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Dermatology Flashcards

Dermatology - do for finals revision, prob only time for questions unfortunately

1
Q

What is the management of hyperhidrosis?

A
  1. Topical aluminium chloride. SE: skin irritation
  2. Iontophoresis: esp if palmar/plantar/axillary
  3. Botulinum toxin: axillary sx
  4. Surgery e.g. transthoracic sympathectomy. Make aware risk of compensatory sweating
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2
Q

What are the stages of wound healing?

A
  1. Haemostasis – vasoconstriction + platelet aggregation, clot formation
  2. Inflammation – vasodilatation, migration of neutrophils + macrophages, phagocytosis of cellular debris + invading bacteria
  3. Proliferation – granulation tissue forms by fibroblasts, angiogenesis, then re-epithelialisation (epidermal cell proliferation + migration)
  4. Remodelling – collagen fibre re-organisation, scar maturation
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3
Q

Pathophysiology acute allergy

A
  • Trigger like foods, drugs, insect bites, contact, sweating, idiopathic - immunological or non-immunological
  • Inflammatory mediators released from mast cell degranulation - major one is histamine
  • Vasodilation + increased capillary permeability
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4
Q

Urticaria

A

Swelling of superficial dermis - pruritic wheals, which are described as erythematous plaques, some discrete + found, some confluent

  • Acute: infection or type 1 allergy, localised/widespread progressing to anaphylaxis
  • Chronic: >6w, may be spontaneous autoimmune cause or inducible from friction/cold/sun etc

M:

  • Acute usually self-resolves
  • If a/w anaphylaxis obv treat for this with 500 micrograms adrenaline 1:1000 IM + 200mg hydrocortisone + antihistamine
  • Chronic causes non-sedating anti-histamines
  • Steroids if severe
  • Avoid NSAIDs + opiates - may aggravate
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5
Q

Angioedema

A

Deeper dermal + SC swelling causing tongue + lip swelling

  • May be with urticaria
  • May be without urticaria: hereditary (rare) or acquired (idiopathic or lymphoproliferative disease/autoimmune/some drugs e.g. ACEi)
  • Angioedema alone - corticosteroids
  • With anaphylaxis - adrenaline 500 micrograms of 1:1000 IM + 200mg hydrocortisone + antihistamine
  • Comps: asphyxia, cardiac arrest
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6
Q

Erythema nodosum

A

Hypersensitivity response in dermis + SC - to Strep, TB, pregnancy, cancer, sarcoidosis, IBD, chlamydia, drugs (OCP, sulfonamides, NSAIDs)

Most common in YA females

Discrete tender nodules usually over shins, may be confluent, appear over 1-2w, leave bruise-like discolouration as resolve over 2-3w, dusky blue/red colour, no atrophy/scarring/ulceration
*May get fever, malaise, arthralgia

No treatment for it just rest, NSAIDs for pain

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7
Q

Erythema multiforme

A

Acute self-limiting inflammation, precipitated by HSV/other infection like Mycoplasma/drugs like COCP penicillin sulphonamides NSAIDs allopurinol/unknown

Classically target lesions on back of hands/shins then spreads to torso, lesions may blister, with no mucosal involvement (or only 1 mucosal surface - if mucosa involved erythema multiforme major), sometimes mild pruritus, UL>LL

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8
Q

Stevens Johnson syndrome

A

Mucocutaneous necrosis triggered by drugs/infection with at least 2 mucosal sites involved, varying skin involvement, leads to epithelial necrosis with few inflammatory cells

Unusual-looking target lesions

M: call for help, supportive, monitor for sepsis/electrolyte imbalance/organ failure

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9
Q

Toxic epidermal necrolysis

A

Usually secondary to a drug reaction causing extensive skin + mucosal necrosis with systemic toxicity. Full-thickness epidermal necrosis + sub epidermal detachment

Drug causes: phenytoin, sulphonamides, allopurinol, penicillins, carbamazepine, NSAIDs

M: stop cause, higher mortality than SJS, ICU for supportive, IV Ig often given or other immunosuppressive

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10
Q

Rash of meningococcal sepsis

A
  • May begin as blanching maculopapular rash
  • Develops to non-blanching purpuric rash on trunk + extremities
  • May develop ecchymoses, haemorrhagic bull + tissue necrosis
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11
Q

Erythroderma

A

Exfoliative dermatitis of at least 90% of skin surface

Cause: eczema, psoriasis, drugs (sulfonamides, gold, sulfonylureas, penicillin, allopurinol, captopril), idiopathic, lymphoma/leukaemia, pemphigus foliaceus, HIV

Skin: inflamed, oedematous, scaly, feels tight + itchy to pt, long-standing causes hair loss/ectropion of eyelid/nail shedding

Systemic: malaise, fever/chills, lymphadenopathy

M: cause if known, emollients + wet wraps to maintain skin barrier, topical steroids, supportive like fluids, swab skin if suspect infection, stop non-essential drugs

Comp: infection, fluid loss/electrolyte imbalance, hypothermia, high output HF, AKI, low albumin + capillary leak syndrome (can lead to hypovolaemic shock + ARDS)

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12
Q

Eczema herpeticum

A

Complication of atopic eczema/other conditions triggered by HSV

Extensive crusted papules, blisters, erosions, a/w fever + malaise

M: antivirals + Abx if bacterial secondary infection

Can lead to herpes hepatitis, encephalitis, DIC or death

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13
Q

Necrotising fasciitis

A

Rapidly-spreading infection of deep fascia + tissue necrosis, due to group A haemolytic strep/anaerobes. Half occur in otherwise healthy people

Severe pain, erythematous blistering necrotic skin, fever + tachycardia, subcutaneous emphysema (crepitus), may have soft tissue gas on XR

M: extensive surgical debridement + IV Abx. Mortality up to 70%

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14
Q

Burns

A
  • Classification: superficial epidermal (red + painful), partial thickness/superficial dermal (pale pink, blistered, painful), partial thickness/deep dermal (white/patches of non blanching erythema, reduced sensation), full thickness (white/brown/black, no blisters, no pain)
  • Wallace’s rule of 9-each of these are 9% of body surface area: H+N, right arm, left arm, anterior right leg, anterior left leg, posterior right leg, posterior left leg, anterior chest, posterior chest, anterior abdomen, posterior abdomen
  • Refer to secondary care any deep dermal/full thickness, superficial of >3% TBSA (or 2% in kids) or if they involve hands/feet/face/perineum/flexure, or if inhalation/electrical/chemical or suspecting NAI
  • Superficial epidermal: analgesia, emollients
  • Superficial dermal: clean, leave blister, non-adherent dressing, avoid creams, r/v in 24h
  • Severe burns: stop burning process, refer complex ones to specialist unit, circumferential e.g. around torso may need escharotomies to divide the burnt skin to improve ventilation/compartment syndrome, excision + grafting
  • IV fluids in adults >15% burns/children >10% using Parkland formula
  • Comps of burns: dehydration as fluid lost into 3rd space, catabolic, immunosuppression e.g. bacterial translocation from gut lumen, sepsis
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15
Q

Cellulitis + erysipelas

A

Spreading bacterial infections: cellulitis involves deep SC tissue, erysipelas more superficial (dermis + upper SC). RF are immunocompromised, wounds, intertrigo in toe webs

Causes: Strep pyogenes, Staph aureus, gram neg in immunocompromised

CF: oedema, erythema, warmth, pain, lymphangitis, sometimes localised blistering/necrosis, systemically unwell (esp erysipelas)

  • Erysipelas more common on face + has more well-defined border
  • Cellulitis most common on LL/arm
  • Skin swabs usually negative unless taken from broken skin
  • Can cause local necrosis, abscess or sepsis

M: flucloxacillin/erythromycin, sterile dressing, analgesia

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16
Q

Staphylococcal scalded skin syndrome

A

Toxin from some strains of staph (e.g. bullous impetigo) - widespread desquamation over hours-days, most common in young children (if in adults more likely immunosuppresed). Often in armpits/groin/orifices then spreads, in newborns umbilical/nappy area. Can get outbreaks

Scald-like appearance, large flaccid bulla, perineal crusting, intra-epidermal blistering, v painful

M: IV anti-staph like flucloxacillin (erythromycin if allergic), paracetamol, skin care e..g petroleum, hydration + electrolytes, recover in 5-7d
If untreated can lead to pneumonia and sepsis

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17
Q

Impetigo

A

V contagious S aureus/Strep pyogenes infection, direct spread

Causes inflamed plaques, golden crusted surface, often around mouth + nose; bullous form from certain staph strains

M: topical fusidic acid if localised, oral flucloxacillin/erythromycin/clarithromycin if widespread, avoid school/work until lesions dry/48h after Abx

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18
Q

Folliculitis

A

Hair follicle infection, usually S aureus. RF: humidity, obesity, DM

Causes pruritic/tender papules + pustules

M: topical antiseptics or Abx or oral Abx

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19
Q

Furuncles

A

Boils - deep infection of hair follicles, usually S aureus

Painful red pus-filled swellings, multiple are ‘carbuncles’

M: hot bathing, if widespread/on face try oral fluclox/erythro/clarithro for 10-14d

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20
Q

Erythrasma + pitted keratolysis

A

Erythrasma: orange/beige rash in large flexures caused by a bacteria, commensal overgrowth, M with topical erythromycin + antiperspirants

Pitted keratolysis: superficial infection of horny layer of skin, small punched out circular lesions on macerated skin, M-topical Abx + antiperspirants

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21
Q

Herpes simplex of skin

A

HSV-1 can sometimes cause painful blisters/gingivostomatitis, or may inoculate into trauma sites causing painful pustules (e.g. herpetic whitlow on fingers)

M: cold sores-topical acyclovir, oral antiviral prophylaxis if recurrent

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22
Q

Viral exanthem

A

Most common skin manifestation of a virus

Erythematous maculopapuler rash mostly on torso + proximal limbs - prob immune complex deposition in dermal bvs

Then there are the specific viral rashes from paeds

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23
Q

Shingles

A

Reactivation of latent VZV:

  • Prodrome of tingling/pain
  • Painful u/l blistering eruption in dermatomal distribution (can be multiple), in crops, may be purulent then crust, lasts 1-2w
  • M: Analgesia, oral acyclovir if given early, high dose IV aciclovir if immunosuppresed
  • Comps: post-herpetic neuralgia, ocular, motor neuropathy
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24
Q

Human papilloma virus

A
  • Common warts: papules with coarse surface, often have small black dots (vessels) within, direct spread
  • Plantar warts - verrucae. Warty papillomatous appearance but flat as on foot

M: often take months-years to clear, may try removal of hyperkeratotic skin with salicylic acid, or cryotherapy

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25
Q

Molluscum contagiosum

A
  • Poxvirus, transmitted by close contact or via contaminated surfaces like towels
  • Majority occur in children esp with eczema
  • Multiple small translucent/pink/white papules, firm, soft white matter inside (can squeeze out), central umbilicated depression. Trunk + flexures in children, may get anogenital, in adults sexual contact may cause them on genitalia/thighs/lowr abdomen
  • M: reassure, resolve in 18m, avoid sharing towels + baths etc, don’t need exclusion from anything, don’t scratch, treatment usually not recommended
  • If problematic: can try squeezing after bath, localised trauma like cryo, emollient + mild topical steroid for itch, topical abx like fusidic acid if looks infected (oedema, crusting)
  • If HIV + extensive lesions urgently refer (sign of more disease), if around eye refer to ophthalmology, if anogenital in adults refer to GUM
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26
Q

Orf

A

Pox virus of sheep/goats - can catch from petting stations - red papules with inflamed border that blisters/turns into pustules, resolve in 4-6w

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27
Q

Dermatophyte skin infection

A

‘Ringworm’ infections as tend to form expanding annular lesion, usually u/l + itchy + asymmetrical, scaly edge.
Don’t give topical steroids! Try antifungal cream like clotrimazole/terbinafine or if widespread oral antifungal
*Tinea corporis: trunk + limbs
*Tinea pedis-athletes foot. moist scaling + fissuring in toe webs, skin white/macerated, may flare as blisters/pustules, no annular lesions
*Tinea capitis: scalp ringworm, spread by close contact, causing scarring alopecia mostly kids, kerion (raised pustular boggy mass), exaggerated inflammatory response with pustules. M-ketoconazole shampoo + oral anti fungal
*Tinea manuum of hand: scaling + dryness in palmar creases
*Tinea crunis of groin, v pruritic
*Tinea unguium-of nail
*Tinea incognito-inappropriate treatment with steroids causing ill-defined lesions

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28
Q

Onychomycosis

A

Fungal nail infection - tinea unguium (dermatophyte infection), usually toenails, more common with age + DM

CF: dystrophic, rough, opaque thickened nail, discoloured white/yellow/beige, usually begins distally/lateral then spreads

M: clip back, 3-6m of oral itraconazole/terbinafine once clippings confirm
(if caused by candida mild topical anti fungal is used)

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29
Q

Candida albicans

A

Commensal yeast in GIT that may overgrow on occluded moist skin

  • Candidiasis: white plaques on mucosal areas, erythema with satellite lesions in flexures
  • Intertrigo of large flexures: irritation, sore, inflamed, ragged peeling edge, may have pustules + satellite lesions
  • Paronychia: chronic nail fold infection from frequent immersion

Usually topical azoles or nystatin

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30
Q

Pityriasis versicolor

A

Due to Malassezia (a yeast commensal)

Scaly pink-brown patches/macules on upper trunk, hypo pigmented (don’t tan), asymptomatic/mild pruritus

M: topical azoles (ketoconazole shampoo) or if fails send scrapings + oral itraconazole. takes months for pigment to change

it can also cause a type of folliculitis

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31
Q

Scabies

A

Mite infestation spread by close contact

  • Intensely pruritic excoriated rash, small red papules/vesicles anywhere but usually not face (esp webs, palms + soles, axillae, nipples, umbilicus, male genitalia), linear/curved burrows
  • M: topical scabicide e.g. permethrin overnight to all skin below the neck + under nails, treat all close contacts at same time even if asymptomatic, repeat after 1w, wash everything at 60 degrees. may also use malathion
  • Pruritus may stay for up to 6w
  • Crusted scabies: variant in immunosuppressed with huge numbers of mites, mild/absent pruritus, v infectious, hyperkeratotic crusted plaques + widespread erythema. Barrier nursing, repeated scabicide treatment
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32
Q

Lice

A
  • Head lice pediculosis capitis: pruritus, excoriations, papules around hairline of neck + ears. Wet combing until all eggs hatched
  • Body lice pediculosis corporis: disease of poverty + neglect with itch, excoriations, post-inflammatory hyperpigmentation, use permethrin/malathion
  • Pubic lice/crabs - Phthiriasis pubis: itching, see near base of hair with eggs further up
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33
Q

Insect bites

A

Papular urticaria caused by arthropods - itchy urticarial lesions, often in clusters, may blister in hot weather, some people react badly to them

Bed bugs: emerge from seams of bedding at night, clustered itchy papules on exposed areas. need property to be treated

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34
Q

Acute vs chronic eczema features

A

Acute: vesicles/bullae within oedematous inflamed skin, scratching causes exudate + crusting

Chronic: dry, lichenification

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35
Q

What are the types of eczema/dermatitis?

A
  • Atopic
  • Seborrhoeic: v common in greasy areas, causes scaling + erythema, may itch, e.g. dandruff (mildest form on scalp), prob triggered by a commensal yeast. chronic course, topical azoles/shampoos
  • Discoid: well demarcated inflamed scaly patches, v itchy, potent topical steroids to clear
  • Asteatotic: affect elderly in winter, can be v pruritic, affects dry areas with scales/inflammed fissures. M-soap substitute, emollients
  • Chronic hand/foot eczema: common, contact dermatitis or no external cause, dry skin esp in people who wash hands a lot
  • Venous: usually in elderly people with h/o varicose veins/venous thrombosis, can be mild erythema + scale or acute exudative rash, signs of venous insufficiency. M: short term moderate steroid, may benefit from compression if ABPI ok, emollients
  • Irritant/allergic contact dermatitis: delayed hypersensitivity 12-24h after contact, manage active eczema + minimise contact
  • Lichen simplex: chronic eczema where skin is lichenified from rubbing, M-topical anti pruritic + short term potent steroid
  • Nodular prurigo: persistent itchy nodular eruption, eroded hyperkeratotic nodules
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36
Q

Cause of atopic eczema

A

Usually develops in early childhood + resolves during teenager years tho may recur

  • Related to a FH of atopy, may have genetic defect in skin barrier
  • Often raised IgE - cause or effect?
  • Exacerbated by infections, allergens, sweating, heat, severe stress, wool; no clear link with food (young children often get type 1 hypersensitivity to foods but eczema is rare)
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37
Q

Features of atopic eczema

A
  • Itchy erythematous dry scaly patches with papules + vesicles
  • Infants: more common face + extensors
  • Children+adults: more common neck/flexors
  • Acute lesions - erythematous, vesicular, exudative
  • Chronic itching - excoriations + lichenification, post-inflammatory hypo/hyperpigmentation
  • May also have nail pitting + ridging, thickened skin, prominent palm creases, ichthyosis vulgarisms
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38
Q

Management of atopic eczema

A
  • Education, avoid known precipitants, only alter diet with expert supervision in infants, emphasise importance of emollients +/- bandages in younger kids, bath oil/soap substitute (avoid soaps!)
  • Topical steroids for flares: usually od/bd to inflamed areas, milder like hydrocortisone for face, don’t skimp
  • Topical immunomodulators like calcineurin inhibitors e.g. tacrolimus ointment. Benefits are dont cause skin atrophy so good for delicate areas, but poorer penetration of thickened areas, ADR-burning when first use but improves, alcohol induced flushing, higher risk skin cancer
  • Topical antiseptics may be added to bathwater if recurrent infection but they’re irritant
  • Oral antihistamines, sedating if sleep affected, for itch
  • Treat viral/bacterial infections
  • Severe cases: phototherapy, immunosuppression with prednisolone/azathioprine/ciclosporin
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39
Q

Complications of atopic eczema

A
  • Bacterial infection - S aureus or strep. Crusted papules/pustules + exudate
  • Viral: molluscs, warts, eczema herpeticum
  • Eye comps: conjunctival irritation, keratoconjunctivitis
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40
Q

Cause of psoriasis

A

Chronic inflammatory disease with hyper proliferation of keratinocytes + inflammatory cells, related to genetic, immunological + environmental factors

Precipitated by trauma, infection, drugs (lithium, BBs, antimalarials, NSAIDs, ACEi, TNF alpha inhibitors), stress, alcohol

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41
Q

Types of psoriasis

A
  • Chronic plaque psoriasis (most common)
  • Guttate: ‘raindrop lesions’, v small circular/oval papules mostly over trunk + prox limbs, red-pink, more in children/YA, a/w Strep sore throat. Most go within 2-3m, may give topical steroids/phototherapy if symptomatic but guidelines are not to give Abx. May be 1st presentation of psoriasis or exacerbation of plaque psoriasis
  • Seborrhoeic in naso-labial folds/behind ear
  • Flexural in body folds, usually red glazed plaques without scale, M-mild steroid/tar or tacrolimus
  • Pustular and erythrodermic: severe types with sterile pustules of inflammatory fluid, needs very potent topical steroids
  • Palmoplantar pustular psoriasis: localised inflammatory pustules but without systemic sx, a/w smoking
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42
Q

Features of plaque psoriasis

A
  • Pink-red, well-demarcated plaques with silver scale
  • May itch, burn or pain
  • Nail changes: pitting, onycholysis, yellow-brown discolouration, subungual hyperkeratosis
  • Mostly extensor surfaces, lower back, ears, scalp
  • Kobner phenomenon: new plaques appear at sites of trauma
  • Psoriatic arthropathy around 5% (so always ask about): symmetrical polyarthritis/asymmetricalmonoarthritis, lone DIP disease, psoriatic spondylosis, flexion deformity of DIPJ
  • Higher prevalence of metabolic syndrome cos of chronic inflammation

Comps: erythroderma, psychological/social effects

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43
Q

Management of psoriasis

A
  • General: avoid precipitants, emollients to reduce scale, explain no cure but can manage
  • Topical therapy for mild disease: mild steroid for face, potent steroid for rest of body; if no improvement in 8w offer vitamin D analogue (e.g. calcipotriol which reduce cell division to reduce the scale + thickness); if no improvement try using steroid BD or add coal-tar preparations (inhibit DNA synthesis); may add diathranol
  • Phototherapy for extensive: UVB light, or photochemotherapy with UVA + psoralen
  • Oral treatment for extensive or severe/systemic involvement: methotrexate, retinoids like acitretin, ciclosporin, mycophenolate mofetil, biologicals like infliximab/etanercept
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44
Q

Venous leg ulcers

A

Large shallow irregular ulcer, painless, exudative granulating base, malleolar area (esp above the medial malleolus)

  • Peripheral pulses present, warm skin, normal ABPI
  • A/w oedema, haemosiderin deposition, lipodermatosclerosis, atrophie blanche (white scarring + dilated caps)
  • M: compression bandaging usually 4 layer (only thing shown to benefit)
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45
Q

Arterial ulcers

A

Painful, small sharply-defined deep ulcer, necrotic base, at pressure or trauma sites + distal areas like toes.

  • Cold skin, weak/absent peripheral pulses, shiny pale skin, loss of hair
  • ABPI <0.8 indicates insufficiency, do Doppler + angiography
  • M: vascular reconstruction
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46
Q

Neuropathic ulcers

A

Abnormal sensation from DM/neuro disease so often don’t notice. Lesion of variable size with granulating base, may be around a keratotic lesion like a callus, occur at pressure sites

  • Warm skin, normal pulses unless neuro-ischaemic
  • XR to exclude osteomyelitis
  • M: wound debridement, regular repositioning, good footwear, nutrition
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47
Q

Lichen planus

A

Chronic inflammation of unknown cause, lichenoid-like rashes may be triggered by ACEi/antimalarials/BBs/gold

  • Clusters of pruritic purple-pink polygonal papules, with Wickham’s striae (fine lacy white streaks)
  • Most common wrist/LL but can be anywhere
  • May fuse into plaques + become hyperkeratotic, may cause post-inflammatory hypopigmentation, may cause a scarring alopecia or involve nails causing a permanent dystrophy, may have Koebner phenomenon
  • 50% have mucosal involvement: white reticular streaks on buccal mucosa, gingivitis, glossitis, anogenital
  • M: resolve in 1-2y, rarely can change to SCC, topical steroids/tacrolimus can help, oral mucosa-mouthwash, severe-oral immunosuppressants
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48
Q

Granuloma annulare

A

Child/YA, self-limiting goes in 2y, usually asymptomatic + cause unknown – small flesh-coloured/erythematous papules, form rings with a dusky centre, often on dorsum of hand/foot

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49
Q

Lichen sclerosus

A

Common inflammatory dermatosis usually at genitals, usually affects females before puberty/after menopause, or males at any age. Increase risk of vulval/penis SCC, can lead to scarring/atrophy which may impede micturition/sexual function. White plaques form due to epidermal atrophy

CF: pruritic/sore shiny/white fissured patches, perianal involvement common (figure of 8 distribution), may have telangiectasia, children may have haemorhagic bullae, can lead to balanitis in males

M: v potent topical steroids + emollients, in children more likely to remit spontaneously, FU women as higher risk of vulval cancer
*Adv biopsy if suspect neoplastic changes e.g. new lesions, erosions, unresponsive to steroids, pigmented areas

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50
Q

Causes of photosensitive rashes

A
  • systemic disease: SLE, porphyria, pellagra
  • drugs like thiazides/teracyclines/amiodarone)
  • skin disease like rosacea
  • idiopathic e.g. polymorphic light eruption (itchy papular rash a few hours after sun, may get vesicles/plaques, last for several days, prob immunological, avoid sun)
51
Q

Role of phototherapy

A

Light has localised immunosuppressive effects

  • Narrow band UVB often for eczema + psoriasis usually a course 3x pw for 6-10w
  • PUVA: UVA with topical/oral psoralen, limited use cos of SCC risk
52
Q

What causes acne vulgaris?

A

Pilosebaceous follicle blocked cos of abnormal keratinisation + more sebum made - overgrowth of Propionibacterium acnes - inflammation

Linked to genetic susceptibility, androgens in puberty cause sebaceous hyperplasia + more sebum

53
Q

Features of acne vulgaris

A
  • Mostly face + upper back + chest as lots of sebaceous glands
  • Mild: open (blackheads) + closed (whiteheads) comedones
  • Mod-severe inflammatory: papules, pustules, nodules, cysts
  • Scarring: hypertrophic or pitted
  • Post-inflammatory hyperpigmentation esp in darker skins

Variants:

  • Infantile from maternal androgens
  • Acneiform eruptions from steroids: pustular folliculitis without comedones
  • Severe cystic acne with abscesses + sinuses
  • Acne fulminans: rare severe with deeply inflamed ulcerated nodes + systemic sx
54
Q

Management of acne vulgaris

A

*General: adv that no specific food triggers, not to do with cleanliness, wash but not too much and avoid harsh soaps, need to persist with treatment for at least 6w for an effect
1. Single topical retinoid or benzoyl peroxide, azelaic acid + salicylic acid. All may cause dry flaking skin
2. Topical combination like retinoid + benzoyl peroxide/antibiotic + benzoyl peroxide
[topical for mild with a few pustules but mostly comedones]
3. Oral Abx for moderate inflammatory with oxytetracycline or doxycycline, 3-4m often before improves. Always prescribe with a non-antibiotic topical to reduce resistance. In females may try a COCP containing cyproterone acetate (reduces sebum)
4. Oral isotretinoin: specialist, 2/3 get long term remission but ADRs are teratogenicity (pregnancy prevention programme, 2 forms contraception), dry skin/eyes/mouth/lips (commonest as this is how it works), low mood (controversial), raised triglycerides, hair thinning, epistaxis from dry nose, intracranial hypertension

55
Q

Acne rosacea

A

Inflammatory facial rash in mid-adulthood, F>M

  • Flushing, diffuse erythema, inflammatory papules + pustules (no comedones)
  • Later fixed erythema cos of dilated bvs, sebaceous gland/soft tissue overgrowth around nose, facial lymphoedema
  • Ocular: blepharitis, keratitis, conjunctivitis
  • A/w triggers like hot drinks, alcohol, sun, temp changes, prolonged topical steroids
  • M: topical metronidazole/azelaic acid for mild (ie no plaques, limited no papules + pustules), oral tetracyclines for flares, sub-antimicrobial doses of doxycycline are anti-inflammatory, laser for prominent telangiectasia, camouflage creams to reduce redness, use high factor sunscreen
56
Q

Perioral dermatitis

A

Rosacea-like rash around mouth, triggered by topical steroids - small inflammatory papules + pustules with scaling, often along nasolabial folds. M-oral tetracycline, weaning off steroids

57
Q

Causes of flushing

A
  • Normal physiological response to emotion
  • Menopause
  • Some drugs e.g. ACEi, CCB
  • Carcinoid syndrome
58
Q

Bullous pemphigoid

A

Blistering skin disorder mostly affecting >60y causing sub-epidermal split

Tense serous/haemorrhagic bullae on an erythematous base, often itch (may be preceded by an itchy rash), usually on trunks + limbs (rarely affects mucosa but it can), can be widespread, can affect eyes causing eyelid fusion/corneal damage

M:

  • wound dressings
  • topical steroids + minocyline if localised
  • oral steroids mod-high dose (for most)
  • tetracycline + nicotinamide combination
  • steroid-sparing immunosuppression where poss as elderly higher risk for ADRs, e.g. azathioprine or methotrexate
59
Q

Pemphigus vulgaris

A

Blistering skin disorder mostly affecting middle aged people, rare + can be life-threatening, a/w Ashkenazi Jewish + Indian populations

Autoantibodies - loss of keratinocyte adhesion - intra-epidermal split, erosions, oral uclers

Causes non-itchy flaccid easily-ruptured blisters, erosions + crusts, often painful, on rupture leave erythematous weeping erosions, often on trunk, 50% involve oral mucosa

M: wound dressings, mouth care, oral high dose steroids/other immunosuppressive agents, high dose IV Ig in severe cases

60
Q

Pemphigus foliaceus

A

Rare variant of pemphigus in which skin splits higher in the epidermis, and MM not involved. Blisters aren’t usually seen, rash with crusted appearance usually in seborrheic areas (scalp, face, chest). M-immunosuppresion

61
Q

Dermatitis herpetiformis

A

Sub-epidermal blistering disorder a/w Coeliac disease, M>F

Causes small intensely itchy vesicles + papules on elbows/extensor of forearms/scalp/buttocks, crusted lesions + erosions from scratching

If do biopsy shows IgA deposits in upper dermis

M: gluten exclusion, dapsone/sulfonamides to help itch + blistering, can stop meds after 2y if remain blister-free

  • Avoid dapsone in cardioresp disease + G6PDH def (screen for this) as causes haemolysis
  • other dapsone ADRs include hepatitis + peripheral neuropathy
62
Q

Epidermolysis bullosa

A

aka mechanobullous disease
Rare group of conditions with defective/absent skin proteins causing fragility meaning trauma induces blisters/erosions
*Simplex: superficial localised blistering, no scarring
*Dystrophica: deeper blistering with scarring, nail/mucosa inc larynx may involved, reduced life expectancy as SCC risk from chronic inflammation
*Junctional: most severe, widespread blistering with areas of absent skin

63
Q

Benign skin tumours list

A
  • Melanocytic naevi (moles): congenital (can be giant, cafe au lait macules, speckled lentiginous naevus), acquired up to early adult. even pigmentation with regular borders, start as flat brown macules (junctional naevi) then grow into dermis (compound naevus), blue naevus when deeper in dermis
  • Seborrheic keratosis/wart: basal cell papilloma, flesh-brown-balck coloured, ‘stuck on appearance’, usually leave but may do curretage/cryosurgery/shave biopsy
  • Dermatofibroma: pink-beige, firm dermal nodules, may have surrounding hyperpigmentation and may be a/w insect bite or trauma
  • Epidermoid/sebaceous cyst: cystic swellings in occluded follicle, have central puncture + keratinous cheese, may get infected
  • Pilar cyst smooth cysts on scalp
  • Pyogenic granuloma: vascular proliferation’s, friable, minor trauma, often face/fingers, excise to exclude amelanocytic melanoma
  • Cherry angioma (angiokeratoma): v common, tiny pinpoint red papules, age-associated
  • Haemangioma: may look brown to naked eye then with dermatoscope see purpley vessels, if also had pigmentation would be suspicious of melanoma angiogenesis
64
Q

What are actinic keratoses?

A

Pre-malignant lesion on sun-damaged skin considered as pre-cancerous SCC (like just 1 AK unlikely to turn into it but if have >10 AKs there is a 15% risk of SCC), caused by UVB damage + poor immune function + long history of being outdoors

Often multiple + varied appearance, sun exposed areas usually, flat/thickened papule or elevated plaque, skin colour/red/pigmented, tender or asymptomatic, may be scaly/rough. If on lip called actinic chelitis

65
Q

What do you do with actinic keratoses?

A
  • May just observe if flat + asymptomatic + single
  • Topical diclofenac for mild
  • Topical 5-FU for 2-3w to cause local inflammation, or topical imiquimod
  • Remove: cryotherapy, curretage+ cautery, superficial surgery, excision
66
Q

Lentigo maligna

A

A precursor to lentigo maligna melanoma that grows slowly over years until invades dermis when it is melanoma. RF are sun damage + age

Slowly changing patch of discoloured skin initially like a freckle then more atypical, often quite big, irregular, variable pigmentation, smooth surface

Needs excision

67
Q

Bowen’s disease

A

SCC in situ, not invaded basement membrane

  • RF: UV, arsenic, ionising radiation, HPV in fingers/nails, immunosuppression
  • One or more irregular patch/plaque, well-defined, like psoriasis but no scale, slowly enlarging, usually red but may be pigmented, erythronychia (red streak under a nail)
  • 5% progress to invasive SCC
  • M: k excision for solitary lesions, 5-FU or imiquimod cream
  • May occur on mucosal genitalia linked to HPV e.g. PIN
68
Q

Keratocanthoma

A

Rapidly-growing epidermal tumours , initially smooth dome shaped papule that develop central necrosis + ulceration, on sun exposed sites

rare in young people

spontaneous resolution in 3m is common but excised to exclude SCC as look similar

69
Q

What is a basal cell carcinoma?

A

Slow growing, locally invasive malignant tumour of epidermal keratinocytes (a tiny proportion metastasise to local LN, and there’s also basosquamous cell carcinoma which is a mix of BCC + SCC so more aggressive)

RF are UV, frequent/severe sunburn in childhood, skin type 1, age, male, immunosuppression, prev skin cancer, genetic predisposition

70
Q

Types of BCC

A
  • Nodular: most common. small skin coloured papule/nodule with surface telangiectasia, pearly rolled edge due to central depression, may have necrotic centre (rodent ulcer) and micro-erosions
  • Superficial: more common in younger, plaque-like slightly scaly thin translucent rolled border, micro-erosions
  • Cystic: soft jelly-like
  • Morphoeic: sclerosing/waxy/scar like plaque, usually on face, indistinct borders, may infiltrate nerves
  • Pigmented
71
Q

Management of BCC

A
  • High risk in H+N refer under 2ww, low risk manage in primary care
  • Excision: 3-5mm margins (nodular, infiltrative, morphoeic, obv also send for histology)
  • Mohs microscopic surgery if in a high risk area/recurrent: excise lesion + borders progressively until specimens free of microscopic tumour
  • Superficial skin surgery like curretage/shave for small well defined nodular/superficial
  • Cryotherapy for small superficial on trunk/limbs: blister crusts + heals leaving white mark
  • 5-FU cream for small superficial but high recurrence rates; topical imiquimod better
  • Radiotheapy if cant have surgery or adjunct for incomplete margins, works by inflammation
72
Q

What is squamous cell carcinoma?

A

Locally invasive malignant tumour of epidermal keratinocytes which can metastasise

RF: chronic UV exposure, pre-existing AK, Bowen’s disease, chronic inflammation, immunosuppression, arsenic

73
Q

How do SCC present and what is the management?

A
  • Keratotic ill-defined nodule which may ulcerate
  • Cutaneous horn: solitary horny lesion that may be hyperkeratotic AK or SCC, local shave curettage or cautery or excision
  • Cutaneous invasive SCC usually arises within an AK but can be from chronic skin disease
  • Sebaceous carcinoma around eyelid, significant metastatic potential

If suspect need 2ww referral

M: excision with 4mm margin if <20mm lesion, or 6mm if >20mm; may do MMS if high risk/important site

74
Q

What problems are associated with psoriasis therapies?

A

*Topical steroids: skin atrophy, systemic absorption, striae. Adv 4w break between steroid courses to reduce risk + reduce rebound sx, don’t use potent for more than 8w at a time or v potent for more than 4w at a time, be more careful with face/flexures/scalp
*Vit D analogues: ADRs uncommon, but don’t use in pregnancy
*Dithranol: wash off after 30m, s/e burning + staining
*Phototherapy: skin ageing + SCC
*Oral methotrexate: BM suppression, hepatic/pulmonary fibrosis, mucositis; men + women avoid pregnancy for 6m after finishing; regular bloods FBC U+E LFT (once weekly until stable’s then 2-3 months); once weekly
administration
*Oral ciclosporin: renal damage HTN, interactions with NSAIDS/erythromycin

75
Q

What is a Marjolin’s ulcer?

A

SCC at sites of chronic inflammation after like 10y e.g. burns, osteomyelitis, venous ulcers. mostly legs

76
Q

Pityriasis rosea

A

An acute self-limiting exanthem that is prob caused by HHV, affecting older children/young adults

  • Rash on torso + proximal limbs
  • Herald patch: initial solitary patch, larger
  • Circular/oval pink macules with fine scale
  • Tend to run along dermatomal lines of the back
  • Usually asymptomatic or mild itch + resolve in 4-8w, if pruritic give mild steroid + emollients
77
Q

What is malignant melanoma?

A

Invasive malignant tumour of epidermal melanocytes that can metastasise (most commonly to LN, lungs, brain, bone, liver)

RF: excess UV, type 1 skin, h/o multiple/atypical moles, FH/PMH melanoma, Parkinson’s disease, precursor lesions

75% arise from normal appearing skin, 25% from existing mole/freckle

78
Q

Features of malignant melanoma

A

Most common on legs in women + trunk in men

ABCDE symptoms (* is major feature)
Asymmetrical shape*
Border irregularity 
Colour irregularity*
Diameter >6mm
Evolution of lesion*
Symptoms: bleeding or itching
79
Q

Types of malignant melanoma

A
  • Superficial spreading: most common, related to intermittent high intensity UV. Spreads out within epidermis then invades into dermis, CF are growing moles with the ABCDE features
  • Nodular: second most common, aggressive, intermittent high intensity UV. Vertical growth plate, may be black/ulcerated/amelanotic, bleeds/oozes
  • Lentigo maligna melanoma: progresses from the precursor, common on face in elderly, related to cumulative UV
  • Acral lentiginous melanoma: rare type on palms/soles/nail beds, no clear link to sun, dark vertical stripes in nail/amelanotic subungual melanoma/enlarging discoloured skin patch
  • Ocular
  • Amelanotic
80
Q

Diagnosis of melanoma

A

Major criteria: change in shape, size or colour

Secondary features: diameter >6mm, inflammation, oozing/bleeding, altered sensation

81
Q

Management of melanoma

A
  • 2ww
  • Excision - so you excise with 2mm margin initially, then based on Breslow thickness do more excision
  • wide margins: 0-1mm thick 1cm margin, 1-2mm thick 1/2cm margin, 2-4mm thick 2-3cm margin, >4mm thick need 3cm margin
  • If stage 3 (LN) need complete removal of LN
  • Follow up routine skin checks annually for 5y + encourage self examination + sun protection
82
Q

What determines prognosis in melanoma?

A
  • Breslow thickness (vertically in mm from top of granular layer to deepest point tumour reaches): high risk if >1.5mm
  • Clark level of invasion: anatomic plane of invasion. 1=in situ, 2=papillary dermis, 3=filled papillary dermis, 4=reticular dermis, 5=SC tissue; less useful than Breslow
  • Melanoma in situ cured by excision as no potential for spread
  • Mets poor prognosis
83
Q

Kaposi’s sarcoma

A

Tumour of vascular + lymphatic endothelium , strong link to HHV-8. Classically causes larger purpuric lesions (not really petechiae)

  • Classic type in elderly males esp Jewish population, slow-growing purple tumours, rarely a major issue
  • Endemic: widespread skin + LN involvement + oedema, in certain areas
  • Immunosuppression: more severe, affects HIV positive people, widespread lesions in skin/bowel/mouth/lungs
84
Q

Senile purpura

A

Occur in elderly population from sun damage, common on extensor surfaces of hands + forearms

Non-Palpable purpura, surrounding skin atrophic, systemically well, don’t need treatment

85
Q

Pyoderma gangrenosum

A

Not actually infection or gangrene!
Can be triggered by trauma, usually a/w IBD/RA/haem cancers/liver disease/SLE

Usually on LL - small red papules then painful erythematous nodules/pustules developing into large ulcers, often purple margins + purulent surface, may have fever + myalgia

Do not debride - makes it worse!

M: high dose oral steroids, long term may need systemic immunosuppresion/dapsone

86
Q

Signs of endocrine disease in the skin

A
  • Acanthosis nigricans: thickened hyper pigmented brown-black velvet texture around large flexures (can also get on tongue), symmetrical, may appear warty. Due to insulin resistance + obesity (more insulin-deposits in skin-hyperplasia), if severe/late onset usually paraneoplastic (GI cancers)
  • DM: fungal infections/recurrent boils, arterial/neuropathic ulcers, gangrene, necrobiosis lipoidica (spreading erythematous patch over shin, yellow-atrophic in centre, may ulcerate), diffuse granuloma annulare, diabetic dermopathy (red-brown flat papules)
  • Hypothyroidism: dry firm gelatinous skin, hair thinning, loss of outer 1/3 of eyebrow
  • Hyperthyroidism: warm, sweaty skin, diffuse alopecia, thyroid acropachy (clubbing w bone changes), pretibial myxoedema (red-brown mucinous shins, may be lumpy + tender)
  • Cushing syndrome: telangiectasia, atrophy, folliculitis ‘steroid acne’, atrophy, striae
87
Q

Signs of metabolic disease in the skin

A
  • Hyperlipidaemia: xanthomas – xanthelasmas (around eyes), tuberous xanthoma (orange-yellow on extensor surfaces), tendon xanthomas, eruptive xanthoma
  • Amyloidosis: macular amyloid itchy brown rippled macules on upper back, or systemic amyloid causing red/brown papules/nodules/plaques
88
Q

Signs of renal disease in the skin

A
  • Pruritis in CKD often intractable
  • Pallor
  • Hyperpigmentation
  • Ecchymoses
  • Renal transplant pt - recurrent viral warts, SCC
  • Nephrogenic fibrosing dermopathy: severe scleroderma-like disease in dialysis pt with rapid onset discolouration, joint contractures, pain
89
Q

Signs of hepatic disease in the skin

A
  • Spider naevi: fill from centre (cf telangiectasia fill from edge), central red papule with surrounding capillaries, blanch on pressure, almost always on upper body. Also a/w pregnancy, cocp and childhood
  • Jaundice
  • Palmar erythema
  • Leuconychia
  • Hyperpigmentation
  • Pruritis - excoriations, lichenification
90
Q

Dermatomyositis

A

Autoimmune

  • Photosensitive rash, facial erythema, magenta rash, peri-orbital oedema, may have bluish-red nodules.plaques
  • M: hydroxychloroquine, sunscreens
91
Q

Scleroderma

A

Autoimmune
Thickened/hardened skin due to abnormal dermal collagen
*Systemic sclerosis - cutaneous + systemic features
*Morphea - cutaneous only
*Skin problems - bluish-red plaques, induration, central white atrophy

M: potent topical/oral steroids or immunosuppressant (depo on severity)

92
Q

SLE skin manifestations

A
  • Discoid lupus: erythematous, scaly, atrophic plaques with telangiectasia esp of face, a/w hypopigmentation/scarring alopecia, 25% also get oral red patches/ulcers, may also get Raynaud’s. <5% develop systemic disease, 30% positive ANF. M-sunscreens, potent topical steroids or hydroxychloroquine or further immunosuppression, usually chronic
  • Subacute SLE: widespread annular lesions, photosensitive, arthralgia + mouth ulcers common, antibodies usually positive
  • SLE: usually p/w other features but skin things are butterfly rash (macular erythema on cheeks + forehead), palmar erythema, dilated nail fold capillaries, splinter haemorrhages, digital infarcts of fingers, livedo reticular
93
Q

Livedo reticularis

A

Causes: idiopathic, systemic disease like RA/SLE/APS, livedoid vasculopathy (a/w painful ulcers, venous insufficiency), polyarteritis nodosa

Bluish-red skin discolouration in lacy pattern, usually limbs, looks worse in cold as caps + venules dilate

94
Q

Behcet’s disease

A

Oral ulcers + 2 out of eye lesions/genital ulcers/skin lesions

Skin features are erythema nodosum, acneiform lesions, thrombophlebitis, blistering at sites of minor injury

95
Q

Sarcoidosis skin manifestations

A

Red-brown dermal papules + nodules esp around eyelids/nostrils, lupus pernio (nose), hypo/hyperpigmentation, erythema nodosum in acute sarcoid

M: dermovate, oral/intralesional steroids, hydroxychloroquine/methotrexate

96
Q

Skin signs in NF1

A

Early: cafe au lait macules >5 lesions, axillary freckling, Lisch nodules n eyes (hyper pigmented iris hamartomas)

Later: neurofibromas

97
Q

Skin signs in tuberous sclerosis

A

Adenoma sebaceum (red papules/fibromas around nose), periungual fibroma (nodules from nail bed), shagreen patches on trunk (flesh coloured plaques), ash-leaf hypo pigmentation, indurated forehead plaque, pitting of dental enamel, cafe au lait patches

98
Q

Seborrhoeic dermatitis

A
  • Adults: chronic inflammation in response to proliferation of a commensal yeast (Malassezia furfur) - eczematous lesions on sebum rich areas like scalp/periorbital/auricular/nasolabial folds, may cause otitis externa/blepharitis. M: OTC things with zinc pyrithione in like H+S or tar like Neutorgena T Gel; topical antifungals like ketoconazole; topical steroids for short periods. tends to recur. Is also a/w HIV + Parkinson’s disease
  • Children: cradle cap of scalp (early on, erythematous rash with coarse yellow scales), or nappy area/face/limb flexures. Mild-mod baby shampoo+oils, severe mild topical steroid (1% hydrocortisone), tends to go spontaneously by 8m
99
Q

Alopecia areata

A

Autoimmune mediated localised well-demarcated patches of hair loss, at edge of loss may have broken ‘exclamation mark’ hairs.

Will regrow in 50% by 1y and up to 90% eventually

If want to treat can try topical steroids, topical minoxidil (a vasodilator), phototherapy, dithranol

100
Q

Pressure ulcers

A

Usually over bony prominences-heel or sacrum.

Waterlow score-screens for pt at risk like with BMI, nutritional status, skin type, mobility + continence

Grading:

  • 1-non blanch able erythema of intact skin, may be oedema/warmth/indurated/hard
  • 2-partial thickness skin loss up to dermis, superficial ulcer, abrasion/blister
  • 3-full thickness skin loss with damage to SC tissue, may extend down to fascia but not through
  • 4-extensive destruction, tissue necrosis of damage to muscle/bone, with or without full thickness skin loss

M:

  • Moist environment with hydrocolloid dressings to help heal, avoid soap
  • Wound swabs only if suspect cellulitis, as majority will be colonised but usually dont need Abx
  • Consider tissue viability nurse
  • Surgical debridement in some cases

Prevention: prevent with frequent repositioning, nutritional support, use of pressure-relieving devices

101
Q

Role of topical treatments

A

Deliver treatment to a specific area to reduce systemic s/e

  • Active ingredients: tar, steroids, immunomodulators, retinoids, Abx
  • Bases: lotion (liquid), cream (oil in water), gel (organic polymers in liquid), ointment (oil with little/no water), paste (powder in ointment)
102
Q

Emollients

A

Used to rehydrate skin + re-establish surface lipid layer, good for dry scaling conditions + as soap substitutes

  • Aqueous cream, emulsifying ointment, liquid paraffin with white soft paraffin, soap substitutes (remove dirt but don’t lather, e.g. Cetaphil or Hydromol)
  • s/e: irritant/allergic reactions (often due to preservatives)
  • often try different types until find best match, apply liberally + regularly, pat skin dry after showering
  • 500g per tub, e.g. hydromol ointment for at night with epimax cream for daytime
103
Q

Topical steroids + examples

A

Mildly potent - hydrocortisone 1%/2.5%

Moderately potent - Eumovate (clobetasone butyrate)

Potent - Betnovate (betamethasone)

Very potent - Dermovate (clobetasol propionate)

Local s/e: skin atrophy, telangiectasia, striae, may mask/exacerbate/cause infections/acne/perioral dermatitis, allergic contact dermatitis, steroid-induced rosacea/folliculitis, tinea incognito

GPs often unduly cautious about steroid creams as tbh severe eczema they really need it

On face usually use 1% hydrocortisone but like if a big flare can use Eumovate

Adv apply thinly, 1-2w course for mild flares, and only use on the inflamed areas

104
Q

Topical antibiotics

A

Used for bacterial skin infections (fusidic acid, mucipirocin, neomycin), acne (e.g. clindamycin in Duac)

105
Q

Topical antiseptics

A

For treating + preventing skin infections like chlorhexidine, cetrimide
S/e local skin irritation

106
Q

Topical retinoids

A

E.g. adapalene - often combined with Abx or benzoyl peroxide (e.g. Epiduo)

S/e local skin irritation, dryness, dont use in pregnancy

107
Q

Topical antifungals

A

Imidazole, terbinafine

108
Q

Oral steroids for skin

A

Prednisolone

S/e: Cushing’s syndrome, immunosuppression, HTN, DM, osteoporosis, cataracts, psychosis, plus the skin s/e

109
Q

Oral aciclovir

A

For viral infections

S/e are GI upset, raised LFTs, reversible neuro reactions, haematological

110
Q

Oral Abx

A

Multiple types used, avoid tetracyclines in <12y due to yellowing teeth

S/e: Gi upset, rashes, anaphylaxis, vaginal candidiasis, Abx-associated C diff, resistance

111
Q

Oral retinoids

A

Isotretinoin, acitretin - for acne or psoriasis

S/e: mucocutaneous reactions like dry skin/lips/eyes, disordered liver function, hypercholesterolaemia, hypertriglyceridaemia, myalgia, arthralgia depression

V teratogenic, need to use condoms + use contraception that isn’t the pill (like a coil or implant) 1 month before, during and at least 1m after isotretinoin, or 2y after Acitretin

112
Q

How much emollient/ointment/steroid should you prescribe?

A
  • 30g of cream/ointment covers a full adult body, 1 fingertip unit covers an area of two palms and is 0.5g –> so depends on condition basically
  • Emollients in 500g tubs. Cream/lotion for red/inflamed/weeping lesions, ointment for dry scaling skin
  • For steroids you need to specify the base ie cream, lotion, ointment
113
Q

What skin investigations may you do?

A
  • Skin swab: from vesicles, pustules, erosions, ulcers and mucosal surfaces for microbial culture. Surface swabs generally not encouraged, try to get deeper into it
  • Skin scrape: from scaly lesions by gentle use of a scalpel/other bluntish thing in suspected fungal infection to show evidence of hyphae/spores, and from burrows in scapies. Scrape it off onto contrasting piece of paper, fold up and put in pot, label and send to micro
114
Q

Causes of pruritus

A
  • Asteatotic eczema, cholinergic urticaria
  • Idiopathic pruritus-usually due to dry skin
  • Iron def anaemia
  • Internal malignancy esp lymphoma
  • DM, CKD, liver disease (esp primary biliary cholangitis)
  • Thyroid disease
  • HIV
  • Polycythaema vera

M: avoid soaps, symptomatic, low dose amitriptyline/gabapentin may help intractable cases. obv treat medical issues

115
Q

Causes of a red swollen leg

A
  • Cellulitis: deeper into SC, diffuse
  • Erysipelas: well defined edge, more superficial , more often systemically unwell
  • Venous thrombosis: pain, swelling, redness, h/o immobility/clotting tendency, cyanotic if completely occluded. Ix Well’s score, D-dimer (both not used in pregnancy tho), doppler US
  • Chronic venous insufficiency: heavy aching leg, worse on standing relief on walking, venous skin changes
116
Q

What skin conditions are a/w pregnancy?

A
  • Polymorphic eruption of pregnancy: pruritic, esp in T3, lesions appear in abdominal striae initially, M may involve emollients/mild topical steroids/oral steroids
  • Pemphigoid gestationis: pruritic blistering lesions, often peri-umbilical then spread to trunk/back/buttocks, usually in T2/3 and rare in 1st pregnancy, usually need oral steroids
117
Q

Oral antihistamines

A

Block histamine receptors so anti-pruritic + type 1 hypersensitivity reactions

  • Non-sedating e.g. cetirizine, loratidine
  • Sedating e..g chlorpheniramine, hydroxyzine. Good for child not sleeping due to eczema/chickenpox but otherwise avoided

SE sedation, anti-cholinergic sx

118
Q

What skin changes are seen in venous insufficiency?

A

blue/purple discolouration, oedema improved in morning, venous congestion + varicose veins, lipodermatosclerosis (erythematous induration creating a ‘champagne bottle’ appearance), stasis dermatitis (eczema with inflammatory papules, scaly + crusted erosions), venous ulcer

119
Q

What allergy tests can be performed?

A
  • Skin prick: most common, cheap, drops of diluted allergen placed on skin then skin pierced with needle, can test many allergens in one session. usually includes histamine as a positive control + sterile water as a negative control, wheal develops if pt has allergy –> useful for food allergies + pollen
  • Radioallergosorbent blood test: determines amount of IgE that reacts specifically with a suspected allergen, e.g. IgE to egg protein. Results from 0 (negative) to 6 (strongly positive), used for food allergies, inhaled allergens, wasp/bee venom, used when skin prick unsuitable like extensive eczema or pt on antihistamines
  • Skin patch testing: for contact dermatitis. 30-40 allergens placed on back, patches removed 48h later then read after a further 48h
120
Q

Complications of burns

A
  • Haemolysis due to damage of erythrocytes by heat and microangiopathy
  • Loss of capillary membrane integrity causing plasma leakage into interstitial space
  • Extravasation of fluids from the burn site causing hypovolaemic shock (up to 48h after injury)- decreased blood volume and increased haematocrit
  • Protein loss –> oedema
  • Secondary infection e.g. Staphylococcus aureus
  • ARDS
  • Risk of Curlings ulcer (acute peptic stress ulcers)
  • Danger of full thickness circumferential burns in an extremity as these may develop compartment syndrome
121
Q

What is the management for athlete’s foot?

A

A topical imidazole (e.g. miconazole), undecenoate, or terbinafine

122
Q

Hirsutism

A

Hirsutism = androgen-dependent hair growth in women,

Causes of hirsutism: PCOS, Cushing’s syndrome, CAH, androgen therapy, obesity (insulin resistance), adrenal tumour, androgen-secreting ovarian tumour, phenytoin, steroids

M: WL if overweight, cosmetic things like waxing/bleaching (not on NHS), consider COCP like co-cyprindiol (Dianette, not long term due to higher risk of VTE) or Yasmin, for facial hair can try topical eflornithine (an anti-protozoal, blocks an enzyme in follicles, CI in pregnancy + breast feeding)

123
Q

Hypertrichosis

A

Hypertrichosis=androgen-independent hair growth

Causes: drugs (minoxidil, ciclosporin, diazoxide), congenital causes, porphyria cutanea tarda, anorexia nervosa

124
Q

What are the causes of acanthosis nigricans?

A

Obesity, PCOS, DM, GI cancers, acromegaly, Cushing’s disease, hypothyroidism, familial, Prader-Willi syndrome, some drugs (oral contraceptive pill, nicotinic acid)

Neuro + special senses (5 decks)

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