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Phase 2a medicine > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is acne?

A

Common chronic disorder affecting hair follicle and sebaceous gland, in which there is expansion and blockage of hair follicle and inflammation

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2
Q

What is the most common form of acne?

A

Acne vulgaris

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3
Q

When does acne most commonly present?

A 
Starts in adolecence
Often resolves in mid-20s
Prevalence ranges from 70-87% in teenagers
Affects - face, back, chest
Usually seen during puberty 13-20
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4
Q

What is the pathology of acne?

A

Narrowing of hair follicle due to hypercornification (adherent cells blocking hair follicles)
Results in increased sebum production - causing skin to feel greasy
Some of sebum becomes trapped in narrow hair follicle
Sebum stagnates at pit of follicle where there is no O2
Creates anaerobic conditions that allows propionibacterium acnes to multiply in the stagnant sebum
P acne breaks down triglycerides in sebum to FFAs resulting in irritation, inflammation and that attracts of neutrophils (due to chemoattractant release)
Results in pus formation and further inflammation since the now full hair follicle is rapidly filled with attracted neutrophils

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5
Q

How does acne present?

A 
Whiteheads - closed comedones
Blackheads - open comedones
Skin-coloured papules
Inflammatory lesions usually occurring when the closed wall of comedones ruptures
Papules (small red bumps)
Pustules (white/yellow spots)
Nodules (large red bumps)
Commonly found on face, chest and upper back
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6
Q

How is acne diagnosed?

A

Normally clinical diagnosis
Skin swabs for microscopy and culture
Hormonal tests in females

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7
Q

How is mild acne treated?

A

Benzyl peroxide gel/cream - increases cell turnover, clears pores and reduces bacterial count, causes dryness due to keratolytic effect
Topical antibiotics - clindamycin gel/erythromycin gel
Topical retinoids - tazarotene gel - inhibit formation and reduce number of microcomedones
S/E - burning, stinging, dryness, scaling

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8
Q

How is severe acne treated?

A

In addition to topical therapy
Oral tetracycline eg oral doxycyclin then oral minocycline
- 4 month min use
- Contraindicated in pregnancy and children
Hormonal treatment
- Indicated when standard antibiotic treatment has failed or when control of menstruation required
- Anti-androgen treatment suppresses sebum production
- Oral co-cyprindiol

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9
Q

What are arterial ulcers?

A

Punched out, painful ulcers higher up leg/feet

Commonly have history of claudication, hypertension, angina/smoking

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10
Q

What factors can increase your risk of arterial ulcers?

A

Arterial disease eg atherosclerosis
Smoking
Hypercholesterolaemia
DM

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11
Q

How do arterial ulcers present?

A

Typically presents as punched out ulcers higher up leg or on feet
Intense pain that is worse when elevated (more pain than venous ulcers)
Leg cold and pale
Ulcer small, sharply defined and has necrotic base
Shiny pale skin and loss of hair
Absent peripheral pulses
Aterial bruits - murmurs heard caused by turbulent blood flow often due to partial obstruction in artery
No oedema

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12
Q

How are arterial ulcers diagnosed?

A

Doppler ultrasound to confirm arterial disease

Ankle brachial pressure index suggests arterial insufficiency

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13
Q

How are arterial ulcers treated?

A

Keep ulcer clean and covered
Analgesia
Vascular reconstruction if appropriate
Never use compression bandages

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14
Q

What is basal cell carcinoma?

A

Tumour of basal keratinocytes (deepest part of epidermis)

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15
Q

How common is basal cell carcinoma?

A

Most common malignant skin cancer
Tends to present later in life
Less aggressive and metastatic than SCC

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16
Q

What can increase your risk of developing basal cell carcinoma?

A

UV exposure
Skin type 1 - skin that burns and doesn’t tan
Ageing

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17
Q

How does basal cell carcinoma present?

A

Non-pigmented in 95%
Occasionally resembles melanoma when pigmented
May ulcerate - when does called rat ulcer
Rarely metastasises but is locally destructive
Slow growing
Locally invasive
Border of ulcerated lesions raised with pearly appearance
Slowly enlarging, shiny nodule on head and neck area, which bleeds following minor trauma and does not heal
Slowly causes local tissue destruction if not treated

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18
Q

How is basal cell carcinoma treated?

A

Surgically excised with wide borders and histology to ensure clear and adequate tumour margins
Superficial BCCs can be managed with non-surgical treatment - cryotherapy, phytodynamic therapy
Radiotherapy in those unable to tolerate surgery

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19
Q

What is cellulitis?

A

Bacterial infection of deep sub-cutaneous tissues

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20
Q

Where does cellulitis mainly affect?

A

Preferentially involves lower extremities

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21
Q

What can cause cellulitis?

A

Group A beta-haemolytic streptococcus - streptococcus pyogenes most common
Staph aureus
MRSA

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22
Q

What can increase your risk of developing cellulitis?

A 
Lymphoedema
Leg ulcer
Immunosuppression
Traumatic wounds
Athletes foot
Leg oedema
Obesity
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23
Q

What is the pathology of cellulitis?

A

Spreads proximally
Other sites that may be infected include abdomen, perianal and periorbital areas
Can also affect just one side of face

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24
Q

How does cellulitis present?

A

Local inflammation - spreading proximally
Hot erythema in affected area
Poorly demarcated margins, swelling, warmth, tenderness
Occasionally will blister especially is oedema prominent
Systemically unwell with pyrexia

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25
Q

How is cellulitis diagnosed?

A

Clinical
Skin swabs usually negative unless taken from broken skin
Serological testing to confirm streptococcal infection

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26
Q

How is cellulitis treated?

A

Antibiotics eg phenoxymethylpenicillin or flucloxacillin
Erythromycin if penicillin allergic
If infection widespread - antibiotics IV for 3-5 days followed by at least 2 weeks of oral therapy
If recurrent, prophylaxis low-dose antibiotics twice daily

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27
Q

What is eczema?

A

Breakdown of skin due to thinning of stratum corneum - meaning there is an increased risk of inflammation

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28
Q

How common is eczema?

A

Genetically complex, familial disease with strong maternal influence
In developed world, 10% of population
Up to 40% will experience an episode of eczema during lifetime
High prevalence in 15-30% children and 2-10% adults
Nearly always itchy

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29
Q

How is eczema classified?

A

Endogenous (atopic) - usually due to hypersensitivity (asthma and food allergy also atopic)
Exogenous - contact dermatitis usually precipitated by chemicals, sweat and abrasives

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30
Q

What can increase your risk of getting eczema?

A

FHx - with faulty gene that codes for filaggrin

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31
Q

What is the pathophysiology of eczema?

A

Not clearly understood
Caused by damaged filaggrin which is skin barrier protein which, if damaged will increase risk of eczema, as exogenous allergens will be able to invade more easily thereby resulting in inflammation
Exacerbated by chemicals, detergents and woollen clothes
Infection either in skin or systemically can lead to an exacerbation, possible by a super-antigen effect

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32
Q

How does eczema present?

A

Commonly found on face and flexure surfaces of limbs
Itchy, erythematous and scaly patches especially in flexure of elbows, knees, ankles, wrists and around neck
Increased dryness of skin
In infants, eczema often starts on cheeks before spreading to the ybody
Very acute lesions may weep or exude and can show small vesicles
Recurrent S aureus infections may be common

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33
Q

How is atopic dermatitis diagnosed?

A 
Clinical diagnosis
High serum IgE in 80%
Must have itchy skin condition in past 6m
Plus 3 or more of
- History of involvement of skin creases
- Personal history of asthma or hay fever
- History of generally dry skin
- Onset in childhood
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34
Q

How is eczema treated?

A

Education and explanation
Avoidance of irritants/allergens
Keep nails short in children so less damage
Complete emollient therapy - E45 cream - application every 4hrs 3/4 times per day 250-500g per week for child, 500-750g per week adult
Topical therapies - topical corticosteroids or topical calcineurin inhibitors
Oral immune modulators

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35
Q

What is malignant melanoma?

A

Malignant tumour of melanocytes

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36
Q

How common is malignant melanoma?

A

Commonly affects younger patients - thus early diagnosis essential
Responsible for most deaths caused by cancer in men
Incidence rising thought to be due to excessive sun exposure and sunburn in childhood
Common in more affluent people and those who drink alcohol heavily - combination of sun exposure and alcohol is carcinogenic to melanocytes

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37
Q

What are the different classifications of malignant melanoma?

A

Superficial spreading malignant melanoma
Nodular - most aggressive
Lentigo maligna - usually on face
Acral - restricted to palms/soles

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38
Q

What risk factors may increase your risk of developing malignant melanoma?

A 
UV exposure - sun tanning and sunbed use
Red hair
High density freckles
Skin type 1 - skin tends to burn and not tan
Atypical moles
Multiple melanocytic naevi
Sun sensitivity
Immunosuppression
FHx
Pale skin
39
Q

How does malignant melanoma present?

A

Commonest site in men = back/chest
Commonest site in women = lower legs
>95% melanomas show v dark colour, black or almost black in part of lesion
ABCDE symptoms and criteria
A - asymmetrical shape
B - border irregularity
C - colour irregularity
D - diameter > 6mm
E - elevation/evolution - change of lesion
Major signs - change in size, shape or colour (usually darkening)
Minor signs - inflammatory, crusting or bleeding, sensory change, itching

40
Q

Name 3 differential diagnoses for malignant melanoma

A

Benign pigmented naevus
Seborrhoeic wart
Pyogenic granuloma

41
Q

How is malignant melanoma treated?

A

Surgical excision curative in early cases
Very wide excision does not improve survival
Has limited sensitivity to radiotherapy so has limited role
For metastatic disease - removal of regional lymph nodes, isolated limb perfusion, radiotherapy, immunotherapy, and chemotherapy
Distant metastases commonest to lung, liver, CNS - but any tissue/organ can be affected

42
Q

What is the prognosis for malignant melanoma?

A 
Thin lesions < 1mm have best prognosis
If over 60, then lower 5yr survival rate
Generally, female advantage in prognosis
Ulceration usually late sign
Poor prognosis if present on trunk vs limb
43
Q

What is necrotising fasciitis?

A

Deep-seated infection of subcutaneous tissue that results in a fulminant and spreading destruction of fascia and fat but initially spares the skin (eventually skin is also destroyed)
High mortality

44
Q

What are the classifications of necrotising fasciitis?

A

Type 1 - caused by a mixture of aerobic and anaerobic bacteria following an abdominal surgery or in diabetes
Type 2 - caused by group A haemolytic step

45
Q

What can increase your risk of getting necrotisin fasciitis?

A

Abdominal surgery

Immunosuppression

46
Q

How does necrotising fasciitis present?

A

Severe pain that is out of proportion to skin findings at initial site of infection that is rapidly followed by tissue necrosis
Infection tracks rapidly along tissue planes, causing spreading erythema, pain and sometimes crepitus (crackling sound when joints move)
In patients with fever, toxicity and pain that is out of proportion to skin findings - necrotising fasciitis should be suspected
Multi-organ failure common and mortality high

47
Q

How is necrotising fasciitis diagnosed?

A

Soft tissue gas seen on x-ray
Raised CRP
Very raised WCC
If necrotising fasciitis suspected then it must be treated aggressively and promptly

48
Q

How is necrotising fasciitis treated?

A

Aggressive and prompt antibiotics for confirmed group A streptococci - type 2 - IV benzylpenicillin and IV clindamycin
If unknown cause - broad spectrum IV antibiotics with IV mentroidazole
Urgent surgical exploration with extensive debridement or amputation if necessary

49
Q

What are neuropathic ulcers?

A

Often painless

Seen over pressure areas of feet such as metatarsal heads or heels owing to repeated trauma

50
Q

Where are neuropathic ulcers most commonly seen?

A

Diabetes and neurological disease due to peripheral neuropathy
Leprosy common cause in some developing countries

51
Q

How do neuropathic ulcers present?

A

Tend to have variable size and may be surrounded by callus

Warm skin and normal peripheral pulses

52
Q

How are neuropathic ulcers treated?

A

Keep ulcer clean and remove pressure or trauma from affected area
Correctly fitting shoes and specialist podiatrist help for diabetics

53
Q

What is psoriasis?

A

Chronic, inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration
Opposite to eczema as hyper-proliferation of skin leading to thickened plaques

54
Q

How common is psoriasis?

A

Affects around 2% population
Onset at any age - uncommon in children, peak prevalence in early adulthood, second peak between 50-60yrs
Occurs equally in men and women

55
Q

What can cause psoriasis?

A

Polygenic
Dependent on certain environmental triggers - infection with group A streptococcus, drugs, UV light, high alcohol use, stress

56
Q

What can increase your risk of getting psoriasis?

A

FHx

57
Q

What is the pathology of psoriasis?

A

T lymphocyte driven disorder to an unidentified antigen
T cell activation results in upregulation of Th1 types T cell cytokines eg interferon-gamma, interleukins, growth factors and adhesion molecules
Upregulation of these cytokines results in increased uncontrolled hyperproliferation of the keratinocytes in the epidermis with an increase in epidermal cell turnover rate

58
Q

How does psoriasis present?

A

Chronic plaque psoriasis - most common
- Well demarcated disc-shaped, salmon-pink slivery plaques on exterior surface of limbs, particularly elbows and knees
- Scalp involvement common and most seen at hair margin
- Thickened epidermis
- New plaques of psoiasis occur at sites of skin trauma
Flexural psoriasis
- Tends to occur later in life
- Well demarcated red, glazed, non-scaly plaques
- Scaling absent
- Confined to flexures
- Can be mistaken for candida intertrigo
Guttate psoriasis
- Most commonly in children and young adults
- Generalised, concentrating on trunk, upper arms and legs
- Explosive eruption of very small circular or oval plaques appears over trunk about 2 wks after streptococcal sore throat
Palmoplantar psoriasis
- Thickening of palms and soles

59
Q

How is psoriasis treated?

A

Chronic plaque psoriasis - emollients, topical vit D analogues, topical corticosteroids, topical retinoids, UVB, coal tar, anti-mitotic
Flexural - topical corticosteroids, topical vit D analogue
Guttate - topical corticosteroid, UVB, coal tar
Palmoplantar - emollients, keratolytic agents, potent topical corticosteroids, phototherapy with UVA, oral retinoid
Anti-TNF biologics

60
Q

What is squamous cell carcinoma?

A

Locally invasive, malignant tumour of squamal keratinocytes

More aggressive than basal cell carcinoma and has high metastatic potential - particularly to lymph nodes

61
Q

How common is SCC?

A

Tends to present in later life

2nd most common skin cancer just below basal cell carcinoma

62
Q

What is in situ SCC called?

A

Bowen’s disease

63
Q

What can increase your risk of getting SCC?

A

UV exposure

Chronic inflammation eg wound scars and immunosuppression

64
Q

How does SCC present?

A

Most common on sun-exposed sites in later life
Lesions often keratotic, rather than ill-defined nodules that may ulcerate
They can grow very rapidly
Ulcerates lesions on the lower lip or ear are often more aggressive
Examination of regional lymph nodes essential to look for metastases

65
Q

How is SCC treated?

A

Surgical excision with minimal margin of 5mm

Radiotherapy is also used - especially non-resectable

66
Q

What is cutaneous vasculitis?

A

Confirmed with skin biopsy

May be an isolated problem or part of a systemic disease with involvement of other organs

67
Q

What is the most common cutaneous vasculitis?

A

Leucocutoclastic vasculitis

68
Q

What can cause vasculitic ulcers?

A 
55-60% idiopathic
Drugs
Infection
Inflammatory disease
Malignant disease
69
Q

How do vasculitic ulcers present?

A

Cutaneous features which may erode and ulcerate are
- Haemorrhagic papules
- Pustules
- Nodules
- Plaques
Purpuric lesions do not blanch with pressure from a glass slide
Pyrexia and arthralgia common

70
Q

How are vasculitic ulcers treated?

A

Analgesia
Support stockings
Daspone (antibiotic) or prednisolone

71
Q

What are venous ulcers?

A

Loss of skin below knee or on leg or foot that takes more than 2 weeks to heal
Result of sustained venous hypertension in superficial veins

72
Q

How common are venous ulcers?

A

Most common type of leg ulcer in developed world
Common in later life and are costly as they are often chronic and recurrent
Affect 1% of population over age 70
Most commonly found on lower leg in a triangle above the ankles

73
Q

What causes venous ulcers?

A

Sustained venous hypertension caused by

  • Incompetent valves in deep/perforating veins
  • Previous DVT
  • Athersclerosis
  • Vasculitis eg RA, SLE
74
Q

What are the risk factors for venous ulcers?

A

Varicose veins or DVT

75
Q

Why does hypertension cause venous ulcers?

A

Increased pressure causes extravasation of fibrinogen through the capillary walls, giving rise to perivascular fibrin deposition, which leads to poor oxygenation of surrounding skin

76
Q

How do venous ulcers present?

A 
Sloping and gradual edges
Ulcer large, shallow, irregular and exudative
Usually in minimal pain
Oedema of lower leg
Venous eczema
Brown pigment from haemosiderin
Varicose veins
Pulses present
Warm skin
77
Q

How are venous ulcers diagnosed?

A

Ankle brachial pressure index normal

Doppler ultrasound to exclude significant arterial disease

78
Q

How are venous ulcers treated?

A

High compression 4 layered bandage
Leg elevation to reduce venous hypertension
Antibiotics for infection

79
Q

Give an example of a topical corticosteroid

A

Hydrocortisone

Betamethasone

80
Q

What are topical corticosteroids used for?

A

Used in inflammatory skin conditions such as eczema to treat disease flares or to control chronic disease where emollients alone are ineffective

81
Q

How do topical corticosteroids work?

A

Have immunosuppressive, metabolic and mineralocorticoid effects
Effects are mostly limited to site of application
Can be prescribed as mild, moderate, strong and very strong

82
Q

What are the main adverse effects of corticosteroids?

A

Uncommon with mild/moderate topical corticosteroids
Stronger ones can cause skin thinning, stir, telangiectasia and contact dermatitis
Can cause perioral dermatitis and acne on the face
Withdrawal can cause rebound worsening initially
Contraindicated if infection present at site or other lesions

83
Q

Give an example of an emollient

A

Aqueous cream
Liquid paraffin
E45

84
Q

What are emollients used for?

A

As a topical treatment for dry and scaling skin disorders eg psoriasis
Used alone or in combination with topical corticosteroids in treatment of eczema
Can reduce skin dryness and cracking in psoriasis

85
Q

How do emollients work?

A

Help replace water content in dry skin
Contains oils or paraffin based products that help to soften the skin and can reduce water loss by protecting against evaporation from the skin surface
Can be used as a soap substitute or moisturiser

86
Q

What are the main adverse effects of emollients?

A

Main tolerability issue is that they cause greasiness of skin and can exacerbate acne on face

87
Q

Give an example of a keratolytic

A

Salicylic acid
Lactic acid
Allantoin

88
Q

What are keratolytics used for?

A

Removal of warts and other lesions of excess skin growth
Treatment of dry skin
Treatment of acne

89
Q

How do keratolytics work?

A

For lesions - keratolytic therapy thins the skin on and around lesion and causes outer layer of skin to loosen and shed
Can also be used to soften keratin in skin, which improves the skin’s moisture binding capacity which is beneficial in dry skin conditions
For acne, it causes cells of epidermis to shed more rapidly which opens clogged pores and neutralises bacteria within
Produces anti-inflammatory effects by suppressing cyclo-oxygenase

90
Q

What are the main adverse effects of keratolytics?

A

At very high concentrations, can produce chemical burns on skin and damage pores
Hypersensitivity reactions can occur
Sun protection should be used with treatment as makes skin more susceptible to UV damage

91
Q

Give an example of a retinoid

A

Acitretin

Tazarotene

92
Q

What can retinoids be used for?

A

Range of inflammatory skin disorders such as severe cystic acne and disorders of skin turnover such as psoriasis
Can also be used in skin cancers

93
Q

How do retinoids work?

A

Incompletely understood - show to induce apoptosis in various cells especially sebaceous gland cells
May amplify production of certain skin proteins that reduce sebum production and exhibit an antimicrobial effect

94
Q

What are the main adverse effects of retinoids?

A

Most common adverse effect is transient worsening of acne, dry and fragile skin, increased susceptibility to sunburn and anaemia
Rarely may cause myalgia, headaches and severe depression
Contraindicated in pregnancy as is severe teratogen

Phase 2a medicine (13 decks)

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