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Phase 3 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What are the functions of skin

A

protection, regulation and sensation

Protection: physical and immunological barruer

  • Primary function of skin
  • protects underlying organs from mechanical impact
  • protects and detects pressure
  • detects variations in extreme temperature and is a berrier to micro-organisms
  • barrier to UV radiation/chemicals

Regulation: physiological

  • body temp via sweat, hair and changes in peripheral circulation (constriction/dilation)
  • fluid balance via sweat and insensible loss
  • synthesis of Vitamin D

Sensation: network of nerve cells that detect and relay changes in the environment (heat, cold touch, pain)

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2
Q

Describe the normal anatomy of the skin

A

3 layers: epidermis, dermis and hypodermis (subcutaneous tissue)

Epidermis:

  • stratified squamous keratinocytes, melanocytes, Langerhan cells and merkel cells
  • Layers from outermost: stratum corneum, stratum granulosum, stratum spinosum, stratum basale

Dermis:

  • fibroblasts, mast cells, blood vessels and skin appendages (hair follicles, sebaceous and sweat glands, nails)
  • superficial papillary layer and inner reticular layer

Subcutaneous tissue:

  • where bigger blood vessels are found and is a major store of adipose tissue
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3
Q

Describe embryoloigcal development of the skin

A
  • Epidermis is derived from the ectoderm
  • Week 5: embryo covered by simple cubodial epithelium
  • Week 7: single squamous layer (periderm) and a basal layer

3rd month: hair appears as epidermal proliferation into dermis

4th month: intermediate layer forms between basal layer and periderm

  • Sweat glands develop as downgrowth’s of epithelial cords into the dermis
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4
Q

What is the role of langerhan cells (LC)?

A
  • members of the dendritic family, residing in basal layers
  • specialise in antigen presentation: acquire antigens in peripheral tissues, travel to regional lymph nodes, present to naive t cells and initiate adaptive immune response and potent cytokine release
  • involved in antimicrobial immunity, skin immunosurveillance, induction of hypersensitivity and the pathogenesis of chronic inflammatory diseases of the skin
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5
Q

How does a skin allergy develop?

A
  • Skin irritation by non-allergenic and allergenic compounds, inducing Langerhan cell migration and maturation
  • Langerhans from epidermis to regional lymph nodes
  • Sensitisation takes 10-14days from initial exposure to allergen
  • Once sensitised to a chemical, allergic contact dermatitis can develop within hours of repeat exposure
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6
Q

How does ultraviolet affect the skin?

A

Direct cellular damage and alterations in immunogenic fxn

  • P53 tumour suppressor genes mutated due to DNA damage: leads to poor suppression of tumour growth and implicated in development of melanoma and non-melanoma skin cancers

Chronic UV exposure: loss of skin elasticity, fragility, abnormal pigmentation, haemorrhage of blood vessels, wrinkles and premature aging

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7
Q

How is the skin protected from UV damage?

A
  • Keratinocytes and melanocytes protect against UV DNA damage: melanocytes are dendritic and protect DNA in keratinocyte nuclei
  • Release melanosomes to protect underlying nucleus
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8
Q

How is Vitamin D synthesised in skin?

A
  • During sunlight exposure, solar UVB photons are absorbed by skin and converted to pre-vitamin D(3)
  • Pre-vitamin D3 undergoes transformation within plasma membrane to active Vitamin D(3)
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9
Q

What are the different types of cutaneous receptors?

A
  • Meissner corpuscles
  • Pacini corpuscles
  • Ruffini corpuscles
  • Free nerve endings associated with merkel cells
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10
Q

Where are each of the different cutaneous receptors found and what is their function?

A

Merkel cell free nerve endings:

  • Base of epidermis
  • Respond to sustained gentle and localised pressure

Meissner Corpuscles

  • Below the epidermis, especially on palmar surfaces
  • Light touch

Ruffini’s Corpuscles

  • Dermis; Deep pressure and stretching

Pacini’s Corpuscles

  • Deep dermis
  • Sensitive to deep touch, rapid deformation of skin surface and around joints for position/proprioception

Other free nerve endings: pain, temperature

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11
Q

What cutaneous receptor(s) sense gentle touch?

A
  • Merkel cell free nerve endings and Meissner corpuscles
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12
Q

What cutaneous receptor(s) sense deep pressure?

A
  • Ruffini and Pacini corpuslces
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13
Q

What cutaneous receptor(s) sense position/proprioception around a joint?

A
  • Pacini Corpuscles
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14
Q

What are the cateogories in the Fitzpatrick skin colour types?

A
  1. Very fair - always burn, can’t tan
  2. Fair - usually burns, sometimes tans
  3. Medium - sometimes burns, usually tans
  4. Olive - rarely burns, always tans
  5. Brown - never burns, always tans
  6. Black - never burns, always tans
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15
Q

Define a macule

A

Flat area of skin change, pale, red, pigmented, usually small

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16
Q

Define a papule

A

Raised lesion on skin about 5mm in size

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17
Q

Define a pustule

A

Small pus-filled lesion usually around 5mm or less

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18
Q

Define a vesicle

A

Tiny fluid-filled blister normally 5mm or less

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19
Q

Define a plaque

A

Elevated area of skin change and redness

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20
Q

Define a bulla

A

Large blister usually 1cm or more

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21
Q

Define erythematous

A

Abnormal redness of the skin

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22
Q

Define ulceration of the skin

A

Loss of epidermis or a skin break

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23
Q

Define acne vulgaris

A

A skin condition characterised by papules, pustules and comedones (white/black heads), especially on the face due to inflamed or infected sebaceous glands and prevalent among adolescents

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24
Q

What is the clinical presentation of acne?

A
  • Pustules, papules and comedones: need all 3 to be diagnosed acne
  • May also have erythema, cysts, scarring

In darker skins: hyperpigmentation (harder to diagnose)

Distribution: face, chest, back/shoulders, legs, scalp

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25
Q

List 3 acne subtypes

A
  • Papulopustular
  • Nodulocystic
  • Comedonal
  • Steroid induced
  • Acne fulminans: severe, sudden onset (hrs), progressive acne

(- Acne rosacea: adult acne, doesn’t fit criteria for acne *NOT acne*. Nose, forehead, cheeks distribution)

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26
Q

Which of the following is not a subtype of acne?

A. Acne fulminans

B. Acne rosecea

C. Comedonal

D. Nodulocystic

A

B. Acne rosecea

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27
Q

What is the general pathophysiology of acne?

A
  • Glandular follicular disorder
  • Lining of sebaceous gland thickens and the oil produced by the sebaceous gland can’t escape
  • Bacteria on the skin loved trapped oil and provoke an inflammatory reaction (red, inflamed spot)
  • Everything builds up from behind until it eventually pops
  • The longer the gland in inflamed, the more trauma there is and more likely to cause scarring
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28
Q

List 3 causes of acne

A
  • Excess oil production
  • Hair follicles clogged by oil and dead skin cells
  • Bacteria
  • Excess androgen production
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29
Q

What treatment options are available for acne vulgaris, and what is their main aim?

A

Reduce plugging (mild)

  • Topical retinoid: slows turnover of follicle lining
  • Topical benzoyl peroxide: dissolves the plug

Reduce bacteria

  • Dual-action antibiotics that reduce bacteria on skin and work as anti-inflammatory agents
  • Topical antibiotics (erythromycin, clindamycin)

Reduce sebum production (moderate)

  • Antiandrogen hormones (OCP)
  • Reduces bacterial resistance

Dietary modification

  • Reduce dairy/glycaemia load eg. milk, chocolate

Isotretinoin (severe)

  • Reduces sebum production, plugging and bacteria
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30
Q

What is isotretinoin?

How does it work?

A
  • Oral retinoid lisenced for severe acne vulargis
  • Concentrated form of Vitamin A
  • Reduces sebum production, plugging (stops blockage of the gland) and bacteria
  • Remission for 80% teenagers
  • 16 week course
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31
Q

List 3 side effects of isotretinoin

A

Trivial: dry mouth, nose bleeds, dry skin

Serious:

  • Deranged liver function
  • Raised lipids
  • Mood disturbance
  • Tetatogenicity (birth defects) therefore need to be on 2 forms of contraceptive and pregnancy test before and every 4 weeks during treatment and one a month after finishing treatment
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32
Q

Define eczema

A
  • Interchangable with dermatitis = inflammation of the skin
  • Inflammatory skin condition of the epidemis in which patches of skin become inflamed, itchy, red and rough (if not itchy - not eczema)
  • Eczema: atopic type from childhood

(Atopy is the genetic tendancy to develop allergic diseases)

  • Dermatitis: exogenous (allergic/contact dermatitis)
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33
Q

What are the causes of eczema?

A
  • Combination of genetic, immune and reactivity to a variety of stimuli
  • Inflammation in eczema primarily due to inherited abnormalities in skin, leading to increased permeability and reduced antimicrobial function
  • Primary cause: abnormalities of Filaggrin (proteins which bind keratin fibres in epidermal cells)
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34
Q

How is eczema classified and list 2/3 examples of each type

A

Endogenous: internal without external trigger

  • Atopic, seborrheic, varicose

Exogenous (Dermatitis): external trigger

  • Contact (allergic, irritant)
  • Photoreaction (allergic, drug)
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35
Q

What is atopic eczema?

Presentation?

Aetiology?

Pathology?

Associations?

A
  • Itchy inflammatory skin condition
  • Bilateral, flexural sites (cubital and popliteal fossa)
  • Aetiology: genetic and immune aetiology
  • Pathology: IgE immunologulins
  • Associations: hayfever, asthma, allergic rhinitis, conjunctivitis
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36
Q

List 3 complications of atopic eczema

A

Bacterial infection (Staph. aureus)

Viral infection

Fatigue

Growth reduction

Psychological impact

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37
Q

How would you manage atopic eczema?

A
  • Emollients (greasy moisturiser)
  • Topical steroids: encourage protective barrier film to redevelop and reduces abnormal immune response
  • Bandages
  • Anti-histamines
  • Antibiotics/antivirals
  • Avoid exacerbating factors
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38
Q

What are the types of contact dermatitis?

A
  • Precipitated by an exogenous agent
  • Irritant contact dermatits: direct noxious effect on skin barrier (due to noxious chemical)
  • Allergic contact dermatitis: Type IV hypersensitivity reaction (immune pathway)
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39
Q

List 3 common causes of allergic contact dermaitits

A
  • Nickel: jewellery, coins
  • Chromate: cement, tanned leather
  • Cobalt: pigment/dyes
  • Colophony: glue, adhesive tape
  • Fragrance: cosmetics, creams, soaps
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40
Q

Define seborrhoeic dermatitis

Aetiology

Typical presentation

Management

A
  • Chronic, scaly inflammatory skin condition

Aetiology: disproportional immune reaction to a small amount of yeast

Presentation

  • Typically face, eyebrows, scalp (often thought to be dandruff) - Worse in teenagers
  • Diagnostic feature for HIV

Management: medicated anti-yeast shampoo (scalp) and anti-microbial, mild steroid moisturiser (face)

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41
Q

Define psoriasis

A

Chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin

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42
Q

How does psoriasis present?

A

Age: two peaks at 20-30 and 50-60yrs

  • Usually bilateral with extensor surface pattern
  • Thickness and scaling: keratinocyte proliferation

- Redness and inflammation: inflammatory infiltrate

  • Red patches of skin covered with thick, silvery scaling
  • Dry cracked skin
  • Swollen and stiff joints
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43
Q

What is the pathogenesis of psoriasis?

A
  • T cell mediated autoimmune disease
  • Abnormal T cell infiltration: release of inflammatory cytokines including interferon, interleukins and TNF causing redness and inflammation

Increased keratinocyte proliferation: causing thickening and scaling

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44
Q

What other conditions is psoriasis connected with?

A
  • Psoriatic arthritis: erosive, inflammatory, destructive arthritis
  • Metabolic syndrome
  • Liver disease
  • Depression
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45
Q

List 3 subtypes of psoriasis

A
  • Erythrodermic
  • Pustular
  • Flexural/Inverse (more psoriasis is extensor driven)
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46
Q

What is management of psoriasis based on?

A
  • Severity
  • Patient preference
  • Patient tolerability
  • Presence of arthropathy
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47
Q

What is the management for psoriasis?

A

1. Topical creams and ointments

  • Moisturisers: reduce dryness and flakiness
  • Steroids: reduce autoimmune response, redness, inflammation
  • Salicylic acid: dissolves thick dead skin

2. Phototherapy light treatment (UVB)

  • Non-specific immunosuppressant therapy
  • Can reduce T cell proliferation
  • Encourages vitamin D and reduces skin turnover
  • Risks: burning (short term), skin cancer (long term)

3. Systemic therapy

  • Immunosuppressants: methotrexate
  • Oral retinoid

4. Biologics

48
Q

What are 3 main skin cancer types?

A
  • Basal cell carcinoma: most common type of skin cancer, develops from basal cells at the bottom of epidermis
  • Squamous cell carcinoma: develops from squamous cells or keratinocytes in upper layers of epidermis
  • Malignant melanoma: Develops from melanocytes (not just unique to skin - brain/bowel)
49
Q

What are the risk factors for developing basal cell carcinoma?

A
  • Caused when a basal cell (at the bottom of the epidermis) develops a mutation in its DNA ie. DNA damage

RFs:

  • Chronic UV radiation exposure from the sun / tanning beds
  • Fair skin
  • Increasing age and male
  • Immunosuppressant drugs
  • Previous BCC or other skin cancer type
  • Repeated prior episodes of sunburn
50
Q

What is the pathogenesis of basal cell carcinomas (BCC)?

A
  • Basal cells are found at the bottom of the epidermis
  • The process of creating new skin cells is controlled by a basal cell’s DNA
  • A mutation in the DNA causes the basal cells to multiply rapidly and continue growing when it would normally die
  • Eventually the accumulating abnormal cells may form a tumour
  • 80% are found on the head and neck ie. UV exposed sites
51
Q

What is the porgnosis of basal cell carcinomas

A
  • Most common type of skin cancer
  • Cured in almost every case
  • Metastatic spread is rare
  • Good prognosis
52
Q

What are the subtypes of basal cell carcinomas?

A

Nodular

Superficial

Pigmented

Morphoeic/Scleroitc

53
Q

How do nodular BCCs present?

A
  • Nodule >0.5cm raised lesion
  • Shiny ‘pearly’ (characteristic feature)
  • Can see cluster of red lines (blood vessels over top)
  • Often ulcerated/depressed centrally, giving rolled edge appearance
  • Neat, rolled edge
  • Commonly seen on the face
54
Q

How do superficial BCCs present?

A
  • Flattened patch
  • Scaly, irregular plaque
  • Rolled, translucent edge with broken blood vessels
  • Stereotypical distribution: sun-exposed sites (shoulders and upper trunk)
55
Q

How do pigmented BCCs present?

A
  • Shiny, raised lesion
  • Domed edge
  • Presence of broken blood vessels
  • Could be mistaken for melanoma due to pigmentation but melanomas aren’t shiny like BCC
56
Q

How do morphoeic/sclerotic BCCs present?

A
  • Waxy, scar like lesion
  • Indistinct margin
  • Shiny, some broken blood vessels
  • Could infiltrate subcutaneous nerves
  • Difficult to diagnose
57
Q

What are the treatment options for a basal cell carcinoma?

A

Gold standard: Surgical excision with 2-4mm margin

  • Highest chance of complete removal and it not returning
  • If large, skin graft may be required

Mohs microscopic surgery: surgery under the microscope in fragile areas eg. tip of nose, around eyes

Curettage and cautery

  • Superficial skin surgery, just need local anaesthesia and no sutures required
  • Appropriate for elderly patients with distinct, small BCC and unfit for bigger surgery
  • Suitable for well-defined, small nodular or superficial BCC

Cyrotherapy

  • Freezing a superficial skin lesion with liquid nitrogen
  • Appropriate for small superficial BCCs on trunk/shoulders

Photodynamic therapy: for low-risk, small superficial BCCs

Liquid imiquimoid/5-fluorouracil cream

58
Q

What are the risk factors for developing a squamous cell carcinoma (SCC)?

A
  • Increasing age and male
  • Sun exposed skin

- Any type of damaged skin: radiotherapy, thermal burn, leg ulcer

  • Previous SCC or other form of skin cancer
  • Atinic keratoses (pre-malignant variant)
  • Smoking
59
Q

What are the clinical features of a squamous cell carcinoma (SCC)?

A
  • Squamous looking ie. keratin crust (NOT skiny)
  • Rolled margin but no broken blood vessels
  • Background skin is more sun-exposed (sub damage)
  • Can ulcerate
  • Proressive type (grows more rapidly than a BCC)

Commonly: face, lips, ears, hands

60
Q

What is the prognosis for a squamous cell carcinoma?

A
  • Good prognosis (99% survival rate if caught early)
  • Cured mostly by surgery
  • Rarely metastasises
61
Q

What are the treatment options for a SCC?

How are SCC in-situs treated?

How can you prevent SCC development?

A

Almost all: surgical excision with 4mm margin

Other options: Curettage and cautery, aggressive cyrotherapy or radiotherapy (if tumour is inoperable, patient is unsuitable for surgery or used as an adjuvant)

For SCC insitu

  • topical imiquimod or 5-fluorouracil cream
  • cyrotherapy
  • photodynamic therapy

Prevention: sub protection

62
Q

What are the risk factors for developing malignant melanoma?

A
  • UV irradiation
  • Sunburns during childhood
  • Fair skin (Skin Type I or II)
  • Genetic markers
  • Personal history of melanoma
  • Immunosuppression
  • Number (>5) and size (>5mm) of melanocytic naevi (moles, non-malignant melanoma)
63
Q

What is the pathogenesis of malignant melanoma?

A
  • Uncontrolled proliferation of melanocytic stem cells that have undergone a genetic transformation due to DNA damage
  • Radial growth phase followed by vertical growth
  • Vertical growth has a worse prognosis
  • Depth of melanoma called Breslow’s depth

Metastatic spread via lymphatics

  • Lymphovascular invasion: tumour cells destroy local blood vessels therefore increasing the risk of spread
  • Lymphatic spread: cells usually metastasis to draining lymph nodes
64
Q

What is the prognosis for malignant melanoma?

A

Prognosis is determined by depth of the melanoma: Breslow’s depth = the depth of the lowest atypical melanocyte

  • Risk of metastasis increases as thickness of melanoma increases
65
Q

What is the progression of melanomas?

A
  • Benign melanocytic naevi and atypical/dysplastic melanocytic naevi are precancerous lesions and spread through the dermis
66
Q

Define Breslow’s depth and Clark’s levels of melanoma

A

Brewlow’s depth (mm): the depth of the lowest atypical melanocyte

Clark’s levels: correlate to the specific layer of skin the tumour has grown into (not as specific as Breslow)

  • Good to combine the two
67
Q

What is the presentation of a melanoma?

A
  • Occur anywhere in the body
  • 1st sign: atypical melanocytic naevi (mole)
  • Pigmented, NOT shiny lesion
  • During radial growth: flat (not invasive/malignant)
  • With vertical growth, it becomes raised: malignant

Symmetry is very important, signs of malignancy:

  • irregular shape, different shades of pigment and tumour lump in the centre
  • ABCDE criteria: asymmetry, border irregularity, colour variation, diameter >6mm, evolving (enlarging, changing)
68
Q

List 3 subtypes of melanomas

A
  • Superficial spreading malignany melanoma: commonest subtype, irregular brown patch
  • Nodular melanoma
  • Acral melanoma (hands, feet, nails)
  • Subungual melanoma (under the nail)

Amelanotic melanoma (no pigment)

69
Q

What are the treatment options for melanomas?

A

Surgical exision

  • Breslow depth <1mm: 1cm margin
  • Breslow depth >1mm: 2cm margin

Immunotherapy

Biologic antibodies

Assessment of lymph nodes and organ spread

Long-term follow-up up to 5 years

70
Q

Outline the function of the skin and identify three organisms found in the normal skin flora

A

Skin: acts as a physical barrier to the environment to prevent infection

  • Colonised with many bacteria

Organisms:

  • Staphococci (S. aureus)
  • Streptococci (A, B, C, G)
  • Anaerobes
  • Yeasts
71
Q

Define cellulitis

A

A spreading bacterial infection of the dermis and subcutaneous tissue, characterised by redness, warmth, swelling and pain. It commonly appears in areas where there is a break in the skin

72
Q

Outline two general and local modifiable and non-modifiable risk factors for developing cellulitis

A

General:

  • Modifiable: venous insufficiency, lymphoedema, immunocompromise, obesity
  • Non-modifiable: pregnancy, Causacian

Local:

  • Modifiable: ulcers, eczema, althlete’s foot, burns, surgical
  • Non-modifiable: trauma, animal/insect bites, tattoos
73
Q

Outline the clinical presentation of cellulitis

A

Local:

  • usually unilateral, usually lower limbs
  • oedema, pain, erythma, warmth (inflammation)
  • dimpled skin
  • treated with oral antibiotics

Can progress into invasive disease (bacteraemia):

  • systemic: fever, chills, hypotension
  • treated with IV antibiotics
74
Q

Outline the pathophysiology of cellulitis

A

There is a break in the skin barrier

  • organisms from the normal skin flora can invade the subcutaneous tissue, potentially into the dermis
  • can breach the deeper dermis
  • can become invasive if they reach the blood supply, then disseminate to the rest of the body
75
Q

Identify 3 causative organisms of cellulutis

A

- Strepococcus pyogenes

- Staph. aureus (inc. MRSA)

Rarer causes:

  • haemophilus influenza
  • strep. viridans
  • Pasteurella multiocida (cat/dog bite)
  • clostridium perfringes
76
Q

Outline the diagnostic process for cellulitis

A

Clinical diagnosis

Investigations may reveal:

  • leucocytosis
  • elevated CRP
  • the causative organism on blood culture
77
Q

Outline the basis for management decisions for cellulitis and the management options

A

Basis:

  • Assess severity: how much of the body is it encompassing, mark the borders and assess over a few days
  • Anatomical site: facial cellulitis can be devastating
  • Co-morbidity: eg. obesity, venous insufficiency
  • Healthcare associated infection: is this necrotising

Options:

  • Surgery (necrotising fasciitis)
  • HDU (High dependency unit)
  • Abx: IV/oral, which abx
78
Q

Identify three causes for hospital admission for a patient with cellulitis

A
  • Significant systemic illness
  • Sepsis syndrome / necrotising fasciitis
  • Severe / Rapidly deteriorating cellulitis
  • Very young or frail
  • Co-morbidities
  • Immunocompromised
  • Facial cellulitis
79
Q

What is the antibiotic recommendation for the following causative agents of cellulitis

S. pyogenes

S. aureus / MRSA

Penicillin allergy

Pasteurella multocida

Clostridium perfringes

A

S. pyogenes: flucloxacillin

S. aureus: flucloxacillin

MRSA: vancomycin

Penicillin allergy: doxycycline, clindamycin or vancomycin

Pasteurella multiocida: co-amoxiclav or doxycycline and metronidazole

Clostridium perfringes: pencillin + flucloxacillin + clindamycin + gentamicin + metronadazole

80
Q

What is the most common causative agent for the follow:

  • Typical cellulitis
  • Typical cellulitis with pus formation
  • Cat/Dog bite
  • Necrotising fasciitis

And what antibiotics are used to treat each

A

Typical cellulitis: strep. pyogenes

  • Flucloxacillin

Typical cellulitis pus forming: S. aureus / MRSA

  • S. aureus: flucloxacillin
  • MRSA: vancomycin

cat/dog bite: pasteurella multocida

  • co-amoxiclav OR doxycycline and metronadazole

necrotising fasciitis: s. pyogenes or clostridium perfringes

  • penicillin + flucloxacillin + clindamycin + gentamicin + metronadazole
81
Q

Identify three complications of cellulitis

A
  • Necrotising fasciitis
  • Gangrene
  • Severe sepsis
  • Infection of other organs eg. osteomyelitis, meningitis
  • Endocarditis
82
Q

Outline the differential diagnosis for suspected cellulitis

A

Statis dermatitis

  • skin condition due to chronic venous insufficiency
  • absense of fever, circumferential, bilateral

Acute arthritis

  • usually poly-joint involvement
  • joint involvement, pain on movement

Pyoderma Gangrenosum

  • associated with IBD
  • ulceration on legs, history of IBD

Hypersensitivity/Drug reaction

  • exposure to allergens, itch, absence of fever and pain

DVT

  • absence of skin changes or fever
  • just painful, swollen area

Necrotising fasciitis

  • severe pain out of proportion
  • swelling, fever, rapid progression, systemic toxicity
83
Q

Define necrotising fasciitis

A

Very severe, rapidly spreading bacterial infection of the soft tissue and fascia over hours

  • medical emergency
84
Q

Outline the clinical presentation of necrotising fasciitis, to differentiate it from typical cellulitis

A

Initially (Hours)

  • Commonly lower leg
  • severe pain at time of presentation and worsens with time
  • erythema and swelling
  • systemically unwell (fever, chills, hypotension)

After a few days

  • Area becomes blackened (necrosis)
  • Skin crepitus
  • Severe pain continues until necrosis/gangrene destroys peripheral nerves, rendering the site painless

Progression:

Painful → painless

Red/Purple → Black

85
Q

Outline the management for necrotising fasciitis

A

Mainstay: surgery

  • Early suspicion and surgical debridement

5 abs used until surgery (Given IV):

  • penicillin
  • flucloxacillin
  • gentamicin: Gram -ve cover
  • clindamycin: switches of exotoxin production and improves mortality
  • metronadazole

Need oxygen and fluids to raise BP

Abx adjusted once blood culture returned with causative organism

86
Q

Define impetigo

Outline the clinical presentation and causative agent

What is the management

A

Def: acute superficial bacterial skin infection (pyoderma)

Clinical presentation:

  • typically children or sports people
  • peri-oral
  • ‘honey-coloured’ crusted lesion and pustules

Causative agent:

  • Staph. aureus (any staph species)

Management:

  • Remove the crust gently, apply anti-septic for 3-5 days and cover the affected area
  • Flucloxacillin indicated if: severe symptoms (fever), more the 3 lesions, high risk of complications, unresolving infection
87
Q

Define scarlet fever and what causes it

A

Def: bacterial infection that presents with a distinctive rash of tiny pink-red spots that cover the entire body

Cause:

  • Group A Streptococcal infection
  • Affects those who have recently had a strep A throat infection or impetigo caused by strains of Group a strep
  • a toxin produced by the bacteria produce the distinctive rash
88
Q

Outline the clinical presentation of scarlet fever

A
  • Usually post-pharyngitic presentation
  • Sudden fever with a sore throat, swollen neck glands, headache, nausea
  • Diffuse red blush
  • Starts on the upper chest and spreads to the trunk, neck and extremeties
  • rash fades over the course of a week and starts to desquamate (peel) over several weeks
  • occlusion of sweat glands gives the skin a sandpapery touch
  • circum-oral pallor
  • red strawberry tongue

Severe cases: high fever and systemic toxicity

89
Q

Outline the management for scarlet fever

A

Once, culture of strep is diagnosed, a course of penicillin is usually started

Other:

  • paracetamol for fever, headache
  • oral antihistamines and emollients
90
Q

Identify the common causative agent causing infection after a bite and outline the management for bites

A

Management

  • Routine prophylaxis only indicated if: deep bite, on the hands, splenectomised or immunocompromised patient
  • Gram stain of wound and blood cultures if systemically unwell
  • Treatment: abx +/- surgical involvement if deep infection
  • Aggressive debridement and abscess drainage

Causative agent: pasteurella multocide

91
Q

Outline the classification of burns

A

1st degree: Superficial (Epidermis only)

  • Dry/red
  • blanches on pressure, painful
  • heals in 7 days

2nd degree: Partial thickness (epidermis and dermis)

  • superficial v deep (involves dermis)
  • blisters
  • progression of superficial to deep: painful to painless
  • heals in <21 days +/- abx/surgery/grafting

3rd degree: full thickness (to subcutaneous tissue)

  • painless, non-blanching
  • requires surgery

4rd degree: involves fascia/muscle/bone

  • healing requires surgery
92
Q

Outline the diagnosis and treatment of infected burns

A

Diagnosis:

  • rapid bacterial colonisation esp. due to hospital organisms
  • diagnosed clinically

Management:

  • need to monitor: infection, hypothermia, acid-base abnormalities and dehydration with burns
  • involves plastic surgeons and microbiology team early
  • surgery

Infected Burns:

  • cleaning, dressing
  • topical antimicrobials
  • Oral/IV abx (directed by culture results)
93
Q

Define tinea, it’s characterisation and classifications

A

Tinea: a skin infection with a dermatophyte (ringworm) fungus

Characterisation:

  • scaly, inflammatory or non-inflammatory patches
  • fungal
  • limited to the epidermis
  • preferentially inhabits warm, moist areas of the skin

Classification:

  • Tinea pedis: foot (athlete’s foot)
  • Tinea corporis: body
  • Tinea capitis: head/scalp
  • Tinea cruris: jock itch
94
Q

Outline the types and presentation of Herpes Simplex Virus (HSV)

What is the diagnosis and treatment?

A

Type 1: stomatitis ‘cold sore’

Type 2: genital herpes

Presentation:

  • primary infection asymptomatic in 60%
  • vesicular, may be painful

Diagnosis: clinical, blood for PCR

Treatment: acyclovir (topical, oral, IV)

95
Q

What conditions can be caused by varicella zoster virus?

A

Chicken Pox

  • self-limiting childhood infection
  • highly infectious, needs a side room
  • Diagnosis: PCR of vesicle fluid
  • In adults: can cause pneumonitis
  • treat at risk individuals with acyclovir

Shingles

  • Reactivation of dormant VZV
  • may be very painful
  • treat at risk patients with acyclovir
96
Q

Identify 3 cutaneous changes seen with thyroid disease

A

Hypothyroidism: dry skin

Grave’s disease: autoimmune hyperthyroidism

  • pretibial myxoedema: characterised by localised thickening of the skin in the pretibial area and localised skin lesions due to the deposition of hyaluronic acid
  • thyroid acropachy: nail changes specific to Grave’s
97
Q

Identify 3 cutaneous changes seen with diabetes

A
  • Necrobiosis lipoidica: waxy appearance, yellow decolouration often on the skins, occassionally ulcerates
  • Diabetic dermopathy
  • Scleredema: cutaneous skin disorder with loss of elasticity
  • Leg ulcers
  • Granuloma annulare
98
Q

Identify 3 cutaneous changes seen with steroid excess

A

Ie. Cushing’s excess

  • Acne: back and chest
  • Striae: exaggerated stretch marks
  • erythema
  • gynaecomastia
99
Q

Identify 2 cutaneous changes with steroid insufficiency

A
  • hyperpigmentation
  • acanthosis nigricans: brown velvety skin in folds eg. axilla, groin
100
Q

Identify 3 cutaneous presentations of Cushing’s Disease

A
  • inc. central adiposity
  • Moon facies and buffalo hump
  • Global skin atrophy: epidermal and dermal components
  • Straie on abdominal flanks, arms, thighs
  • Purpura with minor trauma
101
Q

Identify two cutaneous presentations of excess testosterone and excess progesterone

A

Testosterone:

  • Acne and hirsutism

Progesterone:

  • Acne and dermatitis
102
Q

Identify 3 cutaneous presentations that may indicate underlying systemic infection

A
  • necrolytic migratory erythema: erythematous, scaly plaques found on acral, intriginous and periorificial areas
  • erythema gyratum repens: reddened concentric bands whorled woodgrain pattern. Severe pruritus and peripheral eosinophila
  • acanthosis nigricans: smooth, velvet hyperkeratotic plaques in intertiginous areas eg. axilla, groin
  • erythema annulare
  • sweet’s syndrome
103
Q

How does necrolytic migratory erythema look?

What else can it present with?

How is it treated

A

Morphology:

  • erythematous, scaly plaques found on acral (extremity), intertriginous (eg. axilla) and periorifical areas
  • associated with an islet cell tumour of the pancreas
  • other signs: hyperglycaemia, diarrhoea, weight loss, glossitis

Treatment: removal of the tumour

104
Q

Describe the morphology of erythema gyratum repens.

What condition is it associated with?

How is it treated?

A

Morphology:

  • Reddened concentric bands whorled woodgrain pattern
  • Severe pruritis and pheripheral eosinophila

Condition: strong association with lung cancer

Treat: treat the underlying malignancy

105
Q

Describe the morphology of acanthosis nigricans and identify 3 associated conditions

A

Morphology:

  • Smooth, velvet-like hyperkeratotic plaques in intertriginour areas eg. groin, axilla, neck

Type I: associated with malignancy adenocarcinoma

Type II: familial type

Type III: Associated with obesity and insulin resistance

106
Q

Identify the cutaneous changes seen with Vitamin B deficiency

A

Dementia, diarrhoea, dermatitis

107
Q

Identify 3 cutaneous changes seen with zinc deficiency

Outline 1 cause of zinc deficiency in adults

A
  • pustules
  • bullae
  • scaling
  • acral (extremeties) and perioral distribution

Causes in adults:

  • alcoholism
  • malabsorptive states
  • bowel surgery
  • IBD
108
Q

Outline the clinical presentation of Vitamin C deficiency

A

Scurvy

  • punctate purpura/bruising
  • corkscrew spiral curly hairs
  • patchy hyperpigmentation
  • dry skin and hair
  • non-healing wounds
  • inflamed gums
109
Q

Identify 3 cutaneous changes seen with erythema nodosum and 3 conditions in which it develops

A

Cutaneous changes:

  • tender bilateral erythematous subcutaneous nodules
  • usually found on anterior lower legs, knees and arms
  • ill-defines, warm, oval lesions without ulceration
  • bright red

Conditions it’s associated with:

  • Strep infection
  • pregnancy/ OCP
  • sarcoidosis
  • IBD
110
Q

Identify 3 cutaneous changes seen with pyoderma gangrenosum and 3 conditions in which it may develop

A

Cutaneous changes:

  • rapidly enlarging, very painful ulcer
  • sudden onset at site of minor injury
  • may start as a small pustule, red bumb or blood-blister
  • edge of ulcer: purple and undermined

Associated with:

  • IBD: Crohn’s disease and ulcerative colitis
  • Rheumatoid arthritis
  • Myeloma
111
Q

What conditions are the following associated with:

Alopexia areata hair loss

Hair thinning

Male pattern balding

A

Alopexia: autoimmune

Hair thinning: B12 def, lupus, iron deficiency, hypothyroidism

Male pattern balding: androgen excess

112
Q

What are the two most common skin presentations to primary care?

A
  • Ezcema
  • Psoriasis
113
Q

Identify 3 common benign and 3 worrying skin lesions that GPs see

A

Worrying:

  • melanoma
  • squamous cell carcinoma
  • basal cell carcinoma
  • Any changing pigmented lesion should be referred to dermatology - urgent cancer suspicion*

Benign:

  • Warts
  • Seborrhoeic warts
  • Skin tags
  • Seborrhoeic keratosis
  • Pyogenic granuloma
114
Q

How are the following benign skin lesions managed?

Warts

Seborrhoeic warts

Skin tags

A

Warts: topical salicylic acid or cyrotherapy (freezing)

Seborrhoeic warts: cyrotherapy

Skin tags: do nothing or private sector that bitch

115
Q

Define and outline the clinical presentation of psoriasis

A

Define: a chronic inflammatory skin condition characterised by clearly defined, red and scaly plaques (thickened skin)

  • Overproduction of skin cells causing red, scaly patches

Clincial presentation:

  • Symmetrically distributed red, scaly plaques with well-defined edges
  • Scale is typically silvery-white
  • Common sites: extensor surfaces (elbow, knee), scalp, nails, joints
116
Q

Outline the management for psoriasis

A

Lifestyle: smoking, weight alcohol

Mild: topical agents alone

  • Emollients
  • Salicylic acid
  • topical corticosteroids
  • coal tar

Widespread / Not reponding:

  • Phototherapy, often in combo with topical or systemic agents
  • commonly methotrexate, ciclosporin
117
Q
A

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