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(SG) condensed phase 2a > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Define acne vulgaris

A

Disorder of pilosebaceous follicles in the face and upper trunk

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2
Q

How does acne vulgaris clinically present?

A

Greasy skin with comedones (blackheads), papules and pustules.

Presents just after puberty.

Face 99%, back 60%.

Nodulocystic acne: Severe, with cysts.

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3
Q

What is the pathophysiology of acne vulgaris like?

A

1: Higher than normal sebum production (due to androgens)
2: Excessive deposition of keratin (-> comedone formation)
3: Colonisation of the follicle by Propionibacterium acnes
4: Local release of pro inflammation.

These all contribute to blocked pilosebaceous follicles. Acute inflammation through chronic acne can cause scarring of the skin.

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4
Q

What causes acne vulgaris?

A

Some genetic link.

Onset of puberty brings hormonal changes (increase in androgens).

Infection by Propionibacterium acnes also contributes.

Diet has some unclear effect.

Also worsened by stress.

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5
Q

Epidemiology of acne vulgaris

A

Almost every teenager.

Moderate-severe in about 20% of people

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6
Q

Diagnostic test for acne vulgaris

A

Usually not required

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7
Q

Treatments for acne vulgaris

A

Usually self limiting. Teenagers very sensitive.

First line: Topical agents such as keratolytics (salicylic acid), benzoyl peroxide

Second line: Low dose oral tetracycline (doxycycline)

Third line: Topical retinoid (tretinoin)

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8
Q

Complications of acne vulgaris

A

Scarring, psychosocial factors

Retinoid: Very teratogenic, adverse effect from sunlight.

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9
Q

Sequelae of acne vulgaris

A

Recurrence

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10
Q

Define eczema (dermatitis)

A

Itchy rash of the folds of the elbow/knee

Itchy rash following contact with an irritant

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11
Q

Types of eczema (dermatitis)

A

Atopic

Exogenous (contact dermatitis)

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12
Q

How does atopic eczema clinically present?

A

Itchy red rash, scaling and oozing.

Usually in folds of knee and elbow and around the neck.

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13
Q

How does exogenous (contact dermatitis) eczema clinically present?

A

Sharply demarcated skin inflammation: red, crusting and scaling,

fissures,

hyperpigmentation (if chronic)

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14
Q

What is the pathophysiology of atopic eczema?

A

It is thought that a defect in epithelial barrier function allows antigenic material and irritants to penetrate and come into contact with immune cells -> immune response.

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15
Q

What is the pathophysiology of exogenous (contact dermatitis) eczema?

A

Chemical irritants -> very noticeably demarcated lesion (as if a splash of liquid).

Type IV sensitivity reaction.

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16
Q

What causes atopic eczema?

A

Strong genetic element.

Exacerbating elements include strong detergents, pet hair and some dietary antigens.

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17
Q

What causes exogenous (contact dermatitis) eczema?

A

Exposure to irritants (usually industrial solvents, can be nickel etc)

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18
Q

Epidemiology of atopic eczema

A

Most common form

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19
Q

Epidemiology of exogenous (contact dermatitis) eczema

A

Women more than men

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20
Q

Diagnostic tests for both types of eczema (dermatitis)

A

Clinical

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21
Q

Treatments for atopic eczema

A

Avoid irritants.

Regular emollients to hydrate.

Corticosteroids (hydrocortisone).

Calcineurin inhibitors: tacrolimus (immunosuppressive)

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22
Q

Treatments for exogenous (contact dermatitis) eczema

A

Avoid irritants.

Steroid cream.

Antipruritic creams.

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23
Q

Complications of atopic eczema

A

Scratching can cause exorciations -> broken skin -> Opportunistic S. aureus or herpes simplex infection

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24
Q

Define psoriasis

A

Chronic hyperproliferative disorder with well-demarcated red scaly plaques

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25
Q

Types of psoriasis

A

Chronic plaque psoriasis

Flexural psoriasis

Guttate

Erythrodermic and pustular

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26
Q

How does chronic plaque psoriasis clinically present?

A

Well demarcated, salmon-pink silvery scaling occur on the extensor surfaces of the limbs (elbow, knee).

Scalp involvement is common and most often seen at the hair margin.

Changes fingernail appearance; pitting, whitening, onycolysis and slight bleeding.

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27
Q

How does flexural psoriasis clinically present?

A

Red glazed non-scaly plaques, in flexures (groin, natal cleft, sub-mammary).

No satellite lesions.

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28
Q

How does guttate psoriasis clinically present?

A

Most common in children and young adults.

Explosive eruption of very small teardrop shaped plaques over the trunk 2 weeks after a streptococcal sore throat.

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29
Q

How does erythrodermic and pustular psoriasis clinically present?

A

Most severe.

Potentially life threatening.

Widespread intense inflammation of the skin.

Malaise, pyrexia, circulatory disturbances.

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30
Q

What shape does guttate psoriasis look like?

A

“Raindrop like”

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31
Q

What is the pathophysiology of psoriasis?

A

Abnormally excessive and rapid growth of epidermal layer, as a result of an inflammatory cascade causing premature maturation of keratinocytes.

These keratinocytes then secrete IL-1, IL-6 and TNF-a which signal further inflammation.

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32
Q

What causes chronic plaque psoriasis?

A

Polygenic, but dependent on specific triggers (infection, drugs such as lithium, high alcohol use, stress).

Potentially T lymphocyte driven.

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33
Q

What causes flexural psoriasis?

A

Heat

Trauma

Infection

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34
Q

What causes guttate psoriasis?

A

Genetic predisposition; associated with specific HLA alleles.

Triggered by streptococcal infection.

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35
Q

What causes erythrodermic and pustular psoriasis?

A

Usually occurs secondary to progressively worsening plaque psoriasis

OR precipitated by infection, tar, drugs or the withdrawal of corticosteroids

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36
Q

Epidemiology of chronic plaque psoriasis

A

Most common form.

16-22 and 55-60, double peak of onset.

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37
Q

Epidemiology of guttate psoriasis

A

Usually affects under 30’s

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38
Q

Diagnostic tests for all types of psoriasis

A

Clinical

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39
Q

Treatments for chronic plaque, flexural and guttate psoriasis -

A

Control, not cure.

Topical: reasurrance and emollient. Possibly corticosteroids.

Vitamin D analogues:

Calcipotriol Phototherapy:

Ultraviolet A radiation with photosensitising agent, oral or topical psoralen

Systemic therapy: oral retinoic acid derivatives (acitretin)

Calcineurin inhibitors: tacrolimus (immunosuppressive)

40
Q

Treatment for erythrodermic and pustular psoriasis

A

Bed rest,

emollients,

cool wet dressings,

nutritional support.

Avoid topical tar and phototherapy in the earlier phases

41
Q

Complications of erythrodermic and pustular psoriasis

A

Dehydration,

cardiac failure,

overwhelming infection,

death

42
Q

Sequelae of psoriasis

A

Recurrence

43
Q

Define skin ulceration

A

A sore on the skin accompanied by the disintergration of tissue

44
Q

Types of skin ulceration

A

Venous

Arterial

Neuropathic

Infective

Traumatic

Vasculitic

45
Q

How do skin ulcerations clinically present?

A

Open painful craters, often round, with layers of skin eroded.

Surrounding tissue swollen and tender.

Heals very slowly (healing in 12 weeks is considered acute).

Discharge can also be present.

Serous discharge suggests healing, purulent that it is infected.

46
Q

What is the pathophysiology of skin ulcerations?

A

Wagner’s ulcer grading: 1: Superficial

2: Ulcer deeper to subcutaneous tissue exposing soft tissue or bone
3: Abscess formation underneath
4: Gangrene of part of tissues, limb or foot
5: Gangrene of entire area or foot

47
Q

What causes skin ulcerations?

A

Various causative factors.

Mainly impaired blood circulation, particularly in chronic wounds, such as in bed sores.

Other causes include bacterial/viral infection and possibly cancers.

Venous leg ulcers: Due to impaired circulation or a blood flow disorder.

48
Q

Epidemiology of skin ulcerations

A

More common in the elderly

49
Q

Diagnostic tests for skin ulcerations

A

Culture of discharge.

Edge biopsy.

50
Q

Treatment for skin ulcerations

A

Typically to avoid infection, remove discharge and ease pain.

Leg ulcers: Compression stockings

51
Q

Complications of skin ulcerations

A

Infection

52
Q

Sequelae of skin ulcerations

A

Recurrence

53
Q

Skin cancer - define malignant melanoma

A

Cancer of melanocytes

54
Q

Skin cancer - define squamous cell carcinoma

A

Cancer of the squamous cells

55
Q

Skin cancer - define basal cell carcinoma

A

Cancer of the basal cells

56
Q

Skin cancer - how does malignant melanoma clinically present?

A

Distinguished from moles by;

Asymmetry

Border irregularity

Colour variation

Diameter

Elevation (Evolving?)

57
Q

Skin cancer - how does squamous cell carcinoma clinically present?

A

Ill defined nodules that ulcerate easily and grow rapidly.

Keratotic (hard raised edges).

Sun exposed sites.

58
Q

Skin cancer - how does basal cell carcinoma clinically present?

A

Sun exposed areas.

Early: Small, translucent or pearly and have raised areas with telangiectasia.

Later: Indurated edge and ulcerated centre.

59
Q

Skin cancer - basal cell carcinoma description note

A

‘Rodent ulcer’

60
Q

Pathophysiology of malignant melanoma

A

Melanocytes in the basal layer of the epidermis.

Spread out within the epidermis (if within epidermis then melanoma in situ, if grown through the dermis then invasive).

Metastases can occur virtually anywhere.

61
Q

Pathophysiology of squamous cell carcinoma

A

Arises from the keratinising cells of the epidermis or its appendages.

Locally invasive, and has the potential to metastasise (rarely).

62
Q

Pathophysiology of basal cell carcinoma

A

Slow growing, locally invasive malignant epidermal tumour.

Thought to arise from hair follicles.

Infiltrates local tissues through slow irregular growth of fingerlike outgrowths.

63
Q

What is the cause of malignant melanoma?

A

Strong association with sun exposure.

Those with over 100 moles (or >2 atypical) have 5-20 fold increased risk.

64
Q

What is the cause of squamous cell carcinoma?

A

Strong association with sunlight.

Immunosuppression associated with multiple tumours.

65
Q

What are the causes of basal cell carcinoma?

A

Sun exposure.

Genetic predisposition.

Increasing age,

male sex are RF.

66
Q

Epidemiology of malignant melanoma

A

More common in caucasians

67
Q

Epidemiology of squamous cell carcinoma

A

20% of non melanoma skin cancers

68
Q

Epidemiology of basal cell carcinoma

A

80% of non melanoma skin cancers.

69
Q

Skin cancer - diagnostic test for all 3 types of skin cancer mentioned

A

Clinical -> Biopsy

70
Q

Treatment of malignant melanoma

A

Wide local excision.

Metastases are resistant to all treatments.

71
Q

Treatment of squamous cell carcinoma

A

Local excision.

Occasionally radiotherapy.

72
Q

Treatment of basal cell carcinoma

A

Local excision.

Radiotherapy.

Cryotherapy.

Photodynamic therapy

73
Q

Complication of malignant melanoma

A

Metastasis

74
Q

Complication of squamous cell carcinoma

A

Metastases are rare (5%) but very hard to treat.

75
Q

Complications of basal cell carcinoma

A

Metastases are rare (5%) but very hard to treat.

Damage occurs if local spread reaches other structures.

76
Q

Infection - define cellulitis

A

Poorly demarcated Infection of the dermis and subcutaneous tissue.

77
Q

Infection - define necrotising fascilitis

A

Necrotising infection involving any layer of the deep soft tissue and fascia

78
Q

Infection - types of necrotising fascilitis

A

Type 1: Polymicrobial infection

Type 2: Group A streptococcus

Type 3: Gram-negative monomicrobial infection

Type 4: Fungal infection

79
Q

Infection - how does cellulitis clinically present?

A

Erythema in the involved area (usually lower extremity)

with poorly demarcated margins,

swelling,

warmth

and tenderness.

Erysipelas: Raised and well demarcated.

80
Q

Infection - how does necrotising fascilitis clinically present?

A

Mimics cellulitis.

Important early signs:

Pain,

tenderness

and systemic illness out of proportion to physical signs.

Bullae and ecchymotic skin lesions.

Spreading erythema,

underlying crepitus

and systemic toxicity.

81
Q

Infection - cellulitis - erysipelas note

A

Erysipelas is essentially the superficial form, affecting upper dermis and superficial lymphatics.

82
Q

Infection - pathophysiology of cellulitis

A

Usually follows a breach in the skin.

In some cases no obvious portal, but may be microscopic.

Once organisms enter into the subcutaneous tissue they colonise and multiply.

Can lead to blistering, abscesses and ulceration.

83
Q

Infection - pathophysiology of necrotising fascilitis

A

Deep seating infection of the subcutaneous tissue results in a fulminant and spreading destruction of fascia and fat.

Initially, the skin may be spared.

84
Q

Infection - causes of cellulitis

A

Mostly thought to be Streptococci pyogenes but possibly gram negative organisms,

anaerobes

or fungi can cause it.

85
Q

Infection - necrotising fascilitis - cause of type 1) polymicrobial infection

A

Aerobic and anaerobic bacteria.

Usually in immunocompromised or chronic disease.

Usually follows surgery or in diabetics

86
Q

Infection - necrotising fascilitis - cause of type 2) group A streptococcus

A

Group A streptococcus.

Usually in otherwise well patients

87
Q

Infection - necrotising fascilitis - cause of type 3) gram-negative monomicrobial infection

A

Gram negative monomicrobes.

Includes marine organisms such as Vibrio spp and Aeromonas hydrophil.

These occur if wound exposed to seawater.

88
Q

Infection - necrotising fascilitis - cause of type 4) fungal infection

A

Zygomycetes after traumatic wounds or burns.

89
Q

Epidemiology of necrotising fascilitis

A

500 cases a year (uncommon).

90
Q

Infection - diagnostic test for cellulitis

A

Usually clinical.

Culture possible.

91
Q

Infection - diagnostic test for necrotising fascilitis

A

Clinical.

Bedside finger test: Probing in a 2cm incision with index finger

92
Q

Infection - treatment for cellulitis

A

Rest,

analgesia

and elevate limb.

Empirical antibiotics.

93
Q

Infection - treatment for necrotising fascilitis

A

Early debridement of the affected tissue.

IV broad spectrum antibiotics

94
Q

Infection - complications of cellulitis

A

Abscess formation (needs aspiration and drainage),

gangrene.

95
Q

Infection - complications of necrotising fascilitis

A

Significant mortality rate.

Septic shock

(SG) condensed phase 2a (9 decks)

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