Dermatology Flashcards

(38 cards)

1
Q

Skin cancer

A

1- Melanoma
2-Non Melanoma&raquo_space;> BCC and SCC

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2
Q

Skin Lesion Examination

A

ABCDE Approach
A- Asymmetry
B- Border Irregularity
C- Color variation
D- Diameter > 6mm
E- Evolution ( Increase in size)

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3
Q

Sunburn

A

Exposure to UVB light.
Energy is absorbed by DNA, resulting in damage in the form of pyrimidine dimers.

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4
Q

Molluscum contagiosum

A

A diagnosis of molluscum contagiosum is obvious when a child presents with pearly white hemispherical lesions particularly if they are umbilicated over limbs, trunk or face in various stages of evolution

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5
Q

Dermatitis Herpetiformins

A

-Intensely pruritic vesicles.
- It is usually not responsive to topical steroids but would response well to dapsone.
- Associated with gluten sensitivity and Coeliac disease.

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6
Q

Anthrax

A

Anthrax is caused by the Gram positive, aerobic, non-motile Bacillus anthracis.

It produces serious disease in the herbivore host and carnivores acquire the disease from either consuming the spores from the dead animal or by contact.

In humans, cutaneous disease is most common and a painless, black, indurated eschar frequently forms. Mortality from cutaneous disease is 20% if untreated whereas inhalational anthrax may have a mortality of 90% if untreated.

Inhalational anthrax is associated with a poor yield from sputum culture with the greatest yield from blood culture

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7
Q

Keratocanthoma

A

Keratoacanthomas are rapidly growing, benign skin lesions that often appear as red papules and then develop into a crater filled with keratinous material. They typically reach their maximum size within weeks to months and then spontaneously regress

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8
Q

Lower Lip

A

The most common malignancy in the lower lip is a squamous cell carcinoma

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9
Q

Leishmaniasis

A
  • Cutaneous leishmaniasis
    caused by Leishmania tropica or Leishmania mexicana.
  • Mucocutaneous leishmaniasis
    caused by Leishmania braziliensis.
  • Visceral leishmaniasis (kala-azar)
    mostly caused by Leishmania donovani
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10
Q

DLE

A

Discoid lupus erythematosus is a benign disorder generally seen in younger females. It very rarely progresses to systemic lupus erythematosus (in less than 5% of cases). Discoid lupus erythematosus is characterised by follicular keratin plugs and is thought to be autoimmune in aetiology

Features
erythematous, raised rash, sometimes scaly
may be photosensitive
more common on face, neck, ears and scalp
lesions heal with atrophy, scarring (may cause scarring alopecia), and pigmentation

Management
- topical steroid cream
- oral antimalarials may be used second-line e.g. hydroxychloroquine
- avoid sun exposure

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11
Q

Rosacea

A

Features
typically affects nose, cheeks and forehead
flushing is often first symptom
telangiectasia are common
later develops into persistent erythema with papules and pustules
rhinophyma
ocular involvement: blepharitis
sunlight may exacerbate symptoms

Management
».simple measures
Recommend daily application of a high-factor sunscreen
Camouflage creams may help conceal redness

> > > predominant erythema/flushing
Topical brimonidine gel may be considered for patients with predominant flushing but limited telangiectasia
brimonidine is a topical alpha-adrenergic agonist

> > Mild-to-moderate papules and/or pustules
topical ivermectin is first-line
alternatives include: topical metronidazole or topical azelaic acid

> > > moderate-to-severe papules and/or pustules
combination of topical ivermectin + oral doxycycline

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12
Q

Pyoderma Gangrenosum

A

Oral steroids are the first-line treatment for pyoderma gangrenosum

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13
Q

Bullous pemphigoid

A

Bullous pemphigoid is an autoimmune condition causing sub-epidermal blistering of the skin. This is secondary to the development of antibodies against hemidesmosomal proteins BP180 and BP230.

Bullous pemphigoid is more common in elderly patients. Features include
itchy, tense blisters typically around flexures
the blisters usually heal without scarring
there is stereotypically no mucosal involvement (i.e. the mouth is spared)

Skin biopsy
immunofluorescence shows IgG and C3 at the dermoepidermal junction

Management
referral to a dermatologist for biopsy and confirmation of diagnosis
oral corticosteroids are the mainstay of treatment
topical corticosteroids, immunosuppressants and antibiotics are also used.

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14
Q

Anthrax

A

Anthrax is caused by Bacillus anthracis, a Gram positive rod. It is spread by infected carcasses. It is also known as Woolsorters’ disease. Bacillus anthracis produces a tripartite protein toxin
- Protective antigen
- Oedema factor: a bacterial adenylate cyclase which increases cAMP
- Lethal factor: toxic to macrophages

Features
causes painless black eschar (cutaneous ‘malignant pustule’, but no pus)
Typically painless and non-tender
may cause marked oedema
Anthrax can cause gastrointestinal bleeding

Management
The current Health Protection Agency advice for the initial management of cutaneous anthrax is ciprofloxacin
Further treatment is based on microbiological investigations and expert advice.

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15
Q

Systemic Mastocytosis

A

Systemic mastocytosis results from a neoplastic proliferation of mast cells

Features
- Urticaria Pigmentosa - produces a wheal on rubbing (Darier’s sign)
- flushing
- abdominal pain
- monocytosis on the blood film

Diagnosis
- raised serum tryptase levels
- urinary histamine

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16
Q

Vitiligo

A

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.

Associated conditions
type 1 diabetes mellitus
Addison’s disease
autoimmune thyroid disorders
pernicious anaemia
alopecia areata

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

Management
sunblock 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

17
Q

Koebner phenomenon

A

The Koebner phenomenon describes skin lesions that appear at the site of injury. It is seen in:
- psoriasis
- vitiligo
- warts
- lichen planus
- Lichen sclerosus
- Molluscum contagiosum

18
Q

Alopecia

A

Scarring alopecia
- trauma, burns
- radiotherapy
- lichen planus
- discoid lupus
- tinea capitis*

Non-scarring alopecia
- 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

19
Q

Lichen

A

Lichen
planus: purple, pruritic, papular, polygonal rash on flexor surfaces. Wickham’s striae over surface. Oral involvement common

sclerosus: itchy white spots typically seen on the vulva of elderly women

20
Q

Erythema Nodosum

A

Causes
infection
streptococci
tuberculosis
brucellosis
systemic disease
sarcoidosis
inflammatory bowel disease
Behcet’s
malignancy/lymphoma
drugs
penicillins
sulphonamides
combined oral contraceptive pill
pregnancy

21
Q

Keloid scars

A

Predisposing factors
ethnicity: more common in people with dark skin
occur more commonly in young adults, rare in the elderly
common sites (in order of decreasing frequency): sternum, shoulder, neck, face, extensor surface of limbs, trunk

Keloid scars are less likely if incisions are made along relaxed skin tension lines*

Treatment
early keloids may be treated with intra-lesional steroids e.g. triamcinolone
excision is sometimes required but careful consideration needs to given to the potential to create further keloid scarring

22
Q

Lichen planus

A

Itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
rash often polygonal in shape, with a ‘white-lines’ 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: typically a white-lace pattern on the buccal mucosa
nails: thinning of nail plate, longitudinal ridging

23
Q

Kaposi’s Sarcoma

A

Kaposi’s sarcoma
caused by HHV-8 (human herpes virus 8)
presents as purple papules or plaques on the skin or mucosa (e.g. gastrointestinal and respiratory tract)
skin lesions may later ulcerate
respiratory involvement may cause massive haemoptysis and pleural effusion
radiotherapy + resection

25
Necrobiosis lipoidica diabeticorum
Necrobiosis lipoidica diabeticorum shiny, painless areas of yellow/red skin typically on the shin of diabetics often associated with telangiectasia.
26
Rosacea
Rosacea treatment: mild/moderate: topical ivermectin severe/resistant: combination of topical ivermectin + oral doxycycline
27
Pityriasis Versicolor
1- topical antifungal. NICE advises ketoconazole shampoo as this is more cost effective for large areas 2- if failure to respond to topical treatment then consider alternative diagnoses (e.g. send scrapings to confirm the diagnosis) + oral itraconazole
28
Pompholyx
Pompholyx is a type of eczema which affects both the hands (cheiropompholyx) and the feet (pedopompholyx). It is also known as dyshidrotic eczema. Pompholyx eczema may be precipitated by humidity (e.g. sweating) and high temperatures. Features small blisters on the palms and soles pruritic often intensely itchy sometimes burning sensation once blisters burst skin may become dry and crack Management cool compresses emollients topical steroids
29
Necrotising Fascitis
Management of necrotising fasciitis revolves around immediate surgical debridement nd IV antibiotics
30
Necrotising Fascitis
Type 1 is caused by mixed anaerobes and aerobes (often occurs post-surgery in diabetics). This is the most common type Type 2 is caused by Streptococcus pyogenes
31
Nicotinic acid ( Niacin)
Deficiency of Nicotinic acid ( niacin )(vitamin B3) causes pellagra.
32
Keloid scars
Keloid scars - more common in young, black, male adults
33
Seborrhoeic Dermatitis
Seborrhoeic dermatitis in adults is a chronic dermatitis thought to be caused by an inflammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur (formerly known as Pityrosporum ovale). It is common, affecting around 2% of the general population. Features eczematous lesions on the sebum-rich areas: scalp (may cause dandruff), periorbital, auricular and nasolabial folds otitis externa and blepharitis may develop. Associated conditions include HIV Parkinson's disease Scalp disease management the first-line treatment is ketoconazole 2% shampoo over the counter preparations containing zinc pyrithione ('Head & Shoulders') and tar ('Neutrogena T/Gel') may be used if ketoconazole is not appropriate or acceptable to the person selenium sulphide and topical corticosteroid may also be useful
34
35
Allergy Tests
Skin prick test Most commonly used test as easy to perform and inexpensive. Drops of diluted allergen are placed on the skin after which the skin is pierced using a needle. A large number of allergens can be tested in one session. Normally includes a histamine (positive) and sterile water (negative) control. A wheal will typically develop if a patient has an allergy. Can be interpreted after 15 minutes Useful for food allergies and also pollen Radioallergosorbent test (RAST) Determines the amount of IgE that reacts specifically with suspected or known allergens, for example IgE to egg protein. Results are given in grades from 0 (negative) to 6 (strongly positive) Useful for food allergies, inhaled allergens (e.g. Pollen) and wasp/bee venom Blood tests may be used when skin prick tests are not suitable, for example if there is extensive eczema or if the patient is taking antihistamines Skin patch testing Useful for contact dermatitis. Around 30-40 allergens are placed on the back. Irritants may also be tested for. The patches are removed 48 hours later with the results being read by a dermatologist after a further 48 hours
36
Calciphylaxis
Calciphylaxis lesion are intensely painful, purpuric patches with an area of black necrotic tissue that may form bullae, ulcerate, and leave a hard, firm eschar
37
Calciphylaxis
Calciphylaxis is a rare complication of end-stage renal failure. The underlying mechanism is not clear, however it results in deposition of calcium within arterioles causing microvascular occlusion and necrosis of the supplied tissue. It most commonly affects the skin and presents with painful necrotic skin lesions.
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Treatment of Calciphylaxis
Treatment of calciphylaxis focuses on reducing calcium and phosphate levels, controlling hyperparathyroidism and avoiding contributing drugs such as warfarin and calcium containing compounds