAL BLISTER Types of EB -Several proteins at the DEJ can serve as targets for both inherited and acquired blistering skin diseases. Different levels of blister formation will occur depending on which protein is targeted by inherited genotype phenotype mutations -Simple, junctional and dystrophic are terms given describing the level of the split at the dermal-epidermal junction when the blisters form. -Some of the forms of EB have extracutaneous abnormalities such as muscular dystrophy or pyloric atresia. ( see image) 1)Epidermolysis bullosa simplex (EBS) -Epidermis or uppermost layer of skin cells (keratinocytes) 2)Junctional epidermolysis bullosa(JEB) -Researchers classify junctional epidermolysis bullosa into 2 main types: 1)JEB generalized severe (formerly known as Herlitz JEB) 2) JEB generalized intermediate (formerly known as non-Herlitz JEB). [see image] -Lamina lucida within the basement membrane zone -mutations in the gene producing type 17 collagen. -This condition is characterised by splitting of the skin due to fragile proteins in the dermal-epidermal junction. 3)Dystrophic epidermolysis bullosa(DEB) -Lamina densa and upper dermis 4)Kindler syndrome -Mixed pattern or multiple levels within and beneath the basement membrane zone Mx of genetic blistering skin conditions > Gene therapy >Protein therapy >cell therapy >Drug therapy >prenatal diagnosis There is no specific readily available treatment but several therapies such as, gene, protein, cell and drug therapy are all being piloted at proof of principle and pilot study trial stages. In the absence of a specific treatment and particularly relevant to some of the more severe conditions prenatal diagnosis through DNA analysis is available for families at risk.

What virus causes measles?

Rubeola virus

**which cancer is erythema gyratum repens pathoneumonic of ?

SPECIFIC for an internal tumour , usually lung

** How do you stage melanoma? What do you call the tool? Which is the most important pathological prognostic indicator?

STAGING OF MELANOMA- BRESLOW THICKNESS GUDES PROGNOSIS >Clinical stage 0-melanoma in situ >Stage 1a Breslow< 0.8mm no ulceration >Stage 1b Breslow <0.8mm with ulceration or 0.8-1.0 with or without ulceration or Breslow >1-2 mm without ulceration >Stage 2a Breslow >1-2 mm with ulceration or Breslow >2-4 mm without ulceration >Stage 2b Breslow >2-4 mm with ulceration or Breslow >4mm without ulceration >Stage 2c Breslow >4mm with ulceration NB. the further the stage, the larger the depth !!Which is the most important pathological prognostic indicator? Breslow depth A complete full-thickness excisional biopsy of suspicious lesions with 1 to 3 mm margin of normal skin and part of the subcutaneous fat should be performed. Tumour thickness is the single most important prognostic factor for patients with localised melanoma. This is measured as the Breslow depth or thickness.

** What causes blisters?

See image >Inherited Blistering skin diseases -When an inherited mutation in a gene for one of the proteins of the desmosome exists the desmosomes will not connect the keratinocytes properly. Subsequently there will be widening of spaces between the keratinocytes, the 'brick wall' will fall apart. -The individual keratinocytes will not be closely opposed to one another. -The hemidesmosome will not connect the epidermis and the dermis properly. Subsequently with little trauma the layers will separate easily, and a blister will form. Eg. Junctional epidermolysis bullosa ( a type of epidermolysis bullosa) -mutations in the gene producing type 17 collagen. -This condition is characterised by splitting of the skin due to fragile proteins in the dermal-epidermal junction. >Acquired autoimmune blistering skin diseases If you acquire abnormal autoantibodies against one of these proteins in the dermal-epidermal junction you will have an Acquired Autoimmune Blistering Skin Disease. If autoantibodies are acquired that target one of the proteins within the dermal-epidermal junction a blister will form. Antibody binding within the lamina lucida leads to complement activation and recruitment of inflammatory cells within the lamina lucida, consequently blisters will form through the lamina lucida where the inflammation is occurring. Eg. Bullous pemphigoid A condition in which autoantibodies are acquired against type 17 collagen.

**Internal cancer can affect the skin ,how ? Already mentioned: THROMBOPHLEBITIS -erythema nodosum -dermaeomyoticis -vasculitis -pyoderma gangenosum

Severe acanthuses nigricans & bladder cancer usually due to obesity or insulin resistance but when it develops floridly like this think cancer not specific

**MODERATE STEROIDS

Short periods to axillae or groin Clobetsone butyrate

** What is a Nicorandil leg ulcer?

Skin presentation associated with drugs 5% of patients on nocrandil get oral ulceration drug also affects other areas -genital -perianal -peristomal -eye -GI -cutaneous (skin)

Dermatological investigations

Skin swabs Skin scrapes : suspected fungal infection ABPI - identify the presence and severity of peripheral arterial insufficiency, which is important in the management of leg ulcers. -Measure the cuff pressure of dorsalis pedis or posterior tibial artery using a Doppler and compare it to the pressure of brachial artery. -The ABPI is measured by calculating the ratio of highest pressure obtained from the ankle to highest brachial pressure of the two arms, and is normally >0.8. - Inappropriately high reading will be obtained in calcified vessels (often in diabetics).

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Solar (actinic keratoses) Clinical features >Found on habitually sun-exposed sites (mainly face, ears and hands). >Lesions have a hard scaly crusty surface and no dermal induration. MX >Solar keratoses on the face are predominantly treated by cryotherapy > diffuse lesions may be treated with 5-fluorouracil cream, imiquimod cream or photodynamic therapy.

What happens when someone who is immunocomprised develops "warty lesions"?

Some warty lesions in this situations might be SCC

Commensal organisms that can cause infection What infections does Staph Aureus, a Gram + bacteria staphylococci cause? NB features -envelope absorbs crystal violet stain and appears deep purple -have thick layer of peptidoglycan (made of AA and sugar) -contain lipoteichoic acid (activates human's immune system so it provides protection from host's immune system)

Staph Aureus causes: MSSA-Methicillin-sensitive Staphylococcus aureus, is a skin infection that is not resistant to certain antibiotics. MRSA:Methicillin-resistant Staphylococcus aureus (MRSA) is a bacterium that causes infections in different parts of the body PVL- SA: PVL is a toxin produced by certain types of Staphylococcus aureus. The toxin can kill white blood cells

What causes impetigo? "golden crust"

Staph aureus (50-70%) Strep

**normal skin flora and their characteristics?

Staphylococci :Aureus vs epidermidis -age of patient Micrococcus: body site Corynebacterium: skin level Acinetobacter aerobes Propionobacterium: anaerobes

What causes cellulitis/eryspelas/soft tissue infection?

Streptococcus pyogenes

What are splinter haemorrhages? What are they assoc with

Sub-acute bacterial endocarditis and minor damage of fingers

What is vitiligo?

Symmetrical well defined patches of hypo pigmentation in an ACRAL distribution Aetiology Melanocyte defect drives an autoimmune response leading to melanocyte destruction in susceptible individuals Clinical presentation -skin texture is normal -usually symmetrical with sharp border -associated with other autoimmune conditions, particularly autoimmune thyroid disease

**Internal cancer can affect the skin ,how ? Already mentioned: -erythema norosum -dermaeomyoticis -vasculitis -pyoderma gangenosum

THROMBOPHLEBITIS: inflammation follows line of vein sign of: lung or pancreatic cancer not specific

**NON STEROIDAL DERM TREATMENTS

Tacrolimus

**MILD STEROIDS

To face and neck is appropriate Hydrocortisone

What is carotenaemia?

Too many brussel sprouts not jaundice because the sclera are normal Aetiology increased carotenoids in diet Hyperlidaemic states -hypothyroidism -diabetes mellitus Decreased metabolism -liver disease ? genetic

** young child with eczema What foods account for food-induced atopic eczema? considerations?

Treat eczema, if no GI symptoms or failure to thrive and eczema responds to treatment don't advise dietary manipulation Ask about itch or redness after certain foods (immediately or hours later), diarrhoea, vomiting, and/or poor weight gain. E.g. Milk, egg, wheat, soy, and peanut account for about 75% of the cases of food-induced atopic eczema. Consider asking the person to keep a food diary over 4-6 weeks. In infants, also ask about feeding history (weaning, breastfeeding, or bottle feeding). S uspect food allergy in children with atopic eczema who have reacted previously to a food, with immediate symptoms, or in infants and young children with moderate or severe atopic eczema that has not been controlled by optimum management, particularly if associated with gut dysmotility (colic, vomiting, altered bowel habit) or failure to thrive.

Head lice aka nits

Tx: wet combing if it doesn't work products containing permethrin

Exogenous inflammatory skin conditions **Allergic contact dermatitis What type of immune response is this ? What are common allergens?

Type 4 delayed hypersensitivity immune reaction -Careful history - Investigate with patch testing Common allergens -Nickel -Rubber additives -Medicaments e.g. neomycin -Cosmetics e.g. fragrances, hair dyes B -ase materials e.g. lanolin, preservatives -Resins e.g. colophony, epoxy, formaldehyde

**Pox virus What types exist and what do they cause? characteristics Poxviruses are brick or oval-shaped viruses with large double-stranded DNA genomes. Poxviruses exist throughout the world and cause disease in humans and many other types of animals. Poxvirus infections typically result in the formation of lesions, skin nodules, or disseminated rash.

Types Molluscum contagiosum (pox virus infection) -small pink benign wartlike tumors, umbilicate papupes ( see image) -associated with HIV-positive patient, if it presents in adults consider immunosuppression like HIV -common in childhood -self limiting but can persist for many months -worse in atopic dermatitis Orf Orf virus infection in animals is commonly referred to as sore mouth, scabby mouth, or contagious ecthyma.

**What types of light exist within the solar spectrum ? Which is more carcinogenic?

UVA -longer wavelength -penetrates deeper down into the epidermis -can penetrate through window glass A=ageing, damage caused : -ageing , the sun damages elastic fibres in the dermis within the skin UVB -shorter wavelength, doesn't get through glass -causes more burning than A , B=Burning UVA is more carcinogenic than UVB

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Ulcerated invasive SCC of the lip Clinical features >Generally arises within actinic/solar keratosis but may arise in a normal-appearing vermilion of the lip. >Many affected patients are smokers. >An irregular or firm nodule that ulcerates early. >Cancers on the lip are very likely to metastasise. Mx >Wide surgical excision >Staging investigations for advanced tumours may include ultrasound scanning, lymph node biopsy, CT and/or MRI scan.

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Undifferentiated or anaplastic squamous cell carcinoma Clinical features >May arise within a solar keratosis, within in situ squamous cell carcinoma or de novo. >Predisposing factors include advanced aged, severe solar damage and immunosuppression. >A rapidly growing firm or friable erythematous nodule that frequently ulcerates. >Aggressive tumour with propensity to metastasise. Mx Surgical excision with a wide margin. Careful follow-up is recommended.

Exogenous inflammatory skin conditions Irritant contact dermatitis

Usually starts in webspace Common irritants include soap, detergents High risk occupations: nursing, hairdresser Barrier dysfunction so associated with other eczemas

Dermis ** What is DERMATOFIBROMA?

Very common Firm dermal nodule 5-10mm in diameter Usually red/brown may present as potential skin cancer Asymptomatic Young adults Female>male Arms and legs ? Reaction to minor injury

Epidermis Sebaceous cysts aka : Epidermoid and Pilar Cysts?

Very common Pilar cysts on scalp often run in families Epidermoid cysts on head, neck or trunk Keratin filled epithelial walled cyst Epidermoid cysts usually demonstrate obvious punctum Can get secondarily infected

Endogenous and mixed Atopic Pompholyx

Very itchy small vesicles Hands and feet Heat can be trigger 'Ide reaction' when associated with fungal infection Can be seen in other types of eczema

TESTING My knowledge -SKIN LESIONS What is this skin lesion ? Clinical features? Mx?

Viral wart Clinical features >Well circumscribed verrucous plaque(s) or nodule(s) >Papillomatous skin surface >Frequently arise on prominences (in this case a knee) Mx >Warts are notoriously difficult to get rid of. >Salicylic acid paints, cryotherapy and curettage and cautery would be reasonable options for this lesion.

Viruses What does human papilloma virus (HPV) cause? which strains are responsible for genital warts and which are for cervical cancer?

Viral warts Background · Common usually present in childhood, then spontaneously resolve with developing immunocompetence. · A type of Viral wart called a plantar wart are also called a verruca · Infection occurs in the superficial layers of the epidermis, causing proliferation of the keratinocytes (skin cells) and hyperkeratosis --------->the wart. · HPV is spread by direct skin-to-skin contact or autoinoculation(if a wart is scratched or picked, the viral particles may be spread to another area of skin) · The incubation period can be as long as 1 year · More than 100 HPV subtypes are known, giving rise to a variety of presentations. -The most common strains of HPV are types 2, 3, 4, 27, 29, and 57. >HPV 16 & 18--> 70% of cervical cancers. >Low-risk HPV strains- HPV 6 & 11,--> 90% of genital warts, which rarely develop into cancer. Clinical Presentation · Cutaneous (skin) viral warts have a hard, keratinous surface · A tiny black dot may be observed in the middle of each scaly spot, due to an intracorneal haemorrhage. · Common warts present as papules with a rough, papillomatous and hyperkeratotic surface ranging in size from 1 mm to larger than 1 cm. · They arise most often on the backs of fingers or toes, around the nails—where they can distort nail growth—and on the knees. · Sometimes the warts resemble a cauliflower; these are known as butcher's warts. Types: >Plantar wart aka verrucae aka 2 types 1)Palmoplantar warts (myrmecia, HPV 1): round horny deep painful nodules, most often on weight-bearing sites eg. soles of the foot 2)Mosaic warts: closely grouped, generally presenting as relatively asymptomatic plantar warts, less painful ·Plantar epidermoid cysts are associated with warts. ·Persistent plantar warts may rarely be complicated by the development of verrucous carcinoma. >Plane wart ·Plane warts have a flat surface. ·common sites are the face, hands and shins. · often numerous. · may be autoinoculated by shaving or scratching so that they appear in a linear distribution (pseudo-Koebner response). NB. The Koebner phenomenon describes the appearance of new skin lesions of a pre-existing dermatosis on areas of cutaneous injury in otherwise healthy skin. It is also known as the Köbner phenomenon and isomorphic response. eg. Linear lesions due to the Koebner phenomenon in lichen planus ·Plane warts are mostly caused by HPV types 3 and 10. >Filiform wart ·Filiform warts are on a long stalk like a thread. · commonly appear on the face. · described as digitate (like a finger). >Mucosal wart · Oral warts can affect the lips and even inside the cheeks, where they may be called squamous cell papillomas. · They are softer than cutaneous warts Mx · Many people don't bother to treat viral warts because treatment can be more uncomfortable than warts —they are hardly ever a serious problem. · Warts that are very small and not troublesome can be left alone, and in some cases, they will regress on its own. · However, warts may be painful, and they often look ugly so cause embarrassment. To get rid of them, we have to stimulate the body's immune system to attack the wart virus by putting BAZUKA (Salicylic Acid)2q

** How does our body make vitamin D3? Where? Which populations are at risk of vitamin D deficiency ?

Vitamin D3 is produced in the dermis from cholesterol precursors through the action of UVB Final hydroxylation of vitamin D synthesis takes place in liver & kidney diet isn't good enough to give adequate vitamin D without active supplementation 11-3pm October -march advised for patients to take Vitamin D supplementation At risk groups Counter-intuitive but DARK SKIN TYPES people who cover up people who stay inside Exposing 20% of the body surface to an amount of sunlight =0.5 MED ( minimal erythema dose) is equivalent to ingesting 1400-2000 Its of vitamin D3 -MED different for everyone -those with fair skin need to stay out for shorter time to get MED -but those with dark skin have to stay out for longer to get MEd

**If eruptive Xanthomas present on the skin what metabolic disease can this be an early warning sign of? What do they look like ?

Widespread symmetrical yellow-red papuple -extra cellular lipid deposition in the skin -associated with uncontrolled hypertriglyceridaemia Can mean you are at risk of PANCREATITIS Types of hypertrigglyceridaemia Primary Familial dyslipidaemias Primary genetic susceptibility -metabolic syndrome -treated type 2 diabetes Secondary (drugs etc.) -excess alcohol -drug induced -untreated DM -endocrine disease -renal diesease -liver disease -pregancy -autoimmune disorders

rubella aka german measles

a viral infection characterized by a low-grade fever, swollen glands, inflamed eyes, and a fine, pink rash

What skin issues can ACE inhibitors cause?

angioedema

small vessel vasculitis What is extensive cutaneous(skin) vasculitis ?

associated with CTD , SLE BUT CUTANEOUS VASCULITIS ONLY AFFECTS SKIN, otherwise would be called systemic cutaneous vasculitis is found in about 20% of patients with SLE Can be assoc with presence of cryogobulins & can be associated with systemic involvment NB. photo shows tissue necrosis

Melanocytes Benign melanocytic naevi aka MOLES

benign melanocytic naeviA mole is a common benign skin lesion due to a local proliferation of pigment cells (melanocytes). It is more correctly called a melanocytic naevus melanocytes are dendritic cells in

Endogenous and mixed- Atopic Seborrhoeic dermatitis

caused by lack of biotin, pyridoxine, & riboflavin (7, 6, & 2) Adult and infant Commensal yeasts play a role Patterns - Scalp, T zone face, ears, eyebrows -Pre-sternal, inter-scapular Armpits, groins, umbilicus

Dermatomyositis skin changes?

connective tissue disease involving destruction of the muscle tissue question pt around symptoms of proximal muscle weakness or tenderness SIgns -heliotrope sign on face around eyes Can be caused by underlying B cell lymphoma which can present as nodules n forehead

Scabies

contagious skin disease transmitted by the itch mite

MCQ **2 year old in A & E with her first generalised tonic clonic seziure lasted 5 minuts and self-terminated tired but alert. Temperature 40.1 degrees, tachycardic Blanching papular rash on her face, nappy area and her palms Most likely causative organism of baby's presentation ? A: coxackie virus B: Epstein-Barr Virus (EBV) C: Herpes simplex virus D: Neisseria Meningitidis E: Strep Pneumonia coxackie virus (picornavirus family) non-enveloped, icosahedral, linear, ssRNA virus causes aseptic meningitis and herpangina (fever, mouth blisters) and myocarditisMCQ 2 year old in A & E with her first generalised tonic clonic seziure lasted 5 minuts and self-terminated tired but alert. Temperature 40.1 degrees, tachycardic Blanching papular rash on her face, nappy area and her palms Most likely causative organism of baby's presentation ? A: coxackie virus B: Epstein-Barr Virus (EBV) C: Herpes simplex virus D: Neisseria Meningitidis E: Strep Pneumonia

coxackie virus (picornavirus family) non-enveloped, icosahedral, linear, ssRNA virus causes aseptic meningitis and herpangina (fever, mouth blisters) and myocarditis

** A patient presents with Unilateral hand dermatitis what should you always suspect infection wise?

fungal infection. 2 feet 1 hand

++Methotrexate

gold standard 1st line for psoriasis Also used for - atopic eczema -sacoidosis -other inflammatory skin diseases Very effective in long-term, safe when prescribed correctly slow onset of acton , max benefits 16+ weeks Dose: ONCE WEEKLY dosing 15-25mg max Side effects -Chief adverse effect: bone marrow toxicity -mutagenic: men & women shouldn't take if planning conception -hepatotoxicity, RFS: obesity, Diabetes, alchohol IX -toxicity associated with macrocytosis ALWAYS PRESCRIBE FOLIC ACID

Benign skin lesions not otherwise mentioned Freckles etc

https://dermnetnz.org/cme/lesions/benign-melanocytic-lesions/ https://dermnetnz.org/cme/lesions/benign-keratinocytic-and-adnexal-lesions/

Dermatology Life Quality Index (DLQI)

https://www.bad.org.uk/shared/get-file.ashx?id=1653&itemtype=document

Atrophic scarring from acne?

indented scar that heals below the normal layer of skin tissue. Atrophic scars form when the skin is unable to regenerate tissue. As a result, it leaves behind imbalanced scarring. Atrophic scars are often the result of severe acne or chickenpox.

Commensal organisms that can cause infection What infection do Gram negative organisms cause?

infections including pneumonia, bloodstream infections, wound or surgical site infections, and meningitis in healthcare settings.

Lymphatic Lymphangioma circumscriptum

is an abnormal formation of lymphatic vessels (parts of the body that transport lymph) that appears as a patch of wart-like growths on the skin.

How can diabetes damage larger arteries?

leads to extreme ischameic changes such as gangrene

Spirochaetes characteristics

live in the mouth & water. Some cause STDs like syphilis or systemic diseases like Lyme Disease

**Besides having an underlying skin disease, what else can cause erythroderma?

lymphoma, drugs (e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol, captopril) and idiopathic

**Azathioprine side effects most common steroid sparing agent for inflammatory diesel

mode of action lymphocytes need de novo purine synthesis ( inc. 6-thioguanine,involved in TMPT enzyme production) so they are especially susceptible AZA. AZA disrupts the active metabolites needed to create endogenous purines which is needed for DNA, RNA & cellular proteins -anti B cell Use: -slow onset of action mono therapy in atopic dermatitis Dose: 1-2.5 mg/kg/day SIde effects !!! bone marrow suppression if patient doesn't have good TPMT ( thipurine methyltransferase) enzyme SO routine practice to check for TPMT activity prior to giving AZA

2)Vasculitis skin changes?

more common presentation symmetrical lesions of palpable purpura most common on lower legs and can spread proximally Cause -drugs -infection -collagen disease -IBD -malignancy Complication -skin ulceration like in severe case of rheumatoid disease

What is the prayer sign in diabetes?

patients fingers become stiff unable to put palms together -similar to systemic sclerosis -less recognised -glycosylation of collagen fibres due to diabetes, making them less compliant

How do you tell if a diabetic has small or large blood vessel damage in their skin ?

small subtle atrophic marks diabetic thin spots

** What is the spectrum of malignant melanomas? RFs for malignant melanoma?

spectrum >Congenital melanocytic naevi (moles) -benign -small & medium <20cm-1 in 100 births -Giant>20cm-in 1-50000 births >Acquiredmelanocytes naevi(moles) -benign -more common -the older you are, the less normal it is to get moles 15-60% by the age of 16 years-associated with sunburn, more sunburn, more moles >Atypical (dysplastic ) melancoytic naevi -rather than nice round & brown -high risk of skin cancer >Malignant melonama in situ/Lentigo Maligna -before it becomes invasive >Malignant melanoma -invasive malignancy of melanocytes -more common in elderly 80+ Genesis of moles -Malignancy can arise from a pre-existing mole (naevi) that you have had all your life -50% arise de novo, in an area of skin where you have not had a mole before SO protect all of skin from sun not just were you have moles RFs for malignant melanoma >Age >Sun exposure -intermittent exposure-sunburn-->stay inside most of year then go on holiday and get burnt >country of birth >skin type 1 >Multiple melabocytic naevi >atypical melanocytes naevi >Family hx of MM >Personal hx of MM >use of sunscreen >Immunosupression -HIV -Iatrogeic NB. Sunscreen protection -not going out in peak sun 12pm -staying in -Covering p when you go out Clinical presentation ● The 'ABCDE Symptoms' rule (*major suspicious features): Asymmetrical shape* Border irregularityColour irregularity*Diameter > 6mmEvolution of lesion (e.g. change in size and/or shape)* Symptoms (e.g. bleeding, itching) ● More common on the legs in women and trunk in men Clinical types a) Superfical spreading -commonest - common on the lower limbs, in young and middle-aged adults; related to intermittent high- intensity UV exposure b)nodular -worse prognosis -common on the trunk, in young and middle- aged adults; related to intermittent high-intensity UV exposure c)Lentigo maligna melanoma (See image) -often seen on faces of elderly people, slow growing in situ patch of dysplastic melanocytes-->neoplasia

**What is flexural acanthuses nigricans? **What is true AN associated with ?

symmetrical flexural ,well-defined red brown patches flexural velvety skin changes True acanthuses nigtans is rare and is associated with GI MALIGNANCY Pesuodo acanthus niigricans More commonly seen in insulin resistant states & obesity

Nerve Neurofibromas

tumors consisting predominantly of Schwann cells and some fibroblasts with loosely arranged collagen fibers present in the disease Neurofribromatosis ( hereditary) -Cafe au lait macules ( brown marks) Can lead to a variety of internal pronlems -acoustic neuromas -epilepsy -phaecotochromocytomos

**SUPER POTENT

use when weaker corticosteroids are not effective Clobetasol propionate

**What is lipidermatoscelerosis (LPDS) ?

usually bilateral & symmetrical acute LPDS can be mistaken for cellulitis Chronic changes -woody firm texture -red shiny skin TAG LINE: INVERTED CHAMPAGNE BOTTLE LEGS Pathophysiology -increased hydrostatic pressure in veins causes endothelial cell damage this leakage lead, release of pro inflammatory mediators -release of matriculates metal proteinases (MMP) -get fibrosis & scarring -woody texture -loss of tissue bulk, aka INVERTED CHAMPAGNE BOTTLE LEGS (bulky on top skinny on bottom) Symptoms -itchny so can get excoriations (scratches) Breakdown of connective tissue & more fibrotic tissue being laid down primary lesion: venous stasis

** What is a leg ulcer? What are the different types ? Characteristics?

· In general, there are 3 main types: · Other causes include: - vasculitic ulcers (purpuric, punched out lesions) - infected ulcers (purulent discharge, may have systemic signs) - malignancy (e.g. squamous cell carcinoma in long-standing non-healing ulcers). NB. In clinical practice, there can be mixture of arterial, venous and/or neuropathic components in an ulcer. 1)venous Hx -Often painful, worse on standing - History of venous disease e.g. varicose veins, deep vein thrombosis Common sites -Malleolar area (more common over medial than lateral malleolus) Lesion - Large, shallow(superficial) irregular ulcer - Exudative and granulating base Associated features - Warm skin - Normal peripheral pulses - Leg oedema, haemosiderin and melanin deposition (brown pigment), lipodermatosclerosis( Lipodermatosclerosis is a chronic inflammatory condition characterised by subcutaneous fibrosis and hardening of the skin on the lower legs.), & atrophie blanche (white scarring with dilated capillaries) Ix - Normal ankle/brachial pressure index (i.e. ABPI 0.8-1) Mx - Compression bandaging(after excluding arterial insufficiency) 2)arterial Hx - Painful especially at night, worse when legs are elevated - History of arterial disease e.g. atherosclerosis Common sites - Pressure and trauma sites e.g. pretibial, supramalleolar (usually lateral), and at distal points e.g. toes Lesion - Small, sharply defined deep ulcer - Necrotic base Associated features - Cold skin - Weak or absent peripheral pulses - Shiny pale skin - Loss of hair Ix - ABPI < 0.8 - -->presence of arterial insufficiency - Doppler studies and angiography Mx - Vascular reconstruction - Compression bandaging is contraindicated!!!! 3) neuropathic ulcers. Hx - Often painless -Abnormal sensation - History of diabetes or neurological disease Common sites - Pressure sites e.g. soles, heel, toes, metatarsal heads Lesion - Variable size and depth - Granulating base - May be surrounded by or underneath a hyperkeratotic lesion (e.g. callus) Associated features - Warm skin - Normal peripheral pulses* *cold, weak or absent pulses if it is a neuroischaemic ulcer - Peripheral neuropathy Ix - ABPI < 0.8 --> a neuroischaemic ulcer - X-ray to exclude osteomyelitis Mx - Wound debridement - Regular repositioning, appropriate footwear and good nutrition

** What is Bowen's disease aka SCC insitu?

·Background Precancerous condition , dysplasia purely in epidermis · Occurs on the lower legs of elderly women · Sometimes occurs on hands or nails · Often associated with exposure to mineral oils (carcinogens in engineering industry)and HPV · Fixed non itchy erythematous patches of skin , often multiple, slightly scaly. More cobbled than SK & not as silvery and scaley like psoriasis. · Similar risk factors to solar keratoses · Same mx as solar Keratoses, scales can be picked off · DDx: small patch of eczema

**How do you use topical corticosteroids? side effects?

● Apply thinly and only for short-term use (often 1 or 2 weeks only) ● Only use 1% hydrocortisone or equivalent strength on the face ● Fingertip unit (advised on packaging) - strip of cream the length of a fingertip NB. 1 fingertip unit covers the area of two palms and equals 1⁄2 gram 2FTU=1G -prescribe the weakest potency steroid that is effective avoid applying steroids with emollients as this dilutes effectiveness SIDE EFFECTS - Skin atrophy - Straie - Telangectasia - Hair growth - Tachyphalaxis (diminishing response) - Delayed wound healing - Contact dermatitis - Systemic effects e.g. adrenal suppression Different potencies -weak: face -strong-body prednisolone 5mg=methyleprd 4mg=hydrocortisone 20mg NB. physiological daily secretion of cortisol=5mg prednisolone. Short courses <2 weeks dont unbalance this

How do you prevent pressure sores?

● Pressure sores are due to ischaemia resulting from localised damage to the skin caused by sustained pressure, friction and moisture, particularly over bony prominences. ● Preventative measures involve frequent repositioning, nutritional support, and use of pressure relieving devices e.g. special beds

** Mx of malignant melanoma? Prognosis of malignant melanoma ? What is the name of the criteria to use?

● Surgical excision - definitive treatment ● Radiotherapy may sometimes be usefu l● Chemotherapy for metastatic disease Prognosis ● Recurrence of melanoma based on Breslow thickness (thickness of tumour): <0.76mm thick - low risk, 0.76mm-1.5mm thick - medium risk, >1.5mm thick - high risk ● 5-year survival rates based on the TNM classification (primary Tumour, regional Nodes, Metastases): stage 1 (T <2mm thick, N0, M0) - 90% stage 2 (T>2mm thick, N0, M0) - 80% stage 3 (N≥1, M0) - 40- 50%, and stage 4 (M ≥ 1) - 20-30%