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Dermatology Flashcards

1
Q

Define…

i) Whiteheads.
ii) Blackheads.
iii) Papules.
iv) Macules.
v) Vesicular.
vi) Bulla.
vii) Pustules.

A

i) Closed comedones.
ii) Open comedones.
iii) Elevated, red, small pimple.
iv) Area of skin decolouration.
v) Small cavity, primarily filled with clear fluid.
vi) Large blister, clear fluid.
vii) Small blister with purulent fluid (pus).

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2
Q

What are the common causes of an itch…

i) with a rash?
ii) without a rash?

A

i) Atopic dermatitis, psoriasis, scabies.

ii) Renal failure, jaundice, lymphomas.

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3
Q

ACNE VULGARIS

What is the pathophysiology of acne vulgaris?

A
  • Hair follicle narrows > hypercornification (corneodesmosomes blocking entrance to hair follicles) results in increased sebum production (greasy skin).
  • Some sebum trapped in narrow hair follicle, stagnates at pit of follicle as no oxygen.
  • Anaerobic conditions for Propionibacterium acnes to multiply + breakdown triglycerides in sebum into free fatty acids > irritation, inflammation + neutrophil attraction.
  • Leads to pus formation + further inflammation.
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4
Q

ACNE VULGARIS

What is the aetiology of acne vulgaris?

A
  • Infection by P. acnes.
  • Worsened by stress.
  • Typically starts in adolescence + resolves in mid-20s, increased androgens during puberty.
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5
Q

ACNE VULGARIS

What is the clinical presentation of acne vulgaris?

A
  • Whiteheads + blackheads.
  • Papules.
  • Pustules.
  • Nodules.
  • Commonly found on face, chest + upper back.
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6
Q

ACNE VULGARIS

What are the complications of acne vulgaris?

A
  • Scars.
  • Erythematous macules.
  • Psychological factors.
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7
Q

ACNE VULGARIS

What are the investigations for acne vulgaris?

A
  • Usually clinical.

- Skin swabs for microscopy + culture.

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8
Q

ACNE VULGARIS

What is the treatment for mild acne vulgaris?

A
  • Avoid over-washing, don’t pick at it, healthy diet.

- Topical keratolytics (benzoyl peroxide), retinoids (tazarotene gel) + Abx (erythomycin gel).

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9
Q

ACNE VULGARIS

What is the treatment for moderate acne vulgaris?

A
  • Low dose oral Abx like doxycycline.

- Hormone treatment in women with no C/I to oral contraceptive.

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10
Q

ACNE VULGARIS

What is the treatment for severe acne vulgaris? What must be avoided in pregnancy?

A
  • Oral retinoid like isotretinoin.

- Retinoids are C/I in pregnancy as severe teratogen.

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11
Q

ATOPIC DERMATITIS

What is the pathophysiology of atopic dermatitis?

A
  • Damaged filaggrin (skin barrier protein), allows antigenic material + irritants to penetrate + come into contact with immune cells initiating a response.
  • Breakdown of skin due to thinning of stratum corneum caused by reduced corneodesmosomes meaning increased risk of inflammation.
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12
Q

ATOPIC DERMATITIS

What is the aetiology of atopic dermatitis?

A
  • Significant hereditary predisposition, common in early childhood.
  • Exacerbating factors are infection, strong detergents, cats/dogs + stress.
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13
Q

ATOPIC DERMATITIS

What is the clinical presentation of atopic dermatitis?

A
  • Itchy, erythematous + scaly patches.
  • More common in flexures such as front of elbows, ankles, behind knees.
  • Vesicles + bullae.
  • Oozing.
  • Dry skin.
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14
Q

ATOPIC DERMATITIS

What is the main complication of atopic dermatitis?

A
  • Scratching can lead to broken skin + opportunistic S. aureus or herpes simplex infection, can cause weeping.
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15
Q

ATOPIC DERMATITIS

What are the investigations for atopic dermatitis?

A 
Clinical...
- Itchy skin condition in past 6 months.
- Hx of dry skin, asthma/hayfever.
- Skin creases involved, childhood onset.
High serum IgE
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16
Q

ATOPIC DERMATITIS

What is the generic treatment for atopic dermatitis?

A
  • Avoid irritants.
  • Emollient therapy like E45 cream to trap moisture in skin + increase hydration, acts as an artificial permeability barrier preventing water loss.
  • Bath soap substitutes.
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17
Q

ATOPIC DERMATITIS

What is the first line treatment for atopic dermatitis?

A
  • Low potency topical corticosteroids (hydrocortisone) on face + more potent steroids (betamethasone) on body/soles.
  • Topical immunomodulators like tacrolimus to help sensitive areas.
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18
Q

ATOPIC DERMATITIS

What is the second line + adjuvant treatment for atopic dermatitis?

A
  • UV phototherapy, short courses of oral prednisolone, Abx.

- Bandages, oral anti-histamines.

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19
Q

CONTACT DERMATITIS

What is the pathophysiology of contact dermatitis?

A
  • Chemical irritants cause very noticeably demarcated lesion.
  • Type IV hypersensitivity reaction, delayed type sensitivity, cell-mediated response.
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20
Q

CONTACT DERMATITIS

What is the aetiology of contact dermatitis?

A
  • Exogenous exposure to irritants like chemicals + sweat.
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21
Q

CONTACT DERMATITIS

What is the clinical presentation of contact dermatitis?

A

Sharply demarcated skin inflammation…
- Red, crusting + scaling.
- Hyperpigmentation if chronic.
Itching.

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22
Q

CONTACT DERMATITIS

What are the investigations + treatment for contact dermatitis?

A
  • Patch testing, suspected allergen placed in skin contact.

- Avoid irritants, steroid creams for short periods, antipruritic agents for symptomatic relief.

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23
Q

PSORIASIS

What is the pathophysiology of psoriasis?

A
  • Increased numbers of corneodesmosomes leading to thickening of stratum corneum.
  • T-cell activation results in upregulation of Th1-type T cell cytokines (TGF/TNF-alpha) leading to hyerproliferation of keratinoctes in the epidermis.
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24
Q

PSORIASIS

What is the aetiology of psoriasis?

A 
Polygenic.
Dependent on environmental triggers...
- Group A strep.
- Drugs like lithium.
- UV light, alcohol, stress.
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25
Q

PSORIASIS

What are the associated nail changes in psoriasis?

A
  • Pitting.

- Onycholysis (separation of finger from nail bed).

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26
Q

PSORIASIS

What is the clinical presentation of chronic plaque psoriasis?

A
  • Well-demarcated, salmon-pink silvery scaling lesions on extensor surfaces (knee, elbows).
  • Scalp involvement, most often at hair margin.
  • New plaques at sites of skin trauma (Kobner phenomenon).
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27
Q

PSORIASIS

What is the clinical presentation of flexural psoriasis?

A
  • Red glazed, non-scaly plaques confined to flexures (groin, sub-mammary areas).
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28
Q

PSORIASIS

What is the clinical presentation of guttae (‘raindrop-like’) psoriasis?

A
  • Most commonly children/young adults.

- Explosive eruption of very small circular/oval plaques over trunk about 2 weeks post-strep sore throat.

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29
Q

PSORIASIS

What is the clinical presentation of erythrodermic + pustular psoriasis?

A
  • Most severe + potentially life threatening.

- Widespread intense inflammation of skin which may be associated with malaise, pyrexia + circulatory dsiturbances.

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30
Q

PSORIASIS

What is the first line treatment of psoriasis?

A
  • Reassurance with emollients, avoid triggers.

- Topical therapy with vitamin D analogues (calcipotriol), corticosteroids.

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31
Q

PSORIASIS

What is the second line treatment of psoriasis?

A
  • Phototherapy with UVA radiation.
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32
Q

PSORIASIS

What is the third line treatment of psoriasis?

A
  • Immunosuppression with methotrexate or biological agents like TNF-alpha blockers + monoclonal antibody.
  • Used in resistant disease or severe erythrodermic/pustular psoriasis.
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33
Q

BASAL CELL CARCINOMA

What is the pathophysiology of BCC?

A
  • Slow growing, locally invasive malignant tumour of epidermal keratinocytes.
  • Rarely metastatic, 80% of non-melanoma skin cancers.
34
Q

BASAL CELL CARCINOMA

What is the aetiology of BCC?

A
  • Most common malignant skin tumour.

- Risk factors = increasing age, skin type 1 (burns, doesn’t tan) + sun damage.

35
Q

BASAL CELL CARCINOMA

What is the clinical presentation of BCC?

A
  • Border of ulceration lesion is raised w/ pearly appearance.
  • May have ulcerated centre.
  • Mostly unpigmented.
  • Surface telangiectasia (spider veins).
36
Q

BASAL CELL CARCINOMA

What are the investigations of BCC?

A
  • Clinical + biopsy.
37
Q

BASAL CELL CARCINOMA

What are the treatments of BCC?

A
  • Surgical excision w/ wide borders (5mm), histology to ensure adequate tumour margins.
  • Cryotherapy (extreme cold) + photodynamic (light-sensitive medication) if superficial.
  • Radiotherapy if cannot tolerate surgery.
38
Q

SQUAMOUS CELL CARCINOMA

What is the pathophysiology of SCC?

A
  • Locally invasive, malignant tumour of squamal keratinocytes (in outermost part of epidermis) with potential to metastasise via lymph.
39
Q

SQUAMOUS CELL CARCINOMA
What is…
i) Bowen’s disease?
ii) Keratoacanthoma?

A

i) In situ SCC that is confined to the epidermis.

ii) Benign variant of SCC, unlikely to metastasise.

40
Q

SQUAMOUS CELL CARCINOMA

What are the risk factors for SCC?

A
  • UV exposure.
  • Chronic inflammation.
  • Immunosuppression.
41
Q

SQUAMOUS CELL CARCINOMA

What is the clinical presentation of SCC?

A
  • Lesions grow rapidly + common on sun-exposed sites

- Poorly defined nodule with keratotic (scaly/crust) + ulcerated aeras.

42
Q

SQUAMOUS CELL CARCINOMA

What are the investigations for SCC?

A
  • Clinical + biopsy.
43
Q

SQUAMOUS CELL CARCINOMA

What is the treatment for SCC?

A
  • Keratoacanthoma = biopsy + cryotherapy.
  • Bowen’s = biopsy + surgical excision.
  • Surgical excision with minimal 5mm margin, radiotherapy if non-resectable.
44
Q

MALIGNANT MELANOMA

What is the pathophysiology of malignant melanoma?

A
  • Most malignant form of skin cancer.

- Malignant tumour of melanocytes in basal layer of epidermis where metastases can occur at many places?

45
Q

MALIGNANT MELANOMA

What are the 4 types of malignant melanoma?

A

Nodule MM = rapidly growing pigmented nodule that bleeds/ulcerates.
Superficial spreading MM = large flat irregularly pigmented lesion, grows laterally before vertical invasion
Lentigo MM = nodule on face
Acral lentiginous MM = pigmented lesions on palm/soles.

46
Q

MALIGNANT MELANOMA

What are the risk factors for malignant melanoma?

A
  • UV exposure (tanning/sun beds), red hair, high density freckles, skin type 1, family Hx, pale skin.
47
Q

MALIGNANT MELANOMA

What is the clinical presentation of malignant melanoma?

A
  • Common in back/chest in men, lower legs in women.
  • Major signs = enlargement, colour change (often darker).
  • Minor signs = itching, bleeding, crusting.
48
Q

MALIGNANT MELANOMA

What is the ABCDE criteria for malignant melanoma?

A 
A = asymmetrical shape.
B = border irregularity.
C = colour irregularity (non-uniform).
D = diameter >6mm.
E = elevation/evolution (change of lesion).
49
Q

MALIGNANT MELANOMA

What is the prognosis + investigations for malignant melanomas?

A
  • Breslow lesion (<1mm) = best prognosis.
  • Younger + female = better prognosis.
  • Clinical + biopsy.
50
Q

MALIGNANT MELANOMA

What is the treatment for malignant melanoma?

A
  • Wide surgical excision (1cm margin thin, 3cm thick).
  • Radiotherapy.
  • Metastatic disease responds poorly to all treatments.
51
Q

VENOUS ULCER

What is the pathophysiology of a venous ulcer?

A
  • Defined as loss of skin below knee on leg/foot that takes >2w to heal.
  • Increased pressure causes extravasation of fibrinogen through capillary walls, giving rise to perivascular fibrin deposition, leading to poor oxygenation of surrounding skin.
52
Q

VENOUS ULCER

What is the aetiology + risk factors of venous ulcer?

A
  • Sustained venous HTN (atherosclerosis, previous DVT, incompetent valves).
  • RF = varicose veins, DVT.
53
Q

VENOUS ULCER

What is the clinical presentation of venous ulcer?

A
  • Large, shallow, irregular + exudative.
  • Normal pulses.
  • Painful (worse standing).
  • Oedema.
  • Warm skin, varicose veins.
54
Q

VENOUS ULCER

What are the investigations for venous ulcer?

A
  • Ankle brachial pressure index (ABPI) normal >0.9.

- Skin + ulcer biopsy.

55
Q

VENOUS ULCER

What is the treatment for venous ulcer?

A
  • High compression bandages.
  • Leg elevation.
  • Analgesia.
56
Q

ARTERIAL ULCER

What is the pathophysiology + aetiology/risk factors of arterial ulcer?

A
  • Punched-out, painful ulcers higher up leg/on feet.
  • Hx of claudication, HTN, angina + smoking.
  • Atherosclerosis, smoking, DM.
57
Q

ARTERIAL ULCER

What is the clinical presentation of arterial ulcer?

A
  • Intense pain, worse on elevation.
  • Leg is cold + pale.
  • Absent peripheral pulses.
  • No oedema, necrotic base.
58
Q

ARTERIAL ULCER

What are the investigations for arterial ulcer?

A
  • Ankle brachial pressure index (ABPI) < 0.9

- Doppler studies + angiography.

59
Q

ARTERIAL ULCER

What is the treatment for arterial ulcer?

A
  • Keep ulcer clean + covered.
  • Analgesia.
  • Vascular reconstruction.
60
Q

NEUROPATHIC ULCER

What are the risk factors for neuropathic ulcer?

A
  • DM, neurological disease.
61
Q

NEUROPATHIC ULCER

What is the clinical presentation of neuropathic ulcer?

A
  • Painless.
  • Pressure sites (soles, heels).
  • Peripheral neuropathy.
  • Warm skin + normal pulses.
  • Variable size + depth.
62
Q

NEUROPATHIC ULCER

What are the investigations + treatment for neuropathic ulcer?

A
  • ABPI < 0.9 implies neuroischaemic ulcer, X-ray to exclude osteomyelitis.
  • Wound debridement, keep clean, correctly fitting shoes + specialist podiatrist help for DM.
63
Q

VASCULITIC ULCER

What is the pathophysiology of vasculitic ulcers?

A
  • Vasculitis is inflammatory disorder of blood vessels causing endothelial damage.
  • Cutaneous vasculitis may be isolated or part of systemic disease.
  • Most common = leuokocytoclastic vasculitis, affects small veins.
64
Q

VASCULITIC ULCER

What is the aetiology of vasculitic ulcer?

A
  • Majority idiopathic.

- Drugs, infection, inflammatory disease.

65
Q

VASCULITIC ULCER

What is the clinical presentation of vasculitic ulcer?

A
  • Usually on lower legs.
  • Haemorrhagic papules.
  • Pustules.
  • Nodules.
  • Plaques.
66
Q

VASCULITIC ULCER

What is the treatment for vasculitic ulcer?

A
  • Analgesia, support stockings.
67
Q

CELLULITIS

What is the pathophysiology of cellulitis?

A
  • Bacterial infection of deep sub-cutaneous tissues.
  • Typically affects low leg/arm + spreads proximally.
  • Erysipelas is the superficial form affecting upper dermis + superficial lymphatics.
68
Q

CELLULITIS

What is the aetiology of cellulitis?

A
  • Group A beta-haemolytic strep – pyogenes most common.

- S. aureus, sometimes MRSA.

69
Q

CELLULITIS

What are the risk factors + differentials for cellulitis?

A
  • Lymphoedema, obesity, athletes food, ulcers.

- DVT, septic arthritis, gout.

70
Q

CELLULITIS

What is the clinical presentation of cellulitis?

A
  • Erythema in involved area with poorly demarcated margins, welling, warmth + tenderness.
  • Unilateral.
  • Systemically unwell.
  • Erysipelas = raised + sharply demarcated.
71
Q

CELLULITIS

What are the complications + investigations of cellulitis?

A
  • Necrotising fasciitis, abscesses, septicaemia.

- Clinical exam, bloods = raised WCC, ESR/CRP, cultures.

72
Q

CELLULITIS

What is the treatment for cellulitis?

A
  • Flucloxacillin (or erythromycin if penicillin allergy).
  • Prophylactic low dose phenoxymethylpenicillin.
  • Supportive = leg rest, elevation, analgesia.
73
Q

NECROTISING FASCIITIS

What is the pathophysiology of necrotising fasciitis?

A
  • Life-threatening infection of deep fascia causing necrosis of subcutaneous tissue, rapidly progressive.
74
Q

NECROTISING FASCIITIS

What is the aetiology of necrotising fasciitis?

A
  • Type 1 = polymicrobial with mixture of aerobic + anaerobic bacteria following abdominal surgery or diabetes.
  • Type 2 = Group A haemolytic strep. arises in healthy patients.
75
Q

NECROTISING FASCIITIS

What is the clinical presentation of necrotising fasciitis?

A
  • Intense pain over affected area + underlying muscle.

- Spreading erythema + underlying crepitus (crackling sound when joint moves) with pain + systemic toxicity (fever).

76
Q

NECROTISING FASCIITIS

What are the investigations of necrotising fasciitis?

A
  • Bloods = v high WCC, raised CRP.

- Soft tissue gas seen on XR.

77
Q

NECROTISING FASCIITIS

What is the treatment for necrotising fasciitis?

A
  • Urgent surgical debridement ± amputation.

- Aggressive broad spectrum Abx like benzylpenicillin + clindamycin (+ metronidazole in type 1).

78
Q

GANGRENE

What is the pathophysiology of gangrene?

A
  • Death of tissue from poor vascular supply + is a sign of critical ischaemia.
  • Dry = necrosis in absence of infection, wet = necrosis in presence of infection.
79
Q

GANGRENE

What is the clinical presentation of gangrene?

A
  • Tissues are black + may slough (layer of dead tissue separated from surrounding living tissue).
80
Q

GANGRENE

What is the treatment of gangrene?

A
  • Dry = restore blood supply ± amputation.

- Wet = analgesia, broad-spectrum IV antibiotics, surgical debridement ± amputation.

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