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Phase 2a > Dermatology Diseases > Flashcards

Dermatology Diseases Flashcards

1
Q

What are the two types of eczema?

A

Atopic eczema and contact dermatitis

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2
Q

What is the clinical presentation of eczema?

A
  • Itchy red rash
  • Crusting, scaling and oozing
  • Atopic eczema= Normally in skin folds such as elbow and knee
  • Contact dermatitis= Sharply demarcated skin inflammation
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3
Q

What is the pathophysiology of atopic eczema?

A

A defect om the epithelial barrier (Thinning of stratum corneum due to damaged fillagrin) which allows irritants in to come into contact with T helper 2 cells (CD4) lymphocytes. This leads to inflammation.

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4
Q

What is the aetiology of atopic eczema?

A

Genetics and exacerbating elements

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5
Q

What is the epidemiology of atopic eczema?

A

Most common form

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6
Q

What is the pathophysiology of contact dermatitis?

A

Chemical irritants lead to a type IV hypersensitivity reaction

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7
Q

What is the aetiology of contact dermatitis?

A

Exposure to irritants

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8
Q

What is the epidemiology of contact dermatitis?

A

Women more than men

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9
Q

What is the treatment path of eczema?

A
  1. Avoid irritants
  2. Emollient therapy (E.G. E45)
  3. Topical corticosteroids
  4. Topical calcineurin inhibitor
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10
Q

How much emollient should be applied for eczema?

A

Apply 3-4 times a day

  • 250-500g/week for child
  • 500-750g/week for adult
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11
Q

What topical corticosteroids can be used in eczema?

A

Mild= Hydrocortisone
Moderate= Clobetasol butyrate
Potent= Flucinonide
Very potent= Clobetasol propinate

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12
Q

How is eczema diagnosed?

A

High serum IgE in 80%, and must have itchy skin condition in last 6 months. Plus 3 or more of-

  1. History of involvement of skin creases
  2. History of asthma/ Hay fever
  3. Generally dry skin
  4. Onset in childhood
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13
Q

What are possible complications of eczema?

A

Scratching will lead to broken skin, which then causes opportunistic infection.

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14
Q

What is the most common malignant skin cancer?

A

Basal cell carcinoma

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15
Q

Briefly describe the pathophysiology of basal cell carcinoma

A

Slow growing, locally malignant epidermal tumour. Thought to arise from hair follicles. Infiltrates local tissues through slow irregular growth of fingerlike outgrowths

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16
Q

What are the risk factors for basal cell carcinoma ?

A

UV exposure
Skin type 1: skin that burns and doesn’t tan
Aging

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17
Q

How is basal cell carcinoma diagnosed?

A

Biopsy

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18
Q

What is the clinical presentation of basal cell carcinoma ?

A

Non-pigmented in 95%
Border of ulcerated lesions is raised with peachy appearance
Majority occur in elderly on head and neck
Slowly enlarging, shiny nodule, which bleeds following minor trauma
Slowly causes local tissue destruction
Slowly invasive= Rarely metastasises

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19
Q

How is basal cell carcinoma treated?

A

Surgically excised with white borders and histology to ensure clear and adequate tumour margins
Superficial BCCs can be managed with non surgical treatment= Cryotherapy, photodynamic therapy
Radiotherapy in those unable to tolerate surgery

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20
Q

What are some complications of basal cell carcinoma ?

A

Maetastasis are rare (5%) but very hard to treat. Damage occurs if local spread reaches other structures

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21
Q

What is bowen’s disease?

A

In situ squamous cell carcinoma confined to the epidermis

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22
Q

What is the epidemiology of squamous cell carcinoma?

A

2nd most common skin cancer, just below basal cell carcinoma= 20% of non-melanoma skin cancer

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23
Q

What are the risk factors for squamous cell carcinoma?

A

Age
UV exposure
Chronic inflammation e.g. wound scars

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24
Q

What is the clinical presentation for squamous cell carcinoma?

A

Tends to present in later life
Most common on sun-exposed sites
Lesions are often keratoic, ill defined nodules that may ulcerate
They can grow rapidly
Ulcerations on lower lip or ear are more aggressive
Examinations of the regional lymph nodes is essential to look for metastasis

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25
Q

How is squamous cell carcinoma diagnosed?

A

Biopsy

Examine regional lymph nodes to look for metastasis

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26
Q

How is squamous cell carcinoma treated?

A

Surgical excision with minimal margin of 5mm

Radiotherapy is also used

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27
Q

What are some complications of squamous cell carcinoma?

A

Metastasis are rare (5%) but hard to treat

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28
Q

What is cellulitis?

A

A poorly demarcated bacterial infection of dermis and sub-cutaneous tissue

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29
Q

What is the epidemiology of cellulitis?

A

Preferentially involves lower extremities

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30
Q

What is the aetiology of cellulitis?

A
  • Group A beta-haemolytic strep e.g. S. Pyogenes (Most common)
  • Staph. Aureus
  • MRSA
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31
Q

What are the risk factors for cellulitis?

A
  • Lymphoedema
  • Leg Oedema
  • Obesity
  • Leg Ulcer
  • Immunosuppression
  • Traumatic Wounds
32
Q

Briefly explain the pathophysiology of cellulitis?

A

Typically affects lower leg or arm, and spreads proximally. Other sites that may be affected include the abdomen, perianal and periorbital areas. Can also affect one side of face

33
Q

What are the clinical features of cellulitis?

A
  • Local inflammation with proximal spreading
  • Erythema in affected area with poorly demarcated margins, warmth, swelling and tenderness
  • Occasionally will blister if oedema is severe
  • Systemically unwell with pyrexia
34
Q

How is cellulitis treated?

A
  • Rest, analgesia and elevate limb
  • Antibiotics e.g. oral flucloxacillin or oral phenoxymethylpenicillin
  • Oral erythromycin if penicillin allergic
  • If widespread infection, antibiotics IV for 3-5 days, then 2 weeks oral therapy
  • If recurrent, prophylaxis low dose antibiotics
35
Q

How is cellulitis diagnosed?

A
  • Clinical
  • Skin swabs are usually negative unless taken from broken skin
  • Serological testing to confirm a strep infection
36
Q

What are some possible complications from cellulitis?

A
  • Abscess

- Gangrene

37
Q

What is the epidemiology of malignant melanoma?

A

Commonly affects younger patients
Responsible for the most deaths caused by cancer in men
Incidence is rising due to excessive sun exposure
Common in affluent people and those who excessively drink

38
Q

What are the risk factors for malignant melanoma?

A 
UV exposure
Red hair
High density freckles
Skin type 1
Atypical moles
Immunosuppression
Multiple melanocytic naevi
Family history
39
Q

What are the four types of malignant melanoma?

A

Superficial spreading
Nodular
Lentigo maligna= On face
Acral= On palms/ soles

40
Q

What is the clinical presentation of malignant melanoma?

A 
Commonest site in men is back/chest
Commonest site in women is lower legs
ABCDE
- Asymmetrical shape
- Border irregularity
- Colour irregularity
- Diametre > 6mm
- Elevation/ evolution
Also crusting and bleeding, inflammation, sensory changes, itching
41
Q

What is the differential diagnosis of malignant melanoma?

A

Benign pigmented naevus, seborrhoeic wart, pyogenic granuloma

42
Q

How is malignant melanoma treated?

A
  • Surgical excision is curative in early cases
  • Limited sensitivity to radiotherapy
  • Treatment of metastatic disease
43
Q

What is the prognosis of malignant melanoma?

A
  • Thin lesions have best prognosis
  • Generally there is a female advantage in prognosis
  • Poor prognosis if present on trunk vs limbs
44
Q

What is the most common variant of acne?

A

Acne. Vulgaris

45
Q

What is the epidemiology of acne?

A
  • Usually starts in adolescence
  • Often resolves in mid 20s
  • Affects face, back and chest
  • Prevalence ranges from 70-87% in teenagers
46
Q

Briefly explain the pathophysiology of acne

A

Narrowing of hair follicles due to hypercornification blocking the entrance to hair follicles. Results in increased sebum production. Some sebum becomes trapped in the narrow hair follicle. Sebum stagnates in pit of follicle where there’s no oxygen. This creates anaerobic conditions that allow p. acnes to multiply. P. acnes breaks down triglycerides in sebum into FFAs resulting in inflammation, irritation and attraction of neutrophils= Pus formation.

47
Q

What are the clinical features of acne?

A
  • Whiteheads= Closed comedones
  • Blackheads= Open comedones
  • Skin coloured papules
  • Inflammatory lesions usually occuring when the closed wall of comedones ruptures
  • Papules, pustules, or nodules
48
Q

How is acne diagnosed?

A
  • Clinical diagnosis
  • Skin swabs for culture
  • Hormone test in females
49
Q

How is mild acne treated?

A
  • Benzyl peroxide gel/cream
  • Topical antibiotics
  • Topical retinoids
50
Q

How is severe acne treated?

A
  • Oral tetracyclines e.g oral doxycycline, then oral minocycline
  • Hormone treatment= anti androgen treatment
51
Q

What is the epidemiology of psoriasis?

A
  • 2% of population

- Peak prevalence in early adulthood, 2nd peak at 50-60yrs

52
Q

Briefly explain the pathophysiology of psoriasis?

A

Psoriasis is a T lymphocyte driven disorder to an unidentified antigen T cell activation results in upregulation of Th1 types T cell cytokines. Upregulation of these cytokines results in increased uncontrolled hyperproliferation of the keratinocytes in the epidermis with an increase in epidermal turnover rate.

53
Q

List the types of psoriasis

A
  • Chronic plaque psoriasis
  • Flexural psoriasis
  • Guttate (Raindrop like) psoriasis
  • Palmoplantar psoriasis
  • Erythrodermic and pustular
54
Q

How is general psoriasis treated?

A
  • Topical= Reassurance and emollient. Possibly corticosteroids e.g. hydrocortisone
  • Vit D analogues= Clacipotriol cream
  • Phototherapy= Ultraviolet A radiation with photosensitising agent
  • Systemic therapy= Oral retinoic acid derivatives
  • Calcineurin inhibitors= tacrolimus (immunosuppressants)
  • Ultraviolet B
  • Coal tar
  • Anti-mitotic e.g. dithranol cream
55
Q

What is the epidemiology of neuropathic ulcers?

A

Most commonly found in diabetes and neurological disease due to peripheral neuropathy

56
Q

What are the clinical features of neuropathic ulcers?

A

Ulcers tend to have a variable size and may be surrounded by callus.

57
Q

How are neuropathic ulcers treated?

A
  • Keep ulcer clean and remove pressure or trauma

- Correctly fitting shoes and specialist podiatrist help for diabetics

58
Q

What is the epidemiology of arterial ulcers?

A

Commonly a history of claudication, hypertension, angina or smoking

59
Q

What are the risk factors for arterial ulcers?

A
  • Arterial disease e.g. atherosclerosis
  • Smoking
  • Hypercholesterolaemia
  • Diabetes mellitus
60
Q

How are arterial ulcers diagnosed?

A
  • Doppler ultrasound will confirm arterial disease

- Ankle brachial pressure index suggest arterial insufficiency

61
Q

What are the clinical features of arterial ulcers?

A
  • Typically present as punch-out ulcers higher up the leg or on the feet
  • Intense pain
  • Leg is cold and pale
  • Absent peripheral pulses
  • Ulcer is small, sharply defined and necrotic
62
Q

How are arterial ulcers treated?

A
  • Keep ulcer clean and covered
  • Analgesia e.g. ibuprofen
  • Vascular reconstruction if appropriate
63
Q

What is the epidemiology of venous ulcers?

A
  • Venous ulcers are the most common type of leg ulcer
  • Common in later life
  • Affect 1% of population over 70 yrs
  • Most commonly found on lower leg
64
Q

What causes venous ulcers?

A
  • Sustained venous hypertension = Previous DVT, incompetent leg vein valves, atherosclerosis, vasculitis
65
Q

What are the clinical features of venous ulcers?

A
  • Sloping and gradual edges
  • Ulcer is large, shallow, irregular and exudative
  • Usually minimal pain
  • Oedema
  • Venous eczema
  • Brown pigmentation
  • Varicose veins
66
Q

How are venous ulcers diagnosed?

A
  • Ankle brachial pressure index is normal

- Doppler ultrasound to exclude significant arterial disease

67
Q

How are venous ulcers treated?

A
  • High compression 4 layered bandage
  • Leg elevation
  • Antibiotics if infected
  • Analgesia
  • Support stockings for life
68
Q

A child presents with a weeping rash around the chin and mouth. What is it likely to be, and what pathogen is associated?

A

Impetigo

Strep Pyogenes

69
Q

How would you treat impetigo?

A

Oral flucloxacillin

70
Q

What is necrotising fasciitis?

A

A deep seated infection of the subcut tissue that results in a fulminant and spreading destruction of fascia and fat, but intially spares the skin

71
Q

What are the 2 types of necrotising fasciitis?

A
  • Type one; Anaerobic and aerobic bacteria following abdominal surgery or in diabetics
  • Type 2; Group A beta-haemolytic strep (S. Pyogenes)
72
Q

What are the clinical features of necrotising fasciitis?

A
  • Severe pain that is out of proportion to skin findings
  • Infection track rapidly along the tissue planes, causing spreading erythema , pain and crepitus
  • Fever, toxicity
  • Multi organ failure
73
Q

What are the risk factors for necrotising fasciitis?

A
  • Abdominal surgery

- Immunosuppression

74
Q

How is necrotising fasciitis diagnosed?

A

Soft tissue gas seen on X ray

Raised CRP and WCC

75
Q

How is necrotising fasciitis treated?

A
  • Aggressive and prompt antibiotics for confirmed group A streptococci= Benzylpenicillin and clindamycin
  • If unknown aetiology= IV metronidazole and broad spectrum antibiotics

Phase 2a (31 decks)

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