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Flashcards in Dermatology - Presenting problems Deck (51):
1

What are the three types of leg ulcers?

Leg ulcers are classified according to aetiology. They include:
1) venous
2) arterial
3) neuropathic

Other causes include vasculitis ulcers (purpuric, punched out), infected ulcers (purulent discharge, may have systemic signs) and malignancy (e.g. squamous cell carcinoma in long standing non healing ulcers).

2

What is the history associated with venous ulcers?

- often painful, worse on STANDING (cf. arterial)
- history of venous disease, e.g. varicose veins, DVT

3

What are the key clinical features of venous ulcers?

Venous ulcers are more commonly found on the medial maelleolus.

They are:
- large, shallow and irregular lesions
- exudative (appear "wet") with a granulating base

Skin may be warm and pulses are usually present. Leg oedema, haemosiderin and melanin deposition (brown pigment), lipodermatosclerosis and atrophie blanche (white scarring with dilated capillaries) are all key features.

4

How should venous ulcers be investigated?

Ankle-brachial pressure index (ABPI) is important in non-healing ulcers to assess for poor arterial flow which could impair healing.

A 'normal' ABPI may be regarded as between 0.9 - 1.2. Values below 0.9 indicate arterial disease. Interestingly, values above 1.3 may also indicate arterial disease, in the form of false-negative results secondary to arterial calcification (e.g. In diabetics).

5

How are venous ulcers managed?

- compression bandaging, usually four layer (only treatment shown to be of real benefit)
- oral pentoxifylline, a peripheral vasodilator, improves healing rate
- small evidence base supporting use of flavinoids
- little evidence to suggest benefit from hydrocolloid dressings, topical growth factors, ultrasound therapy and intermittent pneumatic compression

If they fail to heal after 12 weeks or are greater than 10cm2 then skin grafting may be required.

6

What is the history associated with arterial ulcers?

These are also painful at night, but worse when legs are ELEVATED.

History of arterial disease, e.g. atherosclerosis.

7

What are the key clinical features of arterial ulcers?

Located at pressure and trauma sites (e.g. pretibial, supramalleolar (usually lateral), and at distant points e.g. toes.

Appearance:
- small, sharply defined deep ulcer
- necrotic base
- sometimes associated gangrene

Associated features:
- cold skin
- weak or absent peripheral pulses
- shinny pale skin
- loss of hair

8

How should arterial ulcers be investigated and managed?

- ABPI <0.8 = presence of arterial insufficiency
- Doppler studies and ultrasonography

Management is:
- vascular reconstruction
- compression bandage is contraindicated

9

What is the history of neuropathic ulcers?

- Often painless
- Abnormal sensation
- History of diabetes or neurological disease

10

What are the key clinical features of neuropathic ulcers?

Found on pressure sites - e.g. soles, heels, toes, metatarsal heads.

Appearance:
- variable size and depth
- granulating base
- may be surrounded by or underneath a hyperkeratotic lesion (e.g. callus)

Associated features:
- warm skin
- normal peripheral pulses * (*cold, weak or absent pulses if it is a neuroischaemic ulcer)
- peripheral neuropathy

11

How should neuropathic ulcers be investigated and managed?

Investigation:
- ABPI <0.8 suggests neuroischaemic ulcer
- X ray to exclude osteomyelitis

Management:
- wound debridement
- regular repositioning, appropriate footwear and good nutrition

12

What are the differential diagnoses of an itchy eruption?

An itchy (pruritic) eruption can be caused by an inflammatory condition (e.g. eczema), infection (e.g. varicella), infestation (e.g. scabies), allergic reaction (e.g. in some cases of urticaria) or an unknown cause, possibly autoimmune (e.g. lichen planus).

Differentials can be further considered based on whether the itch is generalised or localised.

Generalised = scabies, eczema, pre-bullous pemphigoid, urticaria, xeroderma, psoriasis

Localised = eczema, lichen planus, dermatitis herpetiformis, pediculosis, tinea infections

13

What is the natural history that helps distinguish eczema?

- Personal or family history of atopy
- exacerbating factors (e.g. allergens, irritants)

Chronic lesions are dry and erythematous, whereas acute lesions are erythematous, vesicular and exudative.

Sites are flexible (e.g. flexor aspects in children and adults with atopic eczema)

Associated features can include secondary bacterial or viral infection.

14

How should eczema be investigated?

- Patch testing
- Serum IgE levels
- Skin swab

15

What is the natural history and clinical features of scabies?

- May have history of contact with infected individuals
- Pruritis is worse at night

Common sites of infestation are the sides of fingers, finger webs, wrists, elbows, ankles, feet, nipples and genitals.

Linear burrows (may be tortuous) or rubbery nodules are present on the skin.

16

How is scabies investigated/ managed?

Investigations:
- skin scrape, excoriation of mite and view under microscope

Management:
- Scabicide (e.g. permethrin or melathion)
- Antihistamines

17

What is lichen planus?

Lichen planus is a skin disorder of unknown aetiology, most probably being immune mediated. There is a family history in 10% of cases, and it may be drug induced.

18

What are the features of lichen planus?

- itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
- rash often polygonal in shape, 'white-lace' pattern on the surface (Wickham's striae)
- Koebner phenomenon may be seen (new skin lesions appearing at the site of trauma)
- oral involvement in around 50% of patients
- nails: thinning of nail plate, longitudinal ridging

19

What drugs are known to cause lichenous eruption?

- gold
- quinine
- thiazides

20

How is lichen planus managed?

Topical steroids are the mainstay of treatment.
Extensive lichen planus may require oral steroids or immunosuppression.

21

What diseases should be considered in a papulosuqamous eruption?

These are disorders exhibiting papules and scales. Differentials include psoriasis, pityriasis rosea, lichen planus, atopic eczema and drug eruption.

This is a common presenting complaint that is sometimes associated with itching. Atopic eczema is extremely itchy, psoriasis and pityriasis rosea less so.

22

How can the age of onset of a scaly rash help distinguish the cause?

Atopic eczema often starts in infancy or early childhood, pityriasis rosea and psoriasis between the ages of 15 and 40. Drug eruptions are acute in onset with a clear temporal relationship between starting the medicine and the onset of the rash.

23

How does the site of a rash help distinguish its underlying cause?

For example, flexural sites are involved in atopic eczema and extensor surfaces and scalp in psoriasis. Symmetry sug- gests endogenous disease, such as psoriasis, whereas asymmetry is more common with exogenous causes, such as contact dermatitis or herpes zoster.

24

What can a history of a preceding illness inform you about the cause of a patients rash eruption?

Guttate psoriasis is often preceded by a β-haemolytic streptococcal sore throat. Almost all patients with infectious mononucleosis treated with amoxicillin develop an erythematous maculopapular eruption.

25

What is pityriasis rosea?

A self-limited condition lasting 3–8 weeks. Initially, there is a single 2- to 6-cm annular salmon-colored patch (herald patch) with a peripheral rim of scale, fol- lowed in days to weeks by a generalized eruption involving the trunk and proximal extremities. Individual lesions are similar to but smaller than the herald patch and are arranged in symmetric fashion with long axis of each individual lesion along skin lines of cleavage. Appearance may be similar to that of secondary syphilis.

26

Does pityriasis require treatment?

Disorder is self-limited, so treatment is directed at symptoms; oral antihistamines for pruritus; topical glucocorticoids; UV-B phototherapy in some cases.

27

What are the differentials for a changing pigmented lesion?

A changing pigmented lesion can be benign (e.g. melanocytic naevi, seborrheic wart) or malignant (e.g. malignant melanoma). There are many different types of melanocytic naevi.

28

What is seborrheic keratosis?

Most commonly arise in patients over the age of 50 years, often idiopathic.
Equal sex incidence and prevalence.
Usually multiple lesions over face and trunk.
Flat, raised, filiform and pedunculated subtypes are recognised.
Variable colours and surface may have greasy scale overlying it.
Treatment options consist of leaving alone or simple shave excision.

29

What is the natural history of melanocytic naevi?

These are not usually present at birth but develop during infancy, childhood and adolescence. They are asymptomatic.

30

What are the clinical features of a melanocytic naevi?

This depends on the subtype of naevi:

- CONGENITAL naevi may be large, pigmented, protuberant and hairy

- JUNCTIONAL naevi are small, flat, and dark

- COMPOUND naevi are usually raised, warty and hyperkeratotic

31

How are benign pigmented skin lesions different to malignant melanoma?

Malignant melanoma tends to occur in middle aged to elderly patients, with a history of lesion evolution. They may be symptomatic (e.g. bleeding, itching) and there are often risk factors present.

The lesion can be distinguished by the ABCDE features:
- Asymmetrical shape
- Border irregularity
- Colour irregularity
- Diameter >6mm
- Evolution of the lesion

Excision is required, whereas melanocytic naevi and seborrhoeic warts rarely require removal.

32

What can cause a purpuric eruption?

A purpuric (or non blanching rash) can be thrombocytopaenic (e.g. meningococcal septicaemia, DIC, ITP) or non thrombocytopaenic (e.g. trauma, drugs, aged skin, vasculitis).

Platelet counts and a clotting screen are important to exclude coagulation disorders.

33

What are the characteristics of meningococcal septicaemia?

The history is of acute onset with symptoms of meningitis and septicaemia. The common sites for the rash to develop are the extremities. The petechial rash is not palpable. The patient is also systemically unwell.

Blood cultures, LP and antibiotics are required.

34

What is HSP?

Henoch-Schonlein purpura (HSP) is an IgA mediated small vessel vasculitis. There is a degree of overlap with IgA nephropathy (Berger's disease). HSP is usually seen in children following an infection.

35

What are the clinical features of HSP?

- palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
- abdominal pain
- polyarthritis
- features of IgA nephropathy may occur e.g. haematuria, renal failure

36

What is senile purpura?

This is a purpuric rash that arises in the elderly population with sun damaged skin.
It usually affects the extensor surfaces of hands and forearms.
The lesion is a non palpable purpura, with atrophic and thin surrounding skin.

No investigation or treatment is needed.

37

What are the differentials of a red swollen leg?

Cellulitis/ erysipelas
Venous thrombosis
Chronic venous insufficiency

38

What is vitiligo?

Disorders of skin pigmentation are common presenting complaints. Vitiligo is an autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin. It is thought to affect around 1% of the population and symptoms typically develop by the age of 20-30 years.

39

What are the clinical features of vitiligo?

- well demarcated patches of depigmented skin
- the peripheries tend to be most affected
- trauma may precipitate new lesions (Koebner phenomenon)

Sensation in the depigmented regions is intact (unlike in tuberculoid leprosy). The course is unpredictable, but most patches remain static or enlarge; a few repigment spontaneously.

40

How is vitiligo managed?

- sun block for affected areas of skin
- camouflage make-up
- topical corticosteroids may reverse the changes if applied early
- there may also be a role for topical tacrolimus and phototherapy, although caution needs to be exercised with light-skinned patients

41

What is oculocutaneous albinism? What are the clinical features?

Albinism results from genetic abnormalities in melanin biosynthesis in skin and eyes but the NUMBER of melanocytes is normal (in contrast to vitiligo). It is usually inherited in an autosomal recessive trait. From birth, patients have a complete lack of pigment, resulting in pale skin, white hair and also failure of melanin production in the retina and iris. This causes photophobia, poor vision not correctable with refraction, rotatory nystagmus and alternating strabimus.

42

What conditions are associated with increased pigmentation?

This is mostly due to hypermelanosis but other pigments can occasionally be deposited in the skin, e.g. an orange tint in carotenaemia or a bronze due to haemochromatosis.

43

What is chloasma?

Chloasma describes discrete patches of facial pigmentation that occur in pregnancy and in some women taking oral contraceptives. Diffuse pigmentary change may also occur in Addison's disease, Cushing' syndrome, Nelson's syndrome and chronic renal failure.

44

What drugs are associated with hyperpigmentation?

Amiodarone (slate grey)
Arsenic (diffuse bronze pigmentation)
Bleomycin
Busulfan
Chloroquine (blue grey)

45

What is alopecia?

Alopecia means loss of hair and is a sign rather than a diagnosis. Alopecia may be divided into localised and diffuse, and scarring and non scarring types.

46

What is the difference between scarring and non scarring alopecia?

Scarring alopecia implies destruction of a hair follicle and can be caused by:
- trauma, burns
- radiotherapy
- lichen planus
- discoid lupus
- tinea capitis*

Non scarring alopecia means that the hair follicle has been preserved, and is caused by:
- male-pattern baldness
- drugs: cytotoxic drugs, carbimazole, heparin, oral contraceptive pill, colchicine
- nutritional: iron and zinc deficiency
- autoimmune: alopecia areata
- telogen effluvium (hair loss following stressful period e.g. surgery)
- trichotillomania

47

What is alopecia areata?

Alopecia areata is a presumed autoimmune condition causing localised, well demarcated patches of hair loss. At the edge of the hair loss, there may be small, broken 'exclamation mark' hairs which are pathognomonic.

Hair will regrow in 50% of patients by 1 year, and in 80-90% eventually. Careful explanation is therefore sufficient in many patients. Other treatment options include:
- topical or intralesional corticosteroids
- topical minoxidil
- phototherapy
- dithranol
- contact immunotherapy
- wigs

Larger patches of hair loss carry a worse prognosis for regrowth.

48

What is androgenetic alopecia?

Male-pattern baldness is physiological in men >20 yrs old, although rarely it may be extensive and develop at an alarming pace in the late teens. It also occurs in females, most obviously after the menopause. The distribution is of bitemporal recession and then crown involvement.

49

What investigations should be performed in a patient presenting with alopecia?

These should include FBC, U&Es, LFTs, TFTs, iron studies, an autoantibody profile and, in cases where lupus or lichen planus is suspected, a scalp biopsy.

50

What is hypertrichosis?

A generalised increase in hair, hypertrichosis is commonly a side- effect of drugs, e.g. ciclosporin, minoxidil or diazoxide. Eflornithine inhibits hair growth and may be useful if the cause cannot be removed.

51

What is hirsuitism?

Hirsutism is the growth of terminal hair in a male pattern in a female. The cause of most cases is unknown and, while it may occur in hyperandrogenism, Cushing’s syndrome and polycystic ovary syndrome, only a small minority of patients have a demonstrable hormonal abnormality. Psychological distress is often significant and oral contraceptives containing an anti-androgen (e.g. cypro- terone acetate), laser therapy or topical eflornithine may be beneficial.

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