Dermatology Flashcards

(52 cards)

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?

25
How does basal cell carcinoma present?
- 'Shiny, pearly nodule' | - Rarely ulcerates/metastasises
26
How does squamous cell carcinoma present?
- Ill-defined nodule that ulcerates and grows rapidly - More aggressive than BCC - can metastasise - Premalignant features: solar keratoses and Bowen's disease
27
How does malignant melanoma present?
- 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
Describe the management of basal cell carcinoma
Surgical excision
29
Describe the management of squamous cell carcinoma
Surgical excision
30
Describe the investigation of malignant melanoma
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
Describe the management of malignant melanoma
- If local disease: surgical excision | - If metastatic: radiotherapy, immunotherapy
32
Where are the most common site for venous/arterial/neuropathic ulcers?
Venous: - Medial gaiter region (above medial malleolus) Arterial: - Anterior shin - Foot and ankle Neuropathic: - Foot (especially big toe) and ankle
33
What are the risk factors for an arterial ulcer?
- Arterial disease (atherosclerosis) and its associated risk factors
34
How does an arterial ulcer present?
- Small, punched-out appearance, well defined edges - Necrotic base - Painful - Reduced peripheral pulses - ABPI (ankle brachial pressure index) <0.8
35
How is an arterial ulcer investigated?
- Doppler studies
36
How is an arterial ulcer managed?
- Vascular reconstruction | - Amputation if necessary
37
What are the risk factors for a venous ulcer?
- Varicose veins | - DVT
38
How does a venous ulcer present?
- Large, shallow, irregular edges, exudative - Normal peripheral pulses - ABPI >0.8
39
How is a venous ulcer managed?
Compression bandaging
40
What are the risk factors for a neuropathic ulcer?
- Diabetes mellitus | - Neurological disease
41
How does a neuropathic ulcer present?
- Variable size | - May be surrounded by a callus (found at pressure sites)
42
How is a neuropathic ulcer managed?
- Surgical debridement - Control DM - Advise appropriate footwear - Podiatry
43
What is cellulitis?
Bacterial infection of the deep subcutaneous tissue
44
Which types of bacteria most commonly cause cellulitis?
- Streptococcus pyogenes | - Staphylococcus aureus
45
List some risk factors which may lead to cellulitis
- Immunosuppression - Trauma - Ulcers
46
How does cellulitis present?
5 cardinal signs of inflammation: - Rubor (redness) - Calor (warm) - Tumor (swelling) - Dolor (pain) - Loss of function May be systemically unwell
47
How is cellulitis managed?
Abx: either Flucloxacillin or Benzylpenicillin
48
What is necrotising fasciitis?
Bacterial infection of the deep fascia and tissue necrosis
49
Which types of bacteria most commonly cause necrotising fasciitis?
Group A haemolytic strep
50
List some risk factors which may lead to necrotising fasciitis
- Immunosuppression | - Abdominal surgery
51
How does necrotising fasciitis present?
- Severe pain - Tissue necrosis - Systemically unwell
52
How is necrotising fasciitis managed?
- Surgical debridement | - IV Abx