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Phase 3B > Dermatology > Flashcards

Dermatology Flashcards

1
Q

6 Functions of normal skin

A

(VIPSTAr)
- Protective barrier (against environment)
- Temperature regulation
- Sensation
- Vitamin D synthesis
- Immunosurveillance
- Appearance/ cosmesis

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2
Q

Structures of normal skin

A

= largest organ in the body
- 3 layers: epidermis, dermis, subcutaneous tissue

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3
Q

Epidermis: layers, major cell types

A
  • 5 layers -> Stratum Basale, Stratum Spinosum, Stratum granulosum, Stratum lucidum, Stratum corneum (‘Come Lets Get Sun Burnt’)
  • Each layer represents a different stage of maturation of the keratinocytes. Average epidermal turnover time (migration of cells from basal layer to corneum is about 30 days.
  • Stratum lucidum is a layer that is present mainly in areas of thick skin such as the sole.
  • Composed of 4 major cell types:
    1. Keratinocytes - produce keratin as a protective barrier,
    2. Langerhan cells - present antigens and activate T-lymphocytes for immune protection
    3. Melanocytes - produce melanin, gives pigment to skin and protects cell nuclei from UV DNA damage
    4. Merkel cells - contain specialised nerve endings for sensation
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4
Q

Principles of wound healing

A

‘VIP Room’
* Vascular -> formation of a fibrin clot, through vasoconstriction and platelet aggregation
* Inflammation -> vasodilation. Migration of neutrophils and macrophages.
* Proliferation -> granulation tissue (by fibroblasts) and re-epithelialization.
* Remodelling -> collagen fibre re-organisation, scar maturation

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5
Q

Skin appendages: hair types

A

Hair:
a. lanugo: fine long hair covering shoulders, back and face of fetus/newborn). Typically shed before/shortly after birth.
b. vellus hair: fine, short, blond hair on all body surfaces/ peach fuzz. Develops during childhood.
c. terminal hair: coarse, pigmented, long hair on scalp, eyebrows, eyelashes. After puberty - face (beard), armpits, chest, pubic regions

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6
Q

Hair follicle and growth cycle

A
  • Hair follicle -> divided into hair shaft (keratinised tube) and a hair bulb (actively dividing cells), and melanocytes which give pigment to the hair.
  • Growth cycle -> anagen (long growing phase), catagen (short regressing), telogen (resting/shedding)
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7
Q

Skin appendages: nails

A
  • Made up of a nail plate (hard keratin) which rests on nail bed.
    • Nail bed contains blood capillaries, gives pink colour of nails
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8
Q

Skin appendages: Sebaceous glands

A
  • Produce sebum via hair follicles. Lubricates and waterproofs the skin.
  • Stimulated by conversion of androgens to dihydrotestosterone and therefore become active at puberty.
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9
Q

Skin appendages: Sweat glands

A
  • Regulate body temp and are innervated by the sympathetic nervous system.
  • Eccrine sweat glands -> universally distributed in the skin
  • Apocrine sweat glands -> found in axillae, areola, genital and anus. Only function from puberty and action of bacteria on the sweat produces body odour.
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10
Q

Pathology linked to the epidermis

A
  • Psoriasis -> change in epidermal turnover time - Ulcer, Scales, Crusting, Exudate -> change in surface of the skin or loss of epidermis - Hypo or hyper-pigmented skin -> Changes in pigmentation of skin
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11
Q

Pathology linked to the dermis

A
  • Ulcers, papules, nodules -> changes in contour of skin or loss of dermis
  • Acne, Disorders of hair -> disorders of skin appendages
  • Erythema, Urticaria, Purpura -> changes related to lymphatic and blood vessels
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12
Q

Pathology linked to nails

A
  • Pits and ridges -> abnormalities of nail matrix.
  • Splinter haemorrhage -> abnormalities of nail bed
  • Discoloured nails, thickening of nails -> abnormalities of nail bed
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13
Q

Pathology linked to sebaceous glands

A

Acne -> increased sebum production and bacterial colonisation

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14
Q

Pathology linked to sweat glands

A
  • Hidradenitis suppurativa -> inflammation/infection of apocrine glands.
  • Hyperhidrosis -> overactivity of eccrine glands
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15
Q

Derm Hx: PC

A
  • nature, site and duration of problem
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16
Q

Derm Hx: HPC

A
  • Initial appearance and evolution of lesion
  • Sx (particularly itch and pain) -> systemic, oral/nail/hair loss, joint and muscle
  • Aggravating and relieving factors
  • Previous and current tx (effective or not)
  • Recent contact, stressful events, illness and travel
  • History of sunburn and tanning machines
  • Skin type
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17
Q

Derm Hx: PMH

A
  • history of atopy (e.g. asthma, allergic rhinitis, eczema)
  • history of skin cancer and suspicious skin lesions
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18
Q

Derm Hx: FH + SH

A
  • FH of skin disease
  • Occupation (incl skin contacts at work)
  • Improvement of lesions when away from work
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19
Q

Derm Hx: Further q’s

A
  • medications and allergies
  • impact on QOL
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20
Q

Derm examination: inspect + describe

A
  • Inspect: general, site and number of lesions (distribution)
  • Describe the individual lesion: SCAM
    Size (widest diameter), Shape
    Color
    Associated secondary change
    Morphology, Margin (border)
  • If pigmented, ABCD
  • Asymmetry (lack of mirror image in any of 4 quadrants)
  • irregular Border
  • 2+ Colors within lesion
  • Diameter >6mm
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21
Q

Derm exam: palpate + systemic check

A

Palpate: surface, consistency, mobility, tenderness, temperature
Systemic check: nails, scalp, hair, mucous membranes. General all systems.

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22
Q

Define Macule and Patch

A

Macule: Small (less than 1cm), smooth area of colour change. Ex// freckle, petechiae

Patch: Large (greater than 1cm), smooth area of colour change. Ex// Vitiligo, port wine stain

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22
Q

Define Macule and Patch

A

Macule: Small (less than 1cm), smooth area of colour change. Ex// freckle, petechiae

Patch: Large (greater than 1cm), smooth area of colour change. Ex// Vitiligo, port wine stain

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23
Q

Define Papule, Nodules and Plaque

A
  • Papule: palpable + raised lesion <0.5cm. Ex// wart, mole, acne, angioma, xanthomata
  • Nodule: palpable + raised lesion >0.5cm with deeper component. Ex// Cyst, Pyogenic granuloma.
  • Plaque: palpable flat lesion. Can be scaly. Ex// Psoriasis.
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24
Q

Define Vesicle, Bulla, Pustule

A
  • Vesicle: small <0.5cm, fluid filled blister.
    Ex// Herpes, sunburn, pompholyx
  • Bulla: Large >0.5cm, fluid filled blister.
    Ex// Herpes/infection, sunburn, pemphigoid
  • Pustule: pus-containing raised lesion.
    Ex// Acne
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25
Q

Define Wheal, Scar, Ulcer, Fissure

A
  • Wheal: transient raised lesion due to dermal oedema. Usually with swelling, burning or itching.
    Ex// Hives
  • Scar: New fibrous tissue occurring post-wound healing.
    Ex// Keloid scar
  • Ulcer: Break in skin - Loss of epidermis and dermis. Ex// Leg ulcer
  • Fissure: Epidermal crack often due to excess dryness. Ex// Eczema
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26
Q

Define Naevus, Comedone, Abscess, Purpura

A
  • Naevus: A localise malformation of skin structures
  • Comedone: A plug in sebaceous follicle containing altered sebum, bacteria and cellular debris. Present as open (blackheads) or Closed (whiteheads)
  • Abscess: Localised collection of pus surrounded by damaged and inflamed tissue
  • Purpura: Red/purple non-blanching rash consisting of numerous petechiae (small, round non-blanching red/purple spots).
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27
Q

Nails: define clubbing, koilonychia, oncholysis, pitting

A
  • Clubbing: loss of angle between posterior nail fold and nail plate
    -> suppurative lung disease, cyanotic heart disease, IBD, idiopathic
  • Koilonychia: Spoon-shaped depression of the nail plate
    -> IDA, congenital, idiopathic
  • Onycholysis: Separation of distal end of nail plate from nail bed -> trauma, psoriasis, fungal nail infection, hyperthyroidism
  • Pitting: punctuate depressions of nail plate -> psoriasis, eczema, alopecia
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28
Q

Examples of inflammatory skin conditions? how spread between people? General aims of treatment

A
  • Atopic eczema, acne, psoriasis
  • Not infectious
  • Mx: achieving control and not providing a cure
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29
Q

anatomy/physiology of acne

A
  • An inflammatory disease of the pilosebaceous follicle
  • Causes: hormonal (androgen) -> increase sebaceous glands. Abnormal follicular keratinisation. Bacterial colonisation.

FURTHER:
-SEBACEOUS GLANDS produce oily substance sebum, responsible for keeping the skin and hair moisturized. During adolescence, sebaceous glands will typically ENLARGE and produce more sebum under the influence of hormones.
- BACTERIA Propionibacterium acnes is a normal inhabitant of the skin. It uses sebum as a nutrient for growth and will continue to grow in line with the production of sebum.
- The presence of the bacteria attracts WBC’s to follicle. These immune cells produce an enzyme that damages the wall of the follicle, releasing debris into the hair shaft and deeper in the middle layer of skin to (the dermis). This process causes an inflammatory reaction that gives rise to a little red bump (called a papule), which can then develop into a pus-filled blister (called a pustule)

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30
Q

Presentation of Acne Vulgaris

A
  • Non-inflammatory lesions (mild acne) -> open and closed comedones
  • Inflammatory lesions (moderate-severe) -> papules, pustules, nodules.
  • Commonly affects the face, chest and upper back.
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31
Q

Management of Acne Vulgaris

A
  • Topical therapies (mild acne):
    Benzoyl peroxide (antibac)
    Antibiotics (antibac)
    Retinoids (desquam +
    comedolytic)
  • Oral therapies (moderate to severe):
    Antibiotics e.g. tetracyclines
    Anti-androgens
    Retinoids e.g. Isotretinoin
    (severe)
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32
Q

What is psoriasis

A
  • A chronic inflammatory skin disease due to HYPERPROLIFERATION of KERATINOCYTES in the epidermis and INFLAMMATORY cell infiltration.
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33
Q

Types of psoriasis

A
  • Plaque psoriasis: thickened erythematous lesions with silvery SCALES.
  • Guttate: Commonly children. Many small raised PAPULES across trunk + limbs. Often triggered by STREP throat infection, medication, stress.
  • Pustular: rare, SEVERE form. PUSTULES form under erythematous lesions. (emergency)
  • Erythrodermic: EXTENSIVE ERYTHEMATOUS inflamed areas covering most of the surface area of the skin. Raw exposed areas when skin comes away. (emergency)
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34
Q

Presentation of psoriasis

A

Well-demarcated erythematous SCALY plaques - lesions can be itchy, burning or painful

Signs:
- Auspitz sign -> small points of bleeding when plaques are scraped off
- Koebner phenomenon -> psoriatic lesions at areas of skin affected by trauma
- 50% have associated nail changes

35
Q

Mx of psoriasis

A
  • Emollients

Topical (mild-mod):
- VITAMIN D analogues e.g.
Calcitriol,
- CORICOSTEROIDS
(betamethasone)
- KERATOLYTICS (salicylic
acid)
- COAL TAR scalp therapy

PHOTOTHERAPY (extensive disease)

36
Q

What is eczema

A
  • Eczema (or dermatitis) = papules and vesicles on an erythamatous base
  • atopic eczema most common -> usually in childhood
37
Q

Causes of eczema

A
  • not fully understood
  • often family history of atopy -> eczema, asthma, allergic rhinitis (hayfever)
  • Primary genetic defect in skin barrier function -> exacerbated by infections, allergens, sweating, heat and severe stress
38
Q

Px of eczema

A
  • ITCHY, ERYTHEMATOUS, dry scaly patches
  • Infants: face + extensor
    Children + adults: flexor
  • acute lesions erythematous, vesicular and weepy (exudative)
  • chronic scratching/rubbing can lead to EXCORIATIONS (breaks in the skin) and lichenification (hyperpigmentation and thickening of skin).
39
Q

Mx of eczema

A
  • General: avoid exacerbating factors, frequent emollients, bath oil substitute
  • topical steroids for flare ups (mild-moderate)
  • topical steroid sparing agents -> typically maintenance rather than acute flares
40
Q

Complications of eczema

A
  • secondary bacterial infection (crusty weepy lesions)
  • secondary viral infection -> molluscum contagiosum, viral warts and eczema herpeticum
41
Q

What scoring system is used for psoriasis severity

A

PASI (psoriasis area and severity index) -> 0-5 none to mild, 6-10 moderate, 11+ severe

42
Q

What is nail psoriasis

A

Nail psoriasis, also known as psoriatic nail dystrophy, is due to psoriasis involving the nail matrix or nail bed, resulting in specific and non-specific clinical changes in the nail.

43
Q

Clinical features of nail psoriasis

A
  • Pitting
  • Leukonychia
  • Red spots in lunule
  • Onychorrhexis (longitudinal nail ridge, split, or fissure)
  • Beau lines (transverse lines and ridges)
  • Nail crumbling
44
Q

Specific skin cancer history questions?

A
  • HPC: duration of lesion, any change + what change (size/shape/colour), associated sx (bleeding/itching/crusting)
  • RF’s:
    Where born,
    Lived abroad,
    Travel (where, length), Sunburn previously (blistering episodes), Suncream use,
    Sun beds,
    Occupation,
    Fitzpatrick skin type
45
Q

General skin cancer categories

A
  • Non-melanoma: basal cell carcinoma, squamous cell carcinoma
  • Melanoma: malignant melanoma (most life-threatening)
46
Q

Fitzpatrick skin types

A

1: always burns, never tans
-> very fair, often red/strawberry blonde hair. Blue/green eyes.
2: burns easily, tans poorly
-> fair skin and hair. Pale eyes.
3: sometimes burns, tans easily
-> darker white skin.
4: rarely burns, tans easily
-> Light brown skin/olive skin tones
5: rarely burns, tans easily
-> Brown skin. Usually dark hair and dark eyes.
6: Very rarely burns and tans dark easily
-> Dark brown or black skin

47
Q

What is basal cell carcinoma

A
  • Slow-growing, locally invasive, malignant epidermal skin tumours which are thought to arise from hair follicles.
  • Only rarely metastasises
  • Most common malignant skin tumour
  • Prognosis excellent
48
Q

Risk factors for basal cell carcinoma

A
  • UV exposure, history of frequent sunburn in childhood
  • Skin type I and II, male sex, increasing age
  • Previous history of skin cancer - chance of developing a second BCC within 3 years is 44%.
  • genetic predisposition
49
Q

Presentation of basal cell carcinoma

A
  • Most commonly on head and neck. Rest mainly on trunk and lower limbs.
  • Nodular (most common) -> solitary, shiny/pearly + red nodule or papule with rolled edges and telangiectasia; may be ulcerated.
  • Superficial -> plaque like
  • Morphoeic -> sclerosing/scar-like + skin-coloured, poorly defined borders
  • Pigmented -> brown, blue or greyish lesion (may resemble malignant melanoma)
50
Q

Management of basal cell carcinoma

A
  1. Excision (tx of choice)
  2. Mohs micrographic surgery (high risk, recurrent tumours)
  3. Other e.g. Cryotherapy or topical cream
  4. Radiotherapy - when surgery not appropriate.
51
Q

What is squamous cell carcinoma

A
  • second most common skin cancer
  • arises from the keratinising/squamous cells of the epidermis (that have been pushed upwards from basal cells.)
  • Locally invasive malignant tumour, which has the potential to metastasise (locally or spread to lymph nodes) but still rare.
52
Q

RF’s of squamous cell carcinoma

A
  • excessive UV exposure
  • pre-malignant skin conditions e.g. actinic keratoses
  • chronic inflammation - near chronic leg ulcers, wound scars
  • immunodeficiency
53
Q

Presentation of squamous cell carcinoma

A
  • Keratotic (overgrowth of keratin, scaly/crusty) nodule or tumour that may ulcerate.
  • non-healing ulcer or growth in sun exposed areas - most commonly on skin of head and neck.
54
Q

Mx of squamous cell carcinoma

A
  1. Surgical excision
  2. Mohs micrographic surgery for large, recurrent
  3. Radiotherapy for large, non-resectable tumours
55
Q

What is malignant melanoma

A
  • An invasive malignant tumour of the epidermal melanocytes, which has the potential to metastasise. One of most aggressive cancers.

Further:
- melanoma’s have 2 growth phases: radial and vertical. During the radial growth phase, malignant cells grow in a radial fashion in the epidermis. With time, most melanomas progress to the vertical growth phase, in which the malignant cells invade the dermis and develop the ability to metastasise.

56
Q

RF’s for melanoma

A
  • excessive UV exposure, skin type I and II, history of sunburn (particularly blistering)
  • sunbeds
  • history of multiple moles or atypical moles
  • FH or previous history of melanoma
57
Q

4 Types of melanoma

A

classified according to growth pattern:
- Superficial spreading (most common / 70%) -> large, flat, irregularly pigmented lesion which grows laterally before vertical invasion develops. Trunk and lower limbs in young/middle-aged adults.
- Nodular melanoma (most aggressive) -> rapidly growing pigmented (blue-black) nodule which bleeds or ulcerates. Common on the trunk in young/middle-aged adults.
- Lentigo maligna -> flat, tan-like, large freckles/patch. Can develop into a papule or nodule, signalling invasive tumour. Older patients and mostly on the face.
- Acral lentiginous -> pigmented lesions on the palm, sole and nail. In elderly population, no relation to UV exposure.

58
Q

Presentation of melanoma

A

‘ABCDE symptoms’
Asymmetrical shape*
Border irregularity
Colour irregularity*
Diameter >6mm
Evolution of lesion (e.g. change in size and/or
shape)*
Symptoms (e.g. bleeding, itching)
* = major (2 points scored. Minor is 1 point)
2 week referral for score of 3+.

59
Q

Mx of melanoma

A
  1. Excision +/- radiotherapy
  2. Chemotherapy for metastatic disease

Prognosis depends on stage of melanoma
-> in general, 90% of people diagnosed in England and Wales survived 10+ years.

60
Q

Tumour staging for malignant melanoma

A
  • Tumour size (4)
    T1: <1mm
    T2: 1-2mm
    T3: 2-4mm
    T4: 4+mm
    a = no ulceration present
    b = ulceration present to all stages
  • Lymph nodes (4)
    N0: no regional metastases
    N1: one tumour involved node
    N2: two or three tumour involved nodes
    N3: four+ tumour involved nodes
  • Metastases (2)
    M0: no evidence of distant metastases
    M1: distant metastases (skin, lung, other non-CNS sites, CNS)
  • Overall staging
    0 = tumour is in situ/pre-cancerous
    1 = Tumour size small, no nodal involvement or mets
    2 = Tumour size bigger or ulceration present
    3 = Nodal involvement
    4 = Metastases evident
61
Q

Essential management for all dermatological emergencies

A

i) full supportive care - ABC of resuscitation
ii) withdrawal of precipitating agents
iii) management of associated complicaitons
iv) specific treatment

62
Q

What is urticaria/hives?

A

Is an itchy red blotchy rash resulting from swelling of the superficial part of the skin - can be localised or widespread.
-> Angio-oedema occurs when the deeper tissues, lower dermis and subcutaneous tissues, are involved and become swollen.

63
Q

Pathophysiology of Urticaria

A
  • due to a local increase in permeability of capillaries and small venules. Histamine from mast cell degranulation play major role in swelling/inflammatory response.
64
Q

Presentation of Urticaria

A
  • swelling at epidermis of skin -> central itchy white papule (wheal), surrounded by erythematous flare.
  • individual lesions are typically TRANSIENT - come and go within a few mins to hours. New wheals appearing other places (‘migratory’)
  • may be associated with swelling of the soft tissues of the eyelids, lips and tongue (angio-oedema).
  • can get acute (sx<6wk), chronic (sx>6wk)
65
Q

Triggers/causes of urticaria

A
  • Idiopathic
  • Allergies: foods, bites, stings, medication
  • Viral infections such as hepatitis
  • Bacterial infections
  • Physical stimuli - pressure, heat, cold, firm rubbing
66
Q

Urticaria mx

A
  • identify and treat cause/non specific triggers should be minimised
    1. Non-sedating H1 antihistamines e.g. cetirizine.
    2. Sedating antihistamine e.g. chlorphenamine may be used if itch is interfering with sleep
    3. Corticosteroids for severe acute urticaria and angioedema
67
Q

Complications of urticaria

A

Anaphylaxis -> bronchospasm, facial and laryngeal oedema, hypotension.
-> can lead to asphyxia, cardiac arrest and death. (medical emergency)

Mx: adrenaline, corticosteroids, antihistamines

68
Q

Differences between atopic dermatitis and psoriasis

A

Eczema
- itching more severe in eczema
- scratching can cause excoriations
- atopic history
- common sites: cheeks/face (infants), skin creases (e.g. inside of elbows)

Psoriasis
- Red or silvery scales
- scratching can rip off scales and cause bleeding
- scalp, knuckles, back, knees common sites

69
Q

What is erythema nodosum

A
  • a painful, inflammatory condition characterised by inflammation of subcutaneous fat.
  • It is a hypersensitivity reaction in response to a variety of stimuli
70
Q

Causes of erythema nodosum

A
  • idiopathic (50%)
  • Group A Strep infections
  • Primary tuberculosis (Tb) infection
  • IBD
  • Sarcoidosis
  • Pregnancy
71
Q

Presentation of erythema nodosum

A
  • Prodrome of arthralgia (commonly of ankles and knees), malaise and fever
  • Tender, warm, erythematous nodules. Borders poorly defined.
  • Lesions continue to appear for 1-2 weeks and leave bruise-like discolouration as they resolve.
  • Most commonly at shins.
72
Q

Mx of erythema nodosum

A
  • Treat underlying cause -> could be life threatening
  • Usually self-limiting, supportive therapies:
    bed rest, elevation of affected limbs, NSAIDs
73
Q

What is eczema herpeticum

A
  • A serious/emergency complication of atopic eczema that occurs with infection of the herpes simplex virus (HSV)
    -> eczema causes breaks in the skin which allows the virus in.
74
Q

Presentation of eczema herpeticum

A
  • Extensive groups of itchy painful blisters, erosions (breakdown of outer layer of skin) and crusted papules.
  • Systemically unwell with fever and malaise
75
Q

DDx of eczema herpeticum

A
  • Impetigo. Clinical presentation can be mistaken for impetigo
76
Q

Mx of eczema herpeticum

A
  • Antivirals (e.g. aciclovir)
  • Antibiotics for bacterial secondary infection
77
Q

Complications of eczema herpeticum

A
  • Secondary bacterial infections
  • Herpes hepatitis
  • Encephalitis
  • DIC
  • Death (very rare)
78
Q

What is Erythroderma

A
  • intense redness of the skin covering at least 90% of skin surface area
79
Q

Causes of erythroderma

A
  • Previous skin disease e.g. PSORIASIS (most common), eczema.
  • Drug eruptions
  • Malignancies
80
Q

Presentation of erythroderma

A
  • Hot, erythematous skin covering atleast 90% of skin surface
  • Skin will often show signs of desquamation (peeling) of the skin.
  • Systemically unwell with lymphadenopathy and malaise
81
Q

Mx of erythroderma

A
  • Dermatological emergency - if systemically unwell, admit to ICU or specialist burns unit
  • Treat underlying cause, where known
  • Emollients and wet-wraps to maintain skin moisture.
  • Topical steroids may help to relieve inflammation
82
Q

Complications of erythroderma

A
  • Dehydration
  • Electrolyte imbalance
  • Secondary bacterial infection
  • Hypothermia
  • Cardiac failure
  • mortality ranges from 20-40%.
83
Q

What is erythema multiforme

A
  • skin condition considered to be a hypersensitivity reaction to infections or drugs.
  • HSV is the main precipitating factor
84
Q

Presentation of erythema multiforme

A
  • Target lesions: concentric rings of colour variation -> central dark red area, surrounded by lighter oedematous area, with a peripheral erythematous margin. Lesions can expand to form plaques, several cm in diameter.
  • appear first on extensors - palms, neck and face.
  • may be mucosal involvement but it tends to be mild and limited to just one mucosal surface - oral lesions most common (lips, palate, gingiva)
85
Q

Mx of erythema multiforme

A
  • typically Self-limiting. Supportive - analgesics, mouthwash
  • treat underlying cause
  • Secondary infection of lesions may occur
86
Q

DDx of erytherma multiforme

A
  • SJS
  • TEN
  • Urticaria - In erytherma, lesions are fixed (+ fades over 2-4 weeks) and not migratory/transient (appearances can change in mins-hours. Rash usually settles within a few days).

Phase 3B (1 decks)

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