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RW Dermatology > Clinical Dermatology > Flashcards

Clinical Dermatology Flashcards

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Dermatology Board Prep flashcards
1
Q

Which areas do psoriasis most commonly affect?

A

Extensors

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2
Q

What is the most common type of psoriasis?

A

Psoriasis vulgarise (chronic plaque psoriasis)

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3
Q

What are the main topical treatment soptions for psoriasis?

A

Emollients plus vitamin D analogues (calcipqotriol/calcitriol), coal tar, dithranol, steroid ointments (and possible phototherapy)

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4
Q

What are the systemic treatments possible for psoriasis?

A

Retinas, immunosuppression (methotrexate/ciclosporin), immune modulators

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5
Q

Which bacteria are involved in acne?

A

P. acnes

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6
Q

Of whiteheads and blackheads, which are open and which are closed?

A

Whiteheads - closed and blackheads - open

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7
Q

What are the topical treatments for acne?

A

Benzoyl peroxide (keratolytic/antibacterial), topical Vit A deravitives (retinoids) and topical antibiotics

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8
Q

What systemic treatments are available for acne?

A

Antibiotics and oral retinoids (isoretinoin)

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9
Q

What are the side effects of oral retinoids eg. isotetinoin?

A

Depression, dry skin and teratogenicity

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10
Q

What are the characteristics of rosacea?

A

Flushing of the central face along with papule, pustules and erythema (NO comedones)

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11
Q

What are the treatments of rosacea?

A

Topical metronidazole, isoretinoin if severe, vascular laser for telangiectasia

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12
Q

What is the treatment for lichen planus?

A

Topical steroids (oral if extensive)

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13
Q

What is the appearance of lichen planus?

A

Violaceous (pink/ purple) flat-topped shiny papules

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14
Q

How are bullies pemphigoid and pemphigus differentiated?

A

Bulls pemphigoiD split is Deeper (through DEJ), which pemphiguS is more Superficial

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15
Q

Positive Nikolsky sign

A

Positive result: the top layers of the skin slip away from the lower layers when slightly rubbed

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16
Q

How can BP and pemphigus vulgarise be differentiated clinically?

A

BP is negative for Nikolsky sign while pemphigus vulgarise is positive

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17
Q

What is the investigation for Pemphigoid disorders?

A

immunofluorescence

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18
Q

What is involved in the acute phase of eczema/dermatitis?

A

Papulovescular erythematous lesions, oedema, scaling and crusting

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19
Q

What is involved in the chronic phase of eczema/dermatitis?

A

Thickening (lichenification), elevated plaques and increased scaling

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20
Q

What is common to both the acute and chronic phase of eczema/dermatitis?

A

Itch

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21
Q

What is the pathophysiology of contact allergic dermatitis?

A

Delayed Type IV hypersensitivity reaction

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22
Q

What is the pathophysiology of contact irritant dermatitis?

A

Trauma eg. soap

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23
Q

What is the pathophysiology of atopoic dermatitis?

A

Genetic and environmental factors resulting in inflammation

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24
Q

What is the pathophysiology of drug-induced dermatitis?

A

Type I or IV hypersensitivity reaction

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25
Q

What is the pathophysiology of stasis dermatitis?

A

Physical trauma to skin - hydrostatic pressure

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26
Q

What is the pathophysiology of lichen simplex dermatitis?

A

Physical trauma to skin - scratching

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27
Q

What test can be done for contact allergic dermatitis?

A

Patch testing

28
Q

What is the treatment for irritant contact dermatitis?

A

Topical steroids and emollients

29
Q

Which areas are atopic eczema/dermatitis found?

A

Flexural

30
Q

What is a critical symptom for atopic eczema/dermatitis?

A

Pruritus

31
Q

Lichenification

A

Increased skin markings

32
Q

What does golden crusting in atopic eczema indicate?

A

Staph. aureus infection

33
Q

What causes eczema herpeticum and what does it look like?

A

Herpes simplex virus, looks like monomorphic punched-out lesions

34
Q

What is the diagnostic criteria for atopic eczema/dermatitis?

A
  • Visible or history of flexural rash; Personal history of atopy; generally dry skin; onset before 2yrs
35
Q

What are the treatments of atopic eczema/dermatitis?

A

Emollients; topical steroids; antibiotics for infections; phototherapy (UVB); systemic immunosuppressants

36
Q

Which gene is most associated with atopic eczema?

A

Filaggrin

37
Q

What is the characteristic of discoid eczema?

A

Well defined, round lesions

38
Q

Pruritus

A

A usually unpleasant, poorly localised, non-adapting sensation that provokes the desire to scratch

39
Q

What are the mediators of itch?

A

Chemical mediators (eg. histamine, ACh, PGE2), nerve transmission (unmyelintated C fibres) and opiates in the CNS

40
Q

What are the 4 main categories of causes of itch?

A

Pruritoceptive (trigger in the skin), neuropathic (damage of central/peripheral fibres), neurogenic (opiates on CNS fibres but no damage) and psychogenic

41
Q

What are examples of anti-itch treatments?

A

Anti-histamines, emollients, antidepressants, phototherapy,

42
Q

What is chronic venous insufficiency?

A

Occurs when the valves of the veins do not function correctly and venous drainage is impaired. The failure of the valves allows the blood to flow back down (reflux) into the section of vein below

43
Q

How does chronic venous hypertension lead to leg ulcers?

A

Chronic venous hypertension causes abnormalities in the capillaries in the leg tissues that make them more permeable. This allows fluid, proteins and blood cells to leak into the tissues. They may also cause increased inflammatory response, changes in the structure of the microvasculature and reduced skin and tissue oxygenation. Overall, these effects contribute to greater skin fragility and increased risk of leg ulceration and delayed healing

44
Q

What is the definition of a leg ulcer?

A

Any break in the skin of the lower leg above the ankle that is present more than 4 weeks

45
Q

Which type of leg ulcers are most common?

A

Venous ulcers

46
Q

Which ulcers look ‘punched out’ and deep, and often occur on the foot?

A

Arterial ulcers

47
Q

Which ulcers appear superficial, have shallow edges and rarely involve the foot?

A

Venous ulcers

48
Q

What are signs of venous disease that should be looked for?

A

Varicose veins; atrophie blanche; lipodermatosclerosis; haemosiberin

49
Q

What is lipdermatiosclersis?

A

‘Champagne leg’, a type of panniculitis (inflammation of subcutaneous fat) which cause skin hardening, increased pigmentation, swelling and redness

50
Q

What is a normal ABPI range?

A

0.8-1.3

51
Q

What is the aim of compression treatment?

A

To heal ulcers within 12 weeks

52
Q

What is Imiquimod?

A

An immune modulator which can be used as a cream to treat pre-cancers and BCC

53
Q

Vitiligo

A

‘White spot disease’ - an autoimmune disease with loss of melanocytes due to autoimmune attack

54
Q

Albinism

A

In this disorder there is a genetic partial loss of pigment production

55
Q

Nelson’s Syndrome

A

Melanin stimulating hormone is produced in excess by the pituitary

56
Q

What clinical conditions occurs when venous valves become weak and dilated?

A

Varicose veins

57
Q

What conditions can lead to chronic insufficiency and consequently DVT or venous ulceration?

A

Poor circulation, stasis or immobility

58
Q

What causes skin ulceration following chronic venous insufficiency?

A

Superficial microcirculatory deficiencies

  1. (Venous pressure increases
  2. Damages blood vessels in skin
  3. Skin becomes dry, itchy and inflamed
  4. Cannot heal well due to poor blood supply
  5. Begins to break down
59
Q

What causes thrombosis/embolism following chronic venous insufficiency?

A

Deep venous stasis

60
Q

Which classification is used to determine skin photo type?

A

Fitzpatrick skin prototypes (I to VI)

61
Q

What causes photosensitivity?

A

An abnormal reaction to some component of the electromagnetic spectrum of sunlight and a chromophore (reactive compound) within the skin.

62
Q

Photosensitivity

A

Various symptoms, diseases and conditions caused or aggravated by exposure to sunlight.

63
Q

What is the underlying cause of Porphyria Cutanea Tarda?

A

PCT is due to a defective enzyme in the liver (uroporphyrinogen decarboxylase). This causes an increase in porphyrins in the skin result in photosensitivit

64
Q

What is the typical presentation of PCT?

A

Blisters and fragility, particularly on the backs of hands

65
Q

What investigations can be done for PCT?

A

Wood’s lamp (looking for excessive porphyrins) or skin biopsy

66
Q

What is the underlying cause of Erythropoietic Protoporphyria (EPP)?

A

EPP is due to an inherited deficiency of the enzyme ferrochelatase. Reduced activity of this enzyme causes a build-up of the chemical protoporphyrin in the skin; resulting in photosensitivity

67
Q

What is the most common type of porphyria?

A

Porphyria cutanea tarda

RW Dermatology (10 decks)

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