Dermatology Flashcards

1
Q

Describe the pathological processes which result in acne

A
  • Increased sebum production by sebaceous glands
  • Blockage of pilosebaceous units
  • Follicular epidermal hyperproliferation
  • Infection with Propionibacterium acnes
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2
Q

How does acne vulgaris present?

A

Features of acne vulgaris:

  • Open comedones (blackheads)
  • Closed comedones (white heads)
  • Inflammatory papules and pustules
  • Hypertrophic/keloid scarring
  • Hyperpigmentation
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3
Q

Conservative management of acne vulgaris

A
  • Avoid overwashing

- Avoid picking

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4
Q

Pharmacological management of acne vulgaris

A

1st line

  • Topical benzoyl peroxide
  • Topical clindamycin/erythromycin
  • Topical retinoids

2nd line:

  • Low dose oral antibiotics, e.g. erythromycin, tetracycline
  • Hormonal therapy in women (OCP)

3rd line:
- Oral retinoids (TERATOGENIC!!)

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5
Q

What is the other name given to ‘eczema’?

A

Dermatitis

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6
Q

What are the types of eczema?

A

Atopic eczema and contact dermatitis

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7
Q

What causes atopic eczema?

A

Atopy - hereditary predisposition to developing an allergic reaction (eczema, allergic rhinitis, asthma)

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8
Q

Describe the pathological processes which result in eczema

A
  • Abnormal epithelial barrier function - allows irritant agents to penetrate and reach immune cells
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9
Q

What are the clinical features of atopic eczema?

A
  • Itchy, red, scaly patches

- Commonly presents in flexures (in infants, often presents on the face)

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10
Q

Conservative management of atopic eczema

A
  • Avoid irritants/exacerbating factors, e.g. strong chemicals, dog/cat fur
  • Avoid scratching
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11
Q

Pharmacological management of atopic eczema

A
  • Regular use of emollients
  • Antihistamines and topical corticosteroids in attacks: mild steroids (e.g. hydrocortisone) used on face and more potent steroids (e.g. betamethasone) used on rest of body
  • Immunosuppressants, e.g. ciclosporin, and phototherapy if severe
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12
Q

Complications of eczema

A

Secondary Staph. aureus infection due to broken skin - treat with antibiotics

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13
Q

Distinguishing contact dermatitis from atopic eczema from clinical features…

A
  • Itchy, red, scaly rash (same as atopic eczema)

BUT

  • Unusual pattern of rash (i.e. not in flexures) and clear cut demarcation/odd-shaped rash
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14
Q

Investigations for contact dermatitis

A

Patch testing may be necessary to identify particular allergen

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15
Q

Conservative management of contact dermatitis

A

Avoid allergen

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16
Q

Pharmacological management of contact dermatitis

A
  • Antihistamines and topical corticosteroids used in attacks - mild steroids (e.g. hydrocortisone) used on face and more potent steroids (e.g. betamethasone) used on rest of body
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17
Q

When does psoriasis most commonly present?

A

Late teens/early twenties and 50s/60s

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18
Q

What causes psoriasis?

A

Combination of genes and environmental triggers: e.g. group A strep infection, high alcohol consumption, stress

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19
Q

Types of psoriasis…

A
  • Chronic plaque psoriasis (MOST COMMON)
  • Flexural/inverse psoriasis
  • Guttate (‘raindrop’-like pattern)
  • Erythrodermic and pustular psoriasis
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20
Q

How does chronic plaque psoriasis present?

A
  • Well-demarcated, red plaques covered with silvery scales
  • Commonly affects extensor surfaces and scalp
  • May affect sites of sites of skin trauma (Koebner phenomenon)

Other associated clinical features:

  • Nail changes: pitting/onycholysis/discoloration
  • Psoriatic arthritis
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21
Q

Describe the pathological processes which cause psoriasis

A
  • Keratinocyte hyperproliferation

- Infiltration of inflammatory cells

22
Q

Pharmacological management of psoriasis

A

1st line:

  • Topical vitamin D analogues, e.g. calcipotriol
  • Topical corticosteroids
  • Coal tar preparations
  • Topical retinoids

2nd line:
- Phototherapy

3rd line:

  • Immunosuppressants, e.g. ciclosporin, methotrexate
  • Oral retinoids
23
Q

What are the three types of skin cancer we need to know?

A
  • Basal cell carcinoma
  • Squamous cell carcinoma
  • Malignant melanoma
24
Q

What is the main cause of skin cancer?

A

Sun exposure

25
Q

How does basal cell carcinoma present?

A
  • ‘Shiny, pearly nodule’

- Rarely ulcerates/metastasises

26
Q

How does squamous cell carcinoma present?

A
  • Ill-defined nodule that ulcerates and grows rapidly
  • More aggressive than BCC - can metastasise
  • Premalignant features: solar keratoses and Bowen’s disease
27
Q

How does malignant melanoma present?

A
  • Most common sign is appearance of a new mole or a change in an existing mole
  • Most serious from of skin cancer - metastasises early
28
Q

Describe the management of basal cell carcinoma

A

Surgical excision

29
Q

Describe the management of squamous cell carcinoma

A

Surgical excision

30
Q

Describe the investigation of malignant melanoma

A

ABCDE criteria to distinguish benign from malignant moles:

Asymmetry of mole
Border irregularity
Colour variation
Diameter
Elevation

Then the Glasgow 7 point checklist is used for guidance on referral:

  • Change in size (2 points)
  • Change in shape (2 points)
  • Change in colour (2 points)
  • Diameter >6mm (1 point)
  • Inflammation (1 point)
  • Oozing or bleeding (1 point)
  • Mild itch/altered sensation ( 1 point)

If points add up to 3 or more, urgent suspected cancer pathway referral (2 week wait)

Investigation involves CT scan to check for metastases

31
Q

Describe the management of malignant melanoma

A
  • If local disease: surgical excision

- If metastatic: radiotherapy, immunotherapy

32
Q

Where are the most common site for venous/arterial/neuropathic ulcers?

A

Venous:
- Medial gaiter region (above medial malleolus)

Arterial:

  • Anterior shin
  • Foot and ankle

Neuropathic:
- Foot (especially big toe) and ankle

33
Q

What are the risk factors for an arterial ulcer?

A
  • Arterial disease (atherosclerosis) and its associated risk factors
34
Q

How does an arterial ulcer present?

A
  • Small, punched-out appearance, well defined edges
  • Necrotic base
  • Painful
  • Reduced peripheral pulses
  • ABPI (ankle brachial pressure index) <0.8
35
Q

How is an arterial ulcer investigated?

A
  • Doppler studies
36
Q

How is an arterial ulcer managed?

A
  • Vascular reconstruction

- Amputation if necessary

37
Q

What are the risk factors for a venous ulcer?

A
  • Varicose veins

- DVT

38
Q

How does a venous ulcer present?

A
  • Large, shallow, irregular edges, exudative
  • Normal peripheral pulses
  • ABPI >0.8
39
Q

How is a venous ulcer managed?

A

Compression bandaging

40
Q

What are the risk factors for a neuropathic ulcer?

A
  • Diabetes mellitus

- Neurological disease

41
Q

How does a neuropathic ulcer present?

A
  • Variable size

- May be surrounded by a callus (found at pressure sites)

42
Q

How is a neuropathic ulcer managed?

A
  • Surgical debridement
  • Control DM
  • Advise appropriate footwear
  • Podiatry
43
Q

What is cellulitis?

A

Bacterial infection of the deep subcutaneous tissue

44
Q

Which types of bacteria most commonly cause cellulitis?

A
  • Streptococcus pyogenes

- Staphylococcus aureus

45
Q

List some risk factors which may lead to cellulitis

A
  • Immunosuppression
  • Trauma
  • Ulcers
46
Q

How does cellulitis present?

A

5 cardinal signs of inflammation:

  • Rubor (redness)
  • Calor (warm)
  • Tumor (swelling)
  • Dolor (pain)
  • Loss of function

May be systemically unwell

47
Q

How is cellulitis managed?

A

Abx: either Flucloxacillin or Benzylpenicillin

48
Q

What is necrotising fasciitis?

A

Bacterial infection of the deep fascia and tissue necrosis

49
Q

Which types of bacteria most commonly cause necrotising fasciitis?

A

Group A haemolytic strep

50
Q

List some risk factors which may lead to necrotising fasciitis

A
  • Immunosuppression

- Abdominal surgery

51
Q

How does necrotising fasciitis present?

A
  • Severe pain
  • Tissue necrosis
  • Systemically unwell
52
Q

How is necrotising fasciitis managed?

A
  • Surgical debridement

- IV Abx