Dermatology Flashcards

(32 cards)

1
Q

How does acne present?

A
  • Mild – mostly non-inflamed lesions (open + closed comedones) with a few inflammatory lesions.
  • Moderate – more widespread, with increased number of inflammatory papules and pustules.
  • Severe – widespread inflammatory papules, pustules, nodules, and cysts. Scarring may be present.
  • Conglobate acne ­– rare, severe, most often affects M. extensive inflammatory papules, suppurative nodules (may coalesce to form sinuses), and cysts on trunk and upper limbs.
  • Acne fulminans – sudden, severe inflammatory reaction – deep ulcerations and erosions, may be systemic effects (hospital admission and oral steroids)
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2
Q

How do you manage acne?

A
  1. Tretoin topical (topical retinoid) + topical ABx (erythromycin)
    • Topical benzoyl peroxide
    • Topical azelaic acid
  • Conservative – avoid overcleaning the skin, not caused by poor hygiene. Don’t pick/ squeeze, maintain healthy diet.
  • Mild – topical therapies: Benzoyl peroxide (may bleach clothes), salicylic acid, topical antibiotics (clindamycin), topical retinoids (adapalene)
  • Moderate – severe: oral abx (doxycycline, lymecycline) change after 3 months if no response.
  • COCP (dianette) can be used in conjunction (anti-androgen)
  • Oral retinoids e.g. Isotretinoin may be prescribed when referred to dermatological specialist (SEs, and monitoring)
  • Monitoring: lipid panel, LFTs, women – montly pregnancy tests.
  • SEs: highly teratogenic, dry lips, cheilitis, dry skin, fragile skin, photosensitivity, temporary hair loss, brittle nails, myalgia, depression, abnormal LFTs.
  • Advice: shave instead of wax, emollients, drink minimal alcohol, pregnancy prevention programme for women of childbearing age (2x reliable forms of contraception), daily spf.
  • Scarring – laser resurfacing, dermabrasion, chemical peels.
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3
Q

What is eczema?

A
  • Eczema is an inflammatory skin condition where patches of skin become inflamed, itchy, red, and cracked. Most common form is ‘atopic eczema’.
  • Atopic eczema is a chronic, itchy, inflammatory skin condition presenting most frequently in childhood.
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4
Q

What are some RFs of eczema?

A

filaggrin gene mutation (impairs barrier function of the skin), age <5y, FH, allergic rhinitis, asthma, active/ passive smoking.

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5
Q

How does eczema present?

A
  • Itchy erythematous, dry scaly patches.
  • More common on face and extensor aspects in infants, but on flexors in children and adults.
  • Acute lesions are erythematous, vesicular, and exudative.
  • Chronic scratching can lead to excoriations and lichenification (thickened and leathery)
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6
Q

How is eczema managed?

A
  1. Emollients, bandages, soap substitutes
  2. Acute flare – topical corticosteroids such as hydrocortisone
    1. Hydrocortisone → eumovate →Betnovate → dermovate
    2. Tacrolimus – good steroid sparing agent
    3. Intermittent tropical corticosteroids: hydrocortisone/ desonide
  3. If severe itch or urticaria – non-sedating antihistamine (cetirizine, fexofenadine)
  4. Antibiotics for secondary bacterial infection – flucloxacillin
  5. Immunosuppressants (prednisolone, azathioprine, ciclosporin) for severe, non-responsive cases.
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7
Q

What is the classification of urticaria?

A
  • Acute <6wks
  • Chronic >6wks
  • Spontaneous (chronic) no identifiable cause
  • Autoimmune IgG autoantibodies to IgE receptors
  • Inducible (chronic) response to physical stimulus (temperature, pressure, UV)
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8
Q

How is urticaria managed?

A

  • Conservative: Avoidance of triggers, topical anti puritic agents e.g. calamine to relieve the itch. Chronic - QoL questionnaire
  • 1st: Non-sedating anti-histamine e.g. cetirizine for <6wks:Increase to <4x standard
  • 2nd: Severe – short course of oral corticosteroids (prednisolone 40mg OD for 7d)
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9
Q

What is contact dermatitis and how does it present?

A
  • Irritantnon-immunological inflammatory reaction caused by direct physical/ toxic effects of a irritating substance on the skin (acute/chronic)
    • Common irritants: water, sweating, detergents, solvents, powders, dust, soil
  • Allergictype IV (delayed) hypersensitivity reaction after sensitiation and re-exposure to an allergen.
    • Common allergens: personal care products, metals (nickel, Cu), topical medications (corticosteroids), plants
  • Presentation: itching, burning, swelling, erythema, scaling, rash. Often seen on the hands (response to jewellery)
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10
Q

How do you manage contact dermatitis?

A
  • Conservative: stimulus avoidance (may take 8-12 weeks to see improvement), use gloves etc if cant avoid stimulus.
  • Topical corticosteroids (as can be hard to distinguish allergic, from irritant)
  • Dermatology referral if severe, chronic, recurrent or persistent.
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11
Q

What is psoriasis?

A
  • Chronic inflammatory skin condition characterised by erythematous, inflamed, silvery white scaly plaques and circumsribed papules and plaques.
  • These often affect the elbows, knees, extensor limbs and scalp
  • It can cause itching, irritating, burning and stinging
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12
Q

What are the diff types of psoriasis?

A
  • Chronic plaque psoriasis – most common, well demarcated erythematous, scaly plaques, scalp and extensor regions.
  • Generalized pustular psoriasis – palms and soles, tender, red skin with small white elevations of pus
  • Guttate psoriasis – triggered by strep infection in childhood, small, red, discrete ‘teardrop’ spots over the trunk and limbs.
  • Flexural psoriasis – occurs within skin folds, smooth and shiny red lesions.
  • Erythrodermic psoriasis – total body redness, fire red scales, extremely itchy and painful, scales fall off in sheets
  • Psoriatic arthritis
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13
Q
A

HIV/ AIDS, alcohol, strep infection, UV light exposure, pscyhological stress, trauma, drugs (lithium, anti-malarials, beta blockers, NSAIDs, ACEi)

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14
Q

How is psoriasis managed?

A
  • Immediate same day dermatology referral and assessment for generalized pustular psoriasis, or erythrodermic psoriasis
  • Creams, lotions, gels, emollients for widespread psoriasis. Ointments for thick scale
  • 1st: Mild topical corticosteroid (hydrocortisone) + Vitamin D (Dovobet gel and ointment)
  • 2nd: Phototherapy: Narrow band UVB + methotrexate + ciclosporin, retinoids (acitretin)
    1. Biologics: infilixumab, apremilast + acicretin (oral retinoid)
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15
Q

What is cellulitis?

A

Acute spreading infectin of the skin with visually indistinct borders that principally involve the dermis and subcut tissue

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16
Q

How is cellulitis ixd, mxd?

A

Ix: usually clinical, WCC, ESR, skin swab + culture, skin biopsy, USS (for abscess)

Mx:

  • Conservative: (pain relief, fluids), sterile dressings, elevate leg, compression stockings
  • High dose flucloxacillin (+/- BenPen if rapid deterioration)
  • Admit if à limb/life threatening (Class ¾), rapid deterioration, frail, facial cellulitis, orbital/periorbital cellulitis
    • IV abx – vancomycin
17
Q

What are maligant melanomas?

A
  • Overview: invasive malignant tumour of the epidermal melanocytes with the potential to metastasize.
    • Most common cause of skin cancer related deaths.
  • Risk factors: age, prev BCC/ SCC, XS UV exposure, skin type I, many or atypical moles, FH
  • Pathophysiology
    • Normal melanocytes found in the stratum basal
    • Non-cancerous growth of melanocytes results in moles (benign melanocytic naevi) and freckles.
    • Cancerous growth results in melanoma
      • In situ if confined to epidermis
      • Invasive if spread into dermis
      • Metastatic if spread to other tissues)
18
Q

What are the diff types of malignant melanoma?

19
Q

How are malignant melanomas classified?

A
  • ABCDEF (evolving)
  • Glasgow 7-point checklist
    • Major – change in size, irregular shape, irregular colour
    • Minor – diameter >7mm, inflammation, oozing, change in sensation
  • Breslow thickness (see pic)
20
Q

What Ix are used for malignant melanoma?

A
  • Diagnostic excision, calculate Breslow score / Clark’s level
    • Breslow score measured in vertical mm from the base of the granular layer to the deepest point of tumour involvement
  • TNM staging – sentinel lymph node biopsy, PET-CT
21
Q

How are malignant melanomas treated?

A

Surgical excision (wider excision margin up to 3cm) to ensure complete removal (SLNB)

+/- chemo for metastatic disease

Immunotherapy (iplimumab/ pembrolizumab) if widespread mets

22
Q

What are superficial spreading melanomas? How are they managed?

A
  • Grow slowly and metastasize later on
  • They have a better prognosis than nodular melanomas which invade deeply and metastasize early
  • Management: Chemo - ipililumab
23
Q

What is the ABCDE criterias for the diagnosis of melanoma?

A
  • Assymetry
  • Border - irregular
  • Colour - non uniform
  • Diametes - 7mm
  • Elevation
24
Q

What is a squamous cell caner of the skin?

A
  • Overview: locally invasive malignant tumour of the epidermal keratinocytes, which has the potential to metastasize.
  • Generally arises within an actinic keratosis, or Bowens disease.
  • Ulcerated, crusted, firm irregular lesions on sun exposed sites
  • Presentation: keratotic (scaly, crusty), ill-defined nodule which may ulcerate (common on lip due to smoking)
25
What are some RFs for SCC?
* excessive exposure to sunlight / psoralen UVA therapy * actinic keratoses and Bowen's disease * **immunosuppression** e.g. following renal transplant, HIV * **smoking** * long-standing **leg ulcers (**Marjolin's ulcer) * genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism * HPV
26
How are squamous cell cancers of the skin managed?
* Surgical excision: 4-6mm margin * 4mm if lesion \<20mm * 6mm if lesion \> 20mm * **Mohs micrographic surgery** (high risk, ill-defined, large recurrent tumours) * **Radiotherapy** for large, non-resectable tumours and metastases.
27
What is a basal cell carcinoma?
* Aka rodent ulcer * Slow-growing, locally invasive malignant tumour of epidermal keratinocytes. Rarely metastasizes. Typically affects older people. * Most common skin cancer * Presentation: * **Most** common over head and neck. * **Nodular** (most common)= pearly rolled edge, small, skin coloured papule or nodule, surface telangiectasia (widened venules, thread-like lines on skin), may have necrotic/ulcerated centre. on sun exposed sites. * **Also** – superficial (most common type in younger adults), cystic, sclerosing, keratotic, pigmented.
28
How is BCC managed?
* Surgical excision: **excision** (histological examination – excisional, incisional, punch and shave biopsy) - **4-6mm margin** * **Mohs micrographic surgery** (removal of cancer thin layer at a time), * Other: Cryotherapy, curettage, radiotherapy, phototherapy * TopicalL: For superficial/ low risk BCC: **5FU + imiquimod**
29
What is actinic keratosis?
* Overview: most common precursor lesion for **SCC**. Pre-malignant change of the skin caused by chronic sun exposure. * Risk factors: increasing age, immunosuppression, photosensitivity, XS UV exposure. * Pathophysiology: **XS UV** exposure resulting * **Presentation**: Flat, crusty, thickened papules or plaques. Can be red, pink, brown, or same colour as skin, typically seen on sun exposed areas. Crumbly yellow white scaly crusts on sun exposed skin
30
How is actinic keratosis mxd?
* Conservative: Prevention of further risk – sun avoidance, sun cream * Medical * **5-FU cream** – 2-3w course, skin may become red and inflamed initially so t**opical hydrocortisone** might be used to settle the inflammation * **Topical diclofenac** for mild cases * Removal by **cryotherapy (liquid nitrogen spray)**
31
What is Bowens disease?
* **Overview**: intraepidermal squamous cell carcinoma, also known as an SCC in situ. Atypical keratinocytes found throughout the epidermis without invasion through the basement membrane. * **Risk factors:** More common in elderly females, often found on sun-exposed skin. * **Presentation**: red, scaly patches/ plaques, often on sun exposed areas
32
How is Bowens disease mxd?
* Medical: **Topical 5-FU (OR imiquimod),** cryotherapy, photodynamic therapy * Surgical: excision, curettage + cautery