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Year 2 Clinical > Dermatology: Clinical Cases of Rash > Flashcards

Dermatology: Clinical Cases of Rash Flashcards

1
Q

Examination of general skin in psoriasis reveals?

A

Plaques on extensor surfaces, usually, e.g: extensor elbows, knees and shins

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2
Q

Examination of scalp in psoriasis reveals?

A

Local adherent scale and erythema at the hairline

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3
Q

Nail signs in psoriasis?

A

Nail dystrophy:

Pitting
Onycholysis - lifting up of nail plate that may discolour the nail
Subungual hyperkeratosis (thickening)
Longitudinal ridging

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4
Q

Joint disease in psoriasis?

A

Psoriatic arthritis (joint swelling), e.g: tender hands

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5
Q

Cause of psoriasis?

A

Multi-factorial disease with:

Genetic factors

Environmental factors inc. stress, drugs and infections

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6
Q

What is the most common type of psoriasis and how does it present?

A

Chronic plaque psoriasis (psoriasis vulgaris) presents as:
Symmetrical, sharply dermarcated, scaly and erythematous plaques

Common sites affected are the extensors, scalp, sacrum, hands, feet, trunk and nails

IMAGE 1

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7
Q

What is the Koebner phenomenon?

A

Psoriasis develops in areas of skin trauma, e.g: a scratch mark or scar

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8
Q

What is Auspitz sign?

A

Removal of surface scale reveals tiny bleeding points (dilated capillaries in elongated dermal papillae, which have come close to the surface)

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9
Q

What is guttate psoriasis?

A

Multiple small scaly plaques that tend to affect most of the body, unlike psoriasis vulgaris (where extensors are mostly affected)

Lesions are conc. around the trunk, upper arms and thighs

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10
Q

What is palmoplantar pustular psoriasis?

A

Chronic pustular condition affecting the palms and soles; characterised by thickened, scaly, erythematous skin that easily develops fissures

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11
Q

What is erythrodermis (or widespread pustular) psoriasis?

A

Rare and is a generalised redness of the skin that can be fatal; it may be precipitated by, e.g: infections, alcohol, low Ca2+

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12
Q

Co-morbidities of psoriasis?

A

Psoriatic arthritis, metabolic syndrome (obesity, hypertension, diabetes, dyslipidaemia), Crohn’s disease, cancer, depression, uveitis

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13
Q

Why is life expectancy reduced by 4 years, in patients with severe psoriasis?

A

Increased CV risk (3x for MI)

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14
Q

Topical therapies available for psoriasis?

A

Vitamin D analogues, e.g: calcitriol and calcipotriol

Coal tar

Dithranol

Steroid ointments

EMOLLIENTS

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15
Q

Other, more specialised treatments available for psoriasis?

A

Phototherapy (narrowband UVB and PUVA)

Systemic treatments, such as immunosuppression and immune modulation (with targeted biologic agents)

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16
Q

What is acne vulgaris and how does it develop?

A

Chronic inflammatory disease of the pilosebaceous unit; there is increased sebum production and poral occlusion

Bacterial colonisation of the duct occurs, by P. acnes, and this is followed by dermal inflammation

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17
Q

Distribution of acne vulgaris?

A

Related to sites with the most sebaceous glands, i.e: face, upper back and chest

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18
Q

Morphology of acne vulgaris?

A

Comedones - open (blackhead) and closed (whitehead)

Pustules and papules

Cysts

Erythema

19
Q

Secondary features of acne vulgaris?

A 
Different types of scarring:
Atropic
Hypertrophic
Ice-pick
Texture changes
20
Q

Grading of acne?

A

Mild - scattered papules, putules and comedones

Moderate - numerous papules and pustules along with mild atrophic scarring

Severe - cysts, nodules and significant scarring

21
Q

First-line therapies for acne vulgaris?

A

Topical agents, e.g: keratolytics (benzoyl peroxide) or topical retinoids (isotretinoin)

For inflammatory acne, topical antibiotics are used, e.g: erythromycin or clindamycin

22
Q

Second-line therapies for acne vulgaris?

A

Low-dose oral antibiotic therapy

23
Q

Third-line therapies for acne vulgaris?

A

Oral retinoid drugs, e.g: oral isotretinoin, if:
All other measures have failed
Nodulocystic acne with scarring
Severe psychological disturbance

24
Q

What are retinoids?

A

Synthetic vitamin A analogues that affect cell growth and differentiation

25
Q

Side effects of oral retinoids?

A

Inital aggravation of acne

Very teratogenic - person must be on oral contraceptive or not sexually active (pregnancy test before and monthly during treatment)

26
Q

What is rosacea?

A

Common inflammatory rash predominantly affecting the face, part. nose, chin, cheeks and forehead

Onset is normally in middle-ages and is more common in women

27
Q

Describe the rash in rosacea

A

Papules, pustules and erythema but no comedones (i.e: this is NOT a disease of the pilosebaceous units)

28
Q

Triggers of rosacea?

A

Exacerbated by sudden changes in temp, alcohol and spicy food

29
Q

Other symptoms of rosacea?

A

Rhinophyma (enlarged nose)

Conjunctivitis/gritty eyes

30
Q

Management of rosacea?

A

Reduce aggravating factors, e.g: dietary triggers, sun exposure and AVOID TOPICAL STEROIDS (can worsen the skin)

Topical therapies, e.g: metronidazole, to reduce the demodex mites

Oral therapies, e.g: long-term oral tetracycline and, if severe, isotretinoin (low dose)

Vascular lasers for telangiectasia

Surgery/laser shaving for rhinophyma

31
Q

Characteristics of lichenoid eruptions?

A

Damage and infiltration between the epidermis and dermis

32
Q

Most common types of lichenoid eruptions?

A

Lichen planus

Lichenoid drug eruptions, e.g: ACE inhibitors (normally, a delayed reaction), statins, etc

33
Q

Clinical presentation of lichen planus?

A

Violaceous (pink/purple), flat-topped shiny papules typically affecting volar wrists/forearms, shins and ankles

Wickham’s striae (fine, white lace pattern on papule surface and on the buccal mucosa)

Intensely pruritis

34
Q

Occurrence of lichen planus?

A

Tends to occur in middle age and lasts around 12-18 months before burning out

35
Q

Treatment of lichen planus?

A 
Treat symptomatically: 
Topical steroids (if extensive, oral) - these should be potent/very potent
36
Q

How to differentiate between bullous pemphigoid and pemphigus?

A

Bullous pemphigoiD:
Split is Deeper, through DEJ

PemphiguS:
Split more Superficial, intra-epidermal

37
Q

What is Nikolsky’s sign?

A

Top layers of the skin slip away from the lower layers when slightly rubbed; this indicates a PLANE OF CLEAVAGE WITHIN THE EPIDERMIS , i.e: when the skin is rubbed, exfoliation of the outer layers can occur

Present in Pemphigus vulgaris and Toxic Epidermal Necrolysis, but not in bullous pemphigoid

38
Q

Clinical presentation of bullous pemphigoid?

A

Localised to one area/widespread on the trunk and proximal limbs

There are large, TENSE, BULLAE on an erythematous base; these can burst and leave erosions that do not scar
However, early in disease, there may be urticated itchy plaques rather than bullae

Nikolsky sign (negative) and mucosal lesions are unlikely

39
Q

Clinical presentation of pemphigus vulgaris?

A

Flaccid vesicle/bullae (thin-roofed) typically affecting the scalp, face, axillae and groin

Lesions rupture to leave raw areas (infection risk)

Nikolsky sign +ve and mucosal involvement is very common, e.g: eyes, genitals

40
Q

Prognosis of pemphigus vulgaris?

A

Chronic self-limiting course but the duration varies from months-years

Most patients achieve REMISSION on treatment within 3-6 months

41
Q

Difference between mortality of pemphigus and bullous pemphigoid?

A

If untreated, pemphigus has a very high mortality

Bullous pemphigoid has much lower risk

42
Q

Investigations for pemphigus or bullous pemphigoid?

A

Skin biopsy with direct immunofluorescence

Indirect immunofluorescence

43
Q

Treatment of pemphigoid and pemphigus?

A

Systemic steroids

Other immunosuppressive agents

Topicals, such as emollients, topical steroids, topical anti-sepsis/hygiene measures

IN PEMPHIGOID - tetracycline antibiotics

Year 2 Clinical (119 decks)

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