Dermatology Flashcards

1
Q

**Urticaria, Angioedema, Anaphylaxis **
- Presentation
- Pathophysiology
- Investigation
- Management (doses done separately)
- When to discharge

A

Presentation
* Urticaria - itchy wheals
* Angioedema - tongue/lip swelling
* Anaphylaxis - bronchospasm (wheeze), facial/laryngeal oedema (stridor), hypotension, tachycardia, urticaria, angioedema
Pathophygiolosy
* Causes: Idiopathic, food, drugs, insect bites, latex. Andioedema/urtcaria can be inherited
Investigation (after stabilisation)
* Serum tryptase to confirm anaphylaxis (raised 12h post event)
* All new anaphylaxis should be referred to allergy clinic + epipen given in interim (unless drug induced)
Management
Initial Stabilisation:
* Remove trigger, lie flat (or left side if pregnant), elevate legs
* IM adrenaline (rpt after 5 mins if needed)
* Establish airway, high flow O2, monitoring, IVI bolus
* If refractory (ongoing after 2x IM adrenaline - crit care ?adrenaline infusion)
After Stabilisation:
* PO antihistamines (if persisting skin symptoms)
Discharge Home (biphasic reaction in 20%)
* Fast-track - 2h post symptom resolution - if good response to single dose, complete resolution, adequate supervision
* 6h post symptom resolution - 2 doses of IM adrenaline needed or prev biphasic reaction
* 12h - >2doses needed, pt has severe asthma, possibility of ongoing reaction (e.g. slow-release meds), late at night, difficult access to ED - observe for 12h

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2
Q

Adrenaline Dose for Anaphylaxis

A

< 6 months - 100- 150 micrograms
**6 months - 6 years ** - 150 micrograms
6-12 years - 300 micrograms
Adults - 500 micrograms (0.5ml 1 in 1,000)

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3
Q

Erythema Nodosum
* Presentation
* Pathohysiology
* Management

A

Presentation
* Discrete, tender, erythematous, nodular lesions
* Often over shins
* continue to appear for 1-2/52 then leave bruise-like discolouration
* No scarring, ulceration or atrophy

Causes
* Infection - group A B-haemolytic strep, TB, burcellosis
* Systemic - sarcoidosis, IBD, bechet’s
* Malignancy/Lymphoma
* Drugs - penicillins, sulphonamides, COCP
* Pregnancy

Management
* Supportive - bed rest, leg elevation
* NSAIDs, intralesional or PO steroids
* nodules may also resolve spontaneously

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4
Q

Erythema Multiforme
Presentation
Pathophysiology
Management

A

**Presentation **
* Target lesions. Often hands/feet then spread to torso +/- mild itch
* Major form also has mucosal involvement - normally oral membranes but can be urogenital or ocular (keratitis, conjunctival scarring, uveitis, permanent visual impairment)
Pathophysiology
* Hypersensitivity reaction.
* Triggers:
* Viral: Herpes simplex (most common)
* Bacteria: mycoplasma, streptococcus
* Drugs: penicillin, sulphonamides, carbamazepine, NSAIDs, COCP
* SLE, sarcoidosis, malignancy, idiopathic
Management
* often self-resolves BUT eye involvement needs ophthalmology
* Otherwise supportive: antihistamines, topical steroids (itch), oral washes for mild mucosal involvement (may need hosp admission if bad for support of PO intake)

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5
Q

Stevents Johnson Syndrome
* Presentation
* Pathophysiology
* Management

A

**Presentation **
-Severe systemic reaction w/ at least 2 mucosal sites involved - mucocutaneous necrosis
-Skin involvement can be limited or extensive: - maculopapular rash w/ target lesions, can develop bullae/vesices, nikolsky sign (blisters/erosions when skin is rubbed)
-Sytemic: fever, arthralgia

Pathophysiology
* mostly due to drug reactions: penicillin, sulphonamides, lamotrigine, carbamazepine, phenytoin, allopurinol, NSAIDs, COCP

Management
- Hospital admission for supportive care + to maintain haemodynamic stability
- Mortality = 5-12%

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6
Q

Toxic Epidermal Necrolysis
- Presentation
- Pathophysiology
- Management

A

**Presentation **
-Severe cutaneous drug reaction.
- Prodrmoal ‘flu-like’ illness –> rapid appearance painful erythematous rash + desquamation of skin/mucous membranes
- >30% skin involvement

**Pathophysiology **
- Severe SJS. Drug reaction.

Management
- Supportive: Isolation, fluid/electrolyte balance, nutritional support, pain management, protective dressings.
- Burns unit or ICU management

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7
Q

Erythroderma
- Presetation
- Pathophysiology
- Complications
- Management

A

**Presentation **
- Exfoliative dermatitis involving >90% of skin
- Inflamed, oedematous, scaly skin
- Itch - can be intolerable
- Systemically unwell w/ lymphadenopathy + malaise

Causes
- Prev skin disease (eg. eczema, psoriasis)
-lymphoma
-drugs (eg. sulphonamides, gold, sulphonylureas, penicillin)
-idiopathic

Complications
- Secondary infection, fluid loss, electrolyte imbalance, hypothermia, high-output HF, capillary leak syndrome
- Mortality 20-40%

Management*
- supportive
- Abx for bacterial infection
- Antihistamines may help itch

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8
Q

Necrotising Fascitis
- Classification
- Presentation
- Risk Factors
- Management

A

Classification
Rapidly spreading infection of deep fascia w/ secondary tissue necrosis
- Type 1: mixed anaerobes + aerobes (most common - often group A haemolytic strep)
- Type 2: Streptococcus pyogenes

**Presentation **
- Often presents as rapidly worsening cellulitis w/ pain out of keeping w/ physical appearance
- pain, swelling, erythema, ++tender. Late signs: skin necrosis, crepitus, gas gangrene, fever, tachycardia

Risk Factors/Causes
- Skin: recent trauma, burns, soft tissue infection
- DM (esp if on SLGT-2 inhibitors), IVDU, immunosupression, abdo surgery

Management
- Urgent referral for extensive surgical debridement
- IV abx
- mortality 20%

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9
Q

Eryspelas and Cellulitis
- Presentation
- Pathophysiology
- Management

A

Pathophysiology Both = Spreading infection of skin
- Cellulitis: deep subcutaneous tissue
- Erysipelas: acute superficial cellulitis involving dermis + upper subcutaneous tissue

Causes
- Strep pyogenes + Staph aurerus
- RF: immunosupression, wounds, leg ulcer, minor skin surgery

Presentation
- mostly lower limbs.
- Swelling, erythema, warmth, pain +/- lymphangitis
- Systemically unwell - fever, malaise, rigors (esp erysipelas)
- erysipelas- more well demarcated w/ red raised border
- Complications: local necrosis, abscess, sepsis

Management
- Abx - mild/moderate cellulitis:
- 1st line: flucloxacillin
- If pregnant: erythromycin
- Penicillin allergy: clarithromycin, erythromycin or doxyxyline

-Severe cellulitis:
- Co-amox, cefuroxime, clindamycin, ceftriaxone

  • Supportive care: rest, leg elevation, dressings, analgesia
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10
Q

Staphylococcal Scalded Skin Syndrome
- Presentation
- Pathophysiology
- Management

A

Presentation
- infancy/early childhood
- Develops over hours-days. Often worse in face, neck, axillae, groins.
- Scalded skin appearance –> large flaccid bulla (intraepidermal blistering)
- ++ painful

Pathophysiology
- Due to epidermolytic toxin from benpen resistant (coagulase positive) staphylococci

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11
Q

Tinea
- Pathophysiology
- Classification/Presentation
- Investigation
- Management

A

Pathophysiology
- Superficial fungal infection (fungal infection can be dermatophyte (tinea/ringworm), yeast (candidiasis, malassezia) or mould (aspergillus))

Classification
- *Tinea Capitis *- pathes of broken hair, inflammation,scale - if untreated can cause kerion (raised, pustular, boggy mass)
- *Tinea Corporis *(ringworm) - circular lesions w/ well defined, raised, scaly edge
- Tinea pedis - athlete’s foot - moist scaling/fissuring in toewebs (can spread to sole or dorsal foot)
- *Tinea cruris *(groin/natal cleft)
- Tinea manuum (scaling/dryness in palmar creases)
- *Tinea Unguium *(yellow discolouration, thick/crumbly nail)
- Tinea incognito (due to inadequate tx of tinea - ill-defined/less scaly lesions)

Investigation
- Skin scrapings, hair or nail clippings

Management
- Risk factor management: immunosupression, moist environment
- Tinea corporis: Mild/limited can use topical antifungal cream (e.g. terbinafine or imidazole). If severe/extensive PO antifungal (terbinafine 1st line)
- Tinea capitits: needs PO antifungal + ketoconazole shampoo. PO terbinafine (for trichophyton tonsurans) + griseofulvin (for microsporum infection OR in children)
- Athlete’s foot - topical terbinafine (may then need PO)
- (topical steroids generally avoided due to risk fo tinea incognito, although can be used if marked inflam)

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12
Q

Pityriasis Versicolor and Pityriasis Rosea
- Presentation
- Pathophysiology
- Management

A

Pityriasis Rosea
- Pathophysiology
Unknown pathophys -?viral, bacterial ?non-infective

  • Presentation
    -Self-limiting rash, resolves in 6-10/52, often itchy
    -herald patch (large circular patch on chest, abdo or back) followed by smaller scaly red oval patches - ‘christmas tree’ pattern on chest/back
    -Can be preceded by mild flu-like illness (but not always)
    -mostly in teens/young adults
  • Management
    Emollient + soap substitutes
    if itch: topical steroids, PO antihistamines
    should self-resolve

Pityriasis Versicolor
* Pathophysiology
-Superficial fungal infection w/ melassezia

  • Presentation
  • hypopigmented, pink or brown patches on trunk + scale + mild pruritis
  • Management
  • Topical antifungal (ketokonazole shampoo)
  • If failure to respond send scrapings to confirm diagnosis + give PO itraconazole
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13
Q

Basal Cell Carcinoma
- Presentation
- Risk factors
- Management

A

Presentation
- spow growing, locally invasive malignant tumour (rare to met)
- Various morphological types: Nodular (most common), superficial (plaque-like), cystic, morphoeic (sclerosing), keratotic, pigmented
- Nodular - small skin-coloured papule/nodule w/ surface telangiectasia + pearly rolled edge +/- necrotic/ulcerated centre

Risk Factors/Causes
- UV exposure, hx of frequent/severe sunburn, skin type I, ge, male, immunosupression, prev hx/genetic predisposition

Management
- surgical excision, Mohs micrographic surgery (if high risk/recurrent)
- Radiotherapy (if surgery not appropriate)
- Other: cryotherapy, curretage/cautery, topical photodynamic therapy, topical Tx e.g. imiquimod
- Would need ref if high risk e.g. eyelid, node, ears, eyes

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14
Q

Squamous cell carcinoma
- Presentation
- Risk factors/cause
- Management

A

Presentation
- Locally invasive malignant tumour. potential to met.
- Keratotic, ill-define nodule +/- ulceration

Cause/risk factors
- UV, pre malignant skin conditions (e.g. actinic keratoses/solar keratosis), chronic inflammation (e.g. leg ulcer, wound scar), immunosupression, genetics

Management
- Surgical excision
- MOHS micrographic surgery
- Radiotherapy (for large un-resectable tumours)

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15
Q

Malignant Melanoma

Presentation
Causes/risk factors
Types
Management
Prognosis

A

**Presentation **
- invasive malignant tumour of epidermal melanocytes
- 7 point weighted checklist:
- major - 2 points each
- change in size
- change in shape
- change in colour
- minor - 1 point
- diameter >7mm
- inflammation
- oozing
- change in sensation (including itch)
- 3 or more = 2ww referral
typically on legs in women + trunk in men

**Types **
- nodular - trunk, middle-aged, intermittent high-intensity UV
- Lentigo maligna melanoma - face, elderly, long term UV
- Acral lentiginous- palms/soles/nail beds - elderly -no clear relation to UV

Causes/Risk factors
- UV, skin type I, >100 moles or atypical naevus syndrome, fam hx

Investigations
- do NOT biopsy in primary care -> 2ww if susptected
- In secondary care it is staged - TNM plus AJCC scoring systeem. T is based on breslow thickness:
- Tis - in situ
- T1 - <1mm
- T2 - 1-2mm
- T3 - 2-4mm
- (T1,2,3 can be split into a (no ulceration) + b (ulceration))
- AJCC then splits into stage I - IV

**Management **
- Surgical excision - excision biopsy then wide local excision
- Radiotherapy
- Chemotherapy (if mets)
- Prognosis depends on stage + breslow thickness

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16
Q

Eczema
- Presentation
- Cause
- Management
- Complications

A

Presentation
- Acute: itchy papules + vesicles. Often weepy.
- Chronic: dry scaly itchy patches, erythematous or grey/brown +/- lichenification
- Face + extensors in babies. Flexures in adults.
- Nails can have ridging/pitching

Causes - atopy, fam Hx, exacerbators: infection, allergens, sweating, heat, stress

Management
- avoid exacerbants
- Emollients + soap substitutes
- Topical steroids for active areas
-(Mild: hydrocortisone. Moderate (betnovate (betamethoasone valerate) or eumovate (clobetasone butyrate) or dermovate (clobetasol propionate)
- Topical immunomodulators eg. tacrolimus for maintenance/steroid-sparing
- Phototherapy + immunosupressant (azathioprine, ciclosporin, methotrexate) for severe cases

Complications
- Secondary bacterial infection (fluclox)
- Secondary viral infection e.g.** eczema herpeticum **(herpes simplex) - extensive crusted papules, blisters, erosions + systemically unwell, can -> hepatitis, encephalitis, DIC, death
- Management: PO aciclovir (or IV is v unwell) + treat any secondary bacterial infections. Needs opthalmology input if any eye/eyelid involvement

17
Q

Acne Vulgaris
- Presentation
- Cause
- Management
- Complications

A

Presentation
- non-inflammatory lesiosn (mild) - open/closed comedones (black/whiteheads)
- Inflammatory lesions (mod/severe) - papules, pustules, nodules, cysts
- In pigmented skin - hyperpigmented lesions

Cause/Pathophysiology
- Hormonal (androgens)
- Sebum, abnormal follicular keratinisation, bacterial colonisation (propionibacterium acnes)

Management - step-wise
- Single topical: retinoids, benozyl peroxide
- combination of topicals: antibiotic, retinoids, benzoyl
- PO abx (w/ topical retinoid) - tetrocyclines (but avoid pregnancy + children <12 - can use erythromycin in preg)
- prolonged abx can –> gram -ve folliculitis (tream w/ trimethoprim)
- In women COPC is alternative to PO abx
- Finally: PO isotretinoin (not in pregnancy + only under specialist supervision)

Complications
- post-inflammatory pigmentation, scarring, deformity, psychological + social effects
- Retinoids side effects: teratogenicity (women should use 2 forms of contraception), dry skin,eyes, lips + mouth; low mood (controversial), raised triglycerides, hair thinning, nose bleeds (dry nasal mucosa), intracranial HTN (cant combine w/ tetracyclines due to this), photosensitivity
-

18
Q

Psoriasis
- Presentation
- Types
- Pathophysiology
- Management
- Complications

A

Presentation
- chronic inflammatory condition due to hyperprolferation of keratinocytes + inflammatory cell infiltration
- well-demarcated erythematous scaly plaques (in dark skin can look dark brown/grey/purple) +/- itch/burn/pain
- Auspitz sign - scratch -> bleeding

Types
- chronic plaque - extensor surfaces
- guttate - raindrop - often follow strep infection 2-4/52 prior - mostly resolves spontaneously but can give topical stuff as per normal psoriasis
- seborrhoiec - naso-labial + retro-auricular
- flexural
- pustular (palmar-plantar)
- Erythrodermic (whole body redness)

Pathophysiology/causes
- genetic, immunological + environmental
- Precipitates: trauma (koebner), infection, drugs (B-blockers, lithium, antimalarials, NSAIDs, ACE, infliximab, withdrawal of systemic steroids), stress, alcohol

Management
- Avoid precipitants + use emollients
- Initial:
-OD Vit D AND potent corticosteroid topical for 4/52
-if insufficent extend vit D to 8/52 + make BD (stop steroid after 4/52)
-then either steroid BD for 4/52 or coal tar OD or BD
Can also try dithranol (inhibits DNA synthesis, wash off after 30mins, adverse effects: burning, staining)

(v potent steroids shouldn’t be used for more than 4/52 + potent no more than 8/52)

  • Other options = secondary care:
    Phototherapy (for extensive disease) - UVB + photochemotherapy (psoralen + UVA) - -PUVA can -> SCC
    PO (extensive + severe or w/ systemic involvement) - methotrexate, retinoids, ciclosporin, mycopheonlate mofetil

Scalp psoraisi - 4/52 potent topical steroids
Face,flexural, genital - mild/mod steroids OD or BD (max 2/52)
Flexural + face psoriasis: steroids

Complications
- Erythroderma
- Psoriatic arthropathy- symettrical polyarthritis, asymmetrical oligomonoarthritis, lone distal interphalangeal disease, spondylosis, arthritis mutilans (flexion deformity of distal interphalangeal joints)
- Nail changes (in 50%) - pitting, onycholysis

19
Q

Complications of psoriasis management:
- Topical Steroids
- Vit D analogues
- PUVA (photo chemotherapy)

A

Topical steroids
- skin atrophy, striae, rebound symptoms
- Systemic side effects if using on >10% of body SA
- Duration
Scalp/face/flexures - 1-2 weeks/month
potent steroids - no more than 8/52 at a time
v potent steroids - no more than 4/52 at a time
4/52 break between steroid courses

**Vitamin D analogues ** e.g. calcipotriol, calcitriol, tacalcitol
- adverse effects uncommon + can be used long-term
- Reduce scale/thickness of plaques but not erythema
- Avoid in pregnancy
- max weekly dose 100g in adults

PUVA
- SCC

20
Q

Bullous Pemphigoid
Presentation
Pathophysiology
Management

A

Presentation
- Non-specific itchy rash
- Then tense fluid-filed blisters on erythematous base. Often itchy. Heal without scarring.
- Usually in elderly on trunk/limbs
- mouth sparing/no mucosal involvement

Pathophysiology
- Autoantibodies against antigens between epidermis + dermis (sub-epidermal split)
- Skin biopsy shows IgG + C3 at dermoepidermal junction
- Needs biopsy for diagnosis

Management
- General: wound dressings, monitor for infection
- Topical steroids (main Tx)
- PO: steroids, PO tetracycline + nicotinamide, immunosupressive (azathioprine, mycophenolte mofetil, methotrexate)

21
Q

Pemphigus Vulgaris
- Presentation
- Pathophysiology
- Management

A

Presentation
- Flaccid, easily ruptured blisters –> erosions + crusts
- Often painful + in mucosal areas + skin
- Nikolsky’s sign - spread of bullae w/ horizontal application of pressure
- normally in middle-aged

Pathophysiology
- Autoantibodies against antigens within the epidermis - intra-epidermal split

Management
- General- wound dressings, monitor for infection, PO care if mucosal involvement
- PO: steroids, immunosupressants (methotrexate, azathioprine, cyclophosphamides, mycophenolate mofetil)

22
Q

Vitiligo
- Presentation
- Pathophysiology (including associated conditions)
- Management

A

Presentation
- Patch(es) of depigmentation, often symmetrical
- Can show koebner phenomonem

Pathophysiology
- Destruction of melanocytes
- Autoimmune + associated w/ other autoimmune conditions: Addison’s, T1DM, thyroid disease, alopecia areats, pernicious anaemia

Management
- Suncream
- Topical: steroids (can reverse changes if used early), calcineurin inhibitors (tacrolimus)
- Phototherapy: UVB (but careful in light skin)
- PO immunosupressants: methotrexate, ciclosporin, mycophenolate mofetil
- Camouflage makeup

23
Q

Melasma
- Presentation
- Pathophysiology
- Management

A

Pathophysiology
- Overproduction of melanin.
- Genetic predisposition + triggered by: sun exposure, hormonal changes

Presentation
- Brown macules (freckle-like spots or larger patches w/ irregular border)
- Symmetrical
- Common sites: forehead, upper lips, cheeks, neck, shoulders, upper arms

Management
- lifelong sun protection, stop hormonal contraceptives, cosmetic camoflauge
- Topical treatments to reduce melanin production: hydroquinone, azelaic acid, kojic acid, vit C
- Laser treatment (but caution as can cause post-inflammatory hyperpigmentation)

24
Q

What is shown by the following images?

A

Straberry Naevus (capillary haemangioma)
- Erythematous, raised, multilobed tumours
- Develop rapidly in 1st month of life. Increase in size till 6-9months. Then regress over years.
- Common sites: face, scalp, back (rare: upper resp tract -> obstruction)
- Management: generally nil unless problem e.g. visual field obstruction –> B-blocker (PO or topical)

Pyogenic Granuloma
- Cause: trauma, pregnancy
- intially small red/brown spot –> rapidly progress to raised red/brown/dark lesion - can bleed profusely or ulcerate
- common site: head, upper trunk, hands. Oral mucosa in pregnancy.
- Management - lesions in pregnancy resolve spontaneously post-partum. Others normally persist –> curretage, cauterisation, cryotherapy

Seborrhoeic Keratoses
- benign epidermal skin lesion
- Stuck on appearance w/ keratotic plugs
- Manage: reassurance +/- removal - curretage, cryosurgery, shave biopsy

Keratocanthoma
- Benign epithelial tumour. More in elderly.
- ‘volcano/crater’ - initially smooth + dome shaped, rapid progression to crater centrally filled w/ keratin
- Normally spontaneously regresses in 3/12 w/ scarring BUT - Management: Urgent excision (as difficult to exclude SCC)

Port-wine Stain
- Vascular birthmarks. Do NOT spontaneously resolve + can darken/become raised w/ time
- Can be associated w/ intracranial vasc abnormalities eg. Sturge Weber Syndrome
- Management: cosmetic camouflage, laser therapy

Sebaceous Cyst
- Can be: epidermoid or pilar cysts.
- location: scalp, back, ears, face, upper arm
- Features: central punctum can be present, keratinous soft, cheese-like content
- Asymptomatic doesn’t need treating but can do complete excision (recurrence common)

Erythema Ab Igne
- Reticulated, erythematous patches w/ hyperpigemented telangiectasia
- Causes: heat exposure, hypothyroidism, lymphoedema

Dermatofibroma (histiocytoma)
- benign fibrous skin lesion. Often following injury.
- Features: solitary firm papule/nodule. The overlying skin dimples on pinching the lesion.

25
Q

Seborrhoiec Dermatitis
- Pathophysiology
- Presentation
- Management

A

Pathophysiology
- chronic dermatitis due to inflammatory reaction to Malassezia (fungus - normal skin inhbaitant)
- Associated conditions: HIV, Parkinsons

Presentation
- Eczematous lesions on sebum-rich areas - periorbital, scalp, auricular, nasolabial folds
- can -> otitis externa + blepharitis

Management
Scalp
- 1st line (OTC): zinc pyrithione (Head + shoulders) + Tar (neutrogena T/Gel)
- 2nd line: ketoconazole

Face/Body
- Ketoconazole
- Topical steroids (short term only)

26
Q

Rosacea
- Pathophysiology
- Presentation
- Management

A

Pathophysiology
- unknown aetiology
Presentation
- Flushing, then persistent erythema w/ pustules/papules + telangiectasia
- can -> rhinophyma + blepharitis
- exacerbants: sunlight, alcohol

Managemet
- Mild disease: Topical metronidazole
- Severe disease: PO oxytetracycline
- Other: suncream, camouflage cream, laser therapy (telangienctasia), topical brimonidine gell (predominant flushing), rhinophyma needs derm ref.