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4 - Med > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What are the functions of the skin ? (5)

A
  • Barrier (protect for mechanical, chemical, UV)
  • Thermal regulation
  • Vit D synthesis
  • Sensory organ (pain, pressure, touch)
  • Aesthetics and communication
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2
Q

What are the 3 layers to the skin ? superficial to deep

A
  • epidermis
  • dermis
  • hypodermis (subcutis)
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3
Q

What are the different layers to the epidermis ? how many ? describe a bit. what cells are involved ?

A

Stratum basale, spinosum, granulosum, lucidum, corneum
- mitosis of keratinocytes => progress more superficially (increased keratin production + migration toward the external surface)

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4
Q

What is cornification ? and how long does it take ?

A

the increased keratin production and migration of keratinocytes more superficially
- takes 30-40 days

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5
Q

What are melanocytes ? in which layer of the skin are they found ?

A

melanin producing cells (form the pigment and distribute to surrounding are through dendrites)
- found in the basal layer of the epidermis

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6
Q

what is the purpose of melanin ? how do ppl of darker skin vary melanin/melanocyte-wise ?

A

melanin protects against UV
- ppl of darker skin have same number of melanocytes but produce more melanin (so have greater protection against UV)

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7
Q

What is the dermis ? what is contained within it ?

A

Thick inner portion of skin which consists of connective tissue
- contains nerves, blood vessels, sweat glands, pilisebacious units
- fibroblasts synthesise the extracellular matrix

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8
Q

what are the 2 types of sweat glands ? describe ? distribution ?

A
  • eccrine glands: cover most of the body: clear, odourless
  • Apocrine glands: axillary + genital regions => body odour
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9
Q

What is the hypodermis ?

A

major body store of adipose tissue (Varies in size)
- contains blood and lymph vessels, sweat glands

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10
Q

list some non-melanoma skin cancers ?

A
  • Basal cell carcinoma
  • Squamous cell carcinoma
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11
Q

what is a BCC ?

A

non-melanoma form of skin cancer that rarely metastasises
- most common type of cancer in the world

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12
Q

What cell layer does BCC affect ?

A

affects the stratum basale of the epidermis

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13
Q

what causes BCC development ?

A

develop from mutations (usually PTCH, TP53 genes)

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14
Q

BCC RF ?

A
  • UV radiation (esp acute intermittent at young age)
  • fear skin (Fitzpatrick I,II)
  • skin canc Hx
  • ionising radiation
  • increasing age
  • immunosuppression
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15
Q

describe BCC vs SCC UV RF ?

A
  • SCC (chronic cumulative)
  • BCC (intermittent intense)
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16
Q

what are the different subtypes of BCC ? (4) which most common ? describe each a bit

A
  • Nodular BCC (most common): pearly shiny papule/nodules, telangiectasis, rolled borders, depressed centre
  • Superficial BCC: plaque or patch of well defined scaly pink skin
  • Morpheaform BCC: poorly defined, pale scar of indurated plaque
  • Pigmented BCC: can be difficult to distinguish from melanoma
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17
Q

where on body are BCCs usually located ?

A

SLOW GROWING
face, nose, forehead, cheeks, nasolabial folds

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18
Q

BCC Ix ?

A
  • History + exam + dermoscopy
  • Definitive Dx requires biopsy + histopathological examination
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19
Q

BCC Mx ?

A

depends on subtype/size/location
- Complete surgical removal (wide local excision, Moh’s surgery)
- Radiotherapy (can only be done once in same location so not usually first line)
- topical therapy: 5-flurouracil (effudix), PDT (photodynamic therapy)

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20
Q

BCC complications ?

A
  • reccurance (rodent ulcer)
  • increase risk of other skin canc (including melanoma)
  • aggressive canc can invade and destroy bones
  • very rarely metastasise
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21
Q

What is SCC ?

A

form of non-melanoma skin cancer
- 2nd most common skin can following bcc
- risk of malignancy

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22
Q

SCC aetiology ? which histological skin layer ? which UV in particular ?

A

cancerous mutations occur in keratinocytes of the epidermis - Stratum spinosum (just above basal layer)
- chronic UV exposure (esp UVB) => damage DNA of squamous keratinocytes

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23
Q

SCC RF ?

A
  • UV radiation (esp UVB)
  • immunosuppresion
  • Fitzpatrick types I+II
  • increasing age
  • male
  • smoking
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24
Q

SCC clinical features ? describe lesion ? distribution ?

A

RAPID GROWING
on sun exposed areas (lips, back of hands, upper face, scalp)
- rapid growth, ulcerate/bleed/pain
- morphology: firm to palpate (nodular/plaque like) may ulcerate/bleed, crusty top

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25
Q

SCC Ix + Mx ?

A

2WW for potential SCC
- Biopsy (WLE), CT, MRI, sentinel lymph node biopsy
- If lymph node spread, radiotherapy

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26
Q

name some pre-malignant skin conditions ? why are these concerning ?

A

pre malignant keratinocyte tumours: actinic keratosis, bowens disease
- can progress to become SCCs

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27
Q

What is actinic keratosis ? describe ?

A

pre canc scaly lesions on the skin (10% risk of SSC dev)
- partial thickness dysplasia of epidermal keratinocytes (begins in basal layer, but no invasion through BM cos then would be SCC)
- no ability to metastasise

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28
Q

actinic keratosis Hx ?

A

developed over yrs in sun exposed sites, no rapid growth, no pain, no bleeding
(no ability to metastasise but can become SCC)

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29
Q

what is Bowens disease ? another name for this ? describe it ?

A

SCC in situ: full thickness displays of epidermal keratinocytes (when the cancerous cells are confined to the epidermis)
- no ability to metastasise

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30
Q

Bowens disease Mx ?

A
  • Mx: topical (5-flurouracil), cryotherapy, C+C, PDT
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31
Q

What is melanoma ? arises where ?

A

it is a malignant cancer that arises from melanocyte layer (epidermal basal layer)

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32
Q

melanoma aetiology ?

A

melon occurs when melanocytes time cells undergo genetic transformation and proliferate uncontrollably

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33
Q

what is melanoma in situ ? invasive ? metastatic ?

A
  • in situ ( confined to epidermis
  • invasive (spread to dermis)
  • metastatic (tumour spread to other issues)
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34
Q

what are the subtypes of melanoma ? most common ? most aggressive ? most common in POC ?

A
  • Superficial spreading melanoma (most common)
  • Nodular melanoma (most aggressive)
  • lentigo maligno melanoma
  • Acral lentigenous melanoma (most common in POC)
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35
Q

what is sacral lentigenous melanoma ?

A

no connection to UV exposure
- worse prognosis
- located on soles of feet, nails

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36
Q

melanom RF ?

A
  • personal/FHx of melanoma
  • Pale skin (Fitzpatrick I/II)
    high freckle density
  • Hx of sunburn
  • tanning bed exposure
  • increasing age
  • outdoor occupation
  • UV exposure
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37
Q

describe melanoma lesion ?

A

A: asymmetrical
B: borders: irregular, jagged, poorly defined
C: colour: variation, change
D: diameter: most melanom >6mm
E: elevation, everything else

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38
Q

What is the most important prognostic factor in melanoma ?

A

breslow thickness (the depth that the melanoma extends to)

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39
Q

describe the stages to melanoma ? depends on what ?

A

depends on breslow thickness, if there is lymphatic/metastatic spread
- Stage 0: melanoma in situ
- Stage 1: melanoma <2mm thickness
- Stage 2: melanoma >2mm
- stage 3: melanoma spread to involve local lymph nodes
- Stage 4: metastases to distant sites

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40
Q

Melanoma Mx ?

A

2ww
- side local excision +/- sentinel lymph node biopsy
- radiotherapy, immunothepry

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41
Q

What is psoriasis ?

A

chronic autoimmune inflam condition characterised by clearly demarcated red, scaly patches

42
Q

psoriasis aetiology ? explain

A

autoimmune + T cell mediated => cytokine production => inflam cell infiltration (=> erythema) + keratinocyte proliferation (=> thickened stratum corner => scale)
- rapid federation of stratum corner => thickening of skin

43
Q

what is the relationship between FHx and psoriasis ?

A

1/3 patients have a FHx (genetic component bt no clear genetic link - multifactorial)

44
Q

psoriasis precipitating factors ?

A
  • precipitating: infections (esp strep for guttate), hormonal changes (post partum), initiation/withdrawal of drugs (BB, lithium, ACEI, NSAIDs)
45
Q

psoriasis exacerbating macros ?

A
  • trauma (abrasions, sunburn)
  • alcohol
  • stress
    (sun exposure) (though for most patients this has positive impacts)
46
Q

psoriasis presentaiton ? most common type ?

A
  • chronic plaque psoriases (most common), guttate (more common in kids)
  • Pruritic lesions, pain or urning around lesions,
  • O/E: well demarcated erythematous, silver, scaly plates (commonly over extensor surfaces)
47
Q

psoriasis associated sx ?

A
  • psoriatic arthritis (10-20% patients)
  • Nail psoriasis (pitting, thickening, discolouration, onycoloysis)
  • IBD
48
Q

What screening tool is used to determine if there is joint involvement in psoriasis ?

A

PEST score

49
Q

psoriasis Ix ?

A

clinical dx, if dx unclear then skin biopsy
- PASI (scoring system (psoriasis area + severity index)

50
Q

psoriases Mx ? (4 levels)

A

avoid exacerbating macros, smoking cessation, reduce alchol
- topical therapies: moisturing emolliants, topical corticosteroids, vit D analogue)
- Phototherapy with narrow band UVB (particularly useful in guttate)
- systemic therapies (methotrexate, cycolsporin
- biologics: anti TNF (adalimimab)

51
Q

What is eczema ?

A

chronic atopic condition caused by defects in normal continuity of skin barrier => inflam of skin (sx can really vary)

52
Q

eczema px ? distribution ?

A
  • erythema, swelling, crusting, erosions, fissuring, scaling
  • on flexor surfaces (inside of elbow and knees) and face and neck
  • periods where is it well controlled and then worse (flares)
53
Q

eczema pathophys ?

A

defects in barrier that skin provides => tiny gaps => entrance for irritants/microbes (infection)/ allergens => immune response => inflam

54
Q

what coring system is used to assess severity of dermatology conditions ?

A

DLQI (dermatology life quailed index)

55
Q

what is the overall approach to eczema Mx ?

A

maintenance therapy and mx of flares

56
Q

what is eczema maintenance therapy ?

A

create artificial barrier over skin to compensate with defective one (emollients)
- avoid scratching/scrubbing skin
- avoid harsh soaps/irritants/allergens

57
Q

describe the step-wise approach to eczema flares up mx ?

A
  • emolliants
  • topical steroids
  • systemic tx
  • phototherapy (marrow band UVB)
58
Q
A
59
Q

describe topical steroid use in eczema mx ?

A

use weakest steroid for shortest period
- mild (hydrocortisone), v potent (derogate)

60
Q

describe systemic tx in eczema mx ?

A
  • course of prednisolone
  • methotrexate
  • ciclosporin
  • azathioprine
61
Q

what are eczema pts more prone to infections ?

A

skin barrier breakdown => entry point for infective organisms

62
Q

what is eczema herpeticum ? px ? causative organism ?

A

viral skin infection in patients with eczema caused by HSV or VZV
- px: patient with eczema has developed widespread painful, vesicular rash (sometimes itchy)
- plus systemic sx: fever, lethargy irritably , reduced oral intake, lymphadenopathy

63
Q

eczema herpeticum mx ?

A

viral swab of vesicles
- treat with acyclovir

64
Q

eczema herpeticum complications ?

A

children can be v unwell
- bacterial super infection => more serious illness

65
Q

what is the most common causative organism of bacterial eczema infection ? mx ?

A

s.aureus
- mx: oral Abx (flucloxacillin)

66
Q

What is acne vulgaris ? characterised by ? (what morphology)

A

disorder of the pilosebaceous unit
- characterised by pustules, papule + comedones

67
Q

describe the pathophysiology of acne - what are the 4 contributing factors ?

A

disorder of pilsebacious unit (hair follicle + associated sebaceous gland)
- follicular hyperkeratinisation => blocks pores => comedones
- Increased sebum production (due to androgenic hormones)
- follicular colonisation by P.acnes
- Inflam mediators lead to inflam => scarring

68
Q

what are some acne RF ?

A
  • hormonal shifts (PCOS, CAH, exogenous (steroids, testosterone))
    medications
    high glycaemia index foods
69
Q

acne Px ?

A
  • closed comedome (withhead)
  • open someone (blackhead)
  • papules
  • pustelues
  • nodules
  • cysts
70
Q

Acne Mx ?

A
  • topical therapies: salicylic acid, benzoyl peroxide, topical retinoids
  • systemic therapies: OCP, Abx, isotretinoin
71
Q

list some isotreinion SE ?

A
  • dry skin/lips
  • photosensitivity
  • depression/suicidal ideation
  • TEN
72
Q

What is rosacea ?

A

centrofacial distribution of inflam lesions
- papular pustular roasiae (dome shaped erythematous papule)

73
Q

What is phymatous rosacea ?

A

sebaceous gland hypertrophy + fibrosis (can make nose big)

74
Q

What is ocular rosacea ?

A

can occur with or without cutaneous manifestations
- dry, gritty/itchy eyes, blepharitis

75
Q

how does UV exposure affect rosacea ?

A

makes it worse

76
Q

What is molluscs contagiosum ? how spread ? mx ?

A

benign lesion caused by MCV
- normal in childhood (reassure)
- spread by direct contact
- Mx: none (self limiting and will resolve in months), cryotherapy

77
Q

difference between between seborrhoea keratosis and solar lentigo ?

A

solar lentigo tends to be macular

78
Q

What are leg ulcers ? name 4 common types

A

wounds or breaks in skin that do not heal due to underlying pathology
- venous ulcers
- arterial ulcers
- diabetic foot ulcers
- pressure ulcers

79
Q

describe arterial ulcers ? what causes them ? describe the actual ulcer

A

result form insufficient blood supply to skin due to PAD (absent pulses, pallor, intermittent claudication)
- occur distally (affecting toes/dorsum of foot)
- are smaller + deeper (have well dfine/punched out appearance)
- are painful
- tend to be worse at night

80
Q

describe venous ulcers ? what causes them ? describe the actual ulcer

A

Due to pooling of blood + waste products secondary to venous insufficiency 9hyperpigmentation, venous eczema, lipodermatosclerosis)
- occur in gaiter area
- bigger and more superficial
- irregular sloping border
- more likely to bleed
- pain relieved by elevation

81
Q

What is impetigo ?

A

superficial bacterial infection of the skin
- v contagious nd spread through direct contact (+towels)

82
Q

Most common causative organism of impetigo ? name 2

A
  • s. aureus
  • s. pyogenes
83
Q

what are the 2 different types of impetigo ? describe ? which one is more common

A
  • Non-bullous (most common): crusted honey-coloured lesions
  • bullous: invade intact skin, systemically unwell
84
Q

Impetigo RF ?

A
  • atopic eczema
  • trauma to skin
  • immune suppression
  • burns
  • usually children
85
Q

impetigo Mx ? Dx ?

A
  • clinical Dx
  • if localised: hydrogen peroxide
  • if more widespread: topical Abx
86
Q

What is Erysipelas ? which skin layers does it affect ?

A

(type of cellulitis): superficial form of cellulitis: affects upper dermis + superficial cutaneous lymphatics

87
Q

Erysipelas causative organism ?

A

almost always group A strep (s. pyogenes)

88
Q

Erysipelas px ? where on body ?

A

face, lower legs
- well demarcated, oedema, swollen, tender, fever/malaise/lymphadenopathy

89
Q

Erysipelas Dx ? Mx ?

A
  • clinical dx, consider blood tests
  • Mx: analgesia (as is v painful), elevation/compression (if lower leg), abx (always systemic so oral/IV)
90
Q

What is cellulitis ? causative organisms ?

A

common bacterial infection of lower dermis + submit tissue
- strep pyogenes, s. aureus

91
Q

cellulitis px ?

A
  • unilateral, erythamtous rash (diffuse or well-demarcated), hot, tender, oedematous, blisters, ulcers
  • fever/ malaise/ lymphadenopathy
92
Q

cellulitis mx ?

A
  • similar to erysipelas
  • clinical dx, analgesia, Abx (systemic)
93
Q

difference between cellulitis and erysipelas ?

A

if it spreads to lower dermis then it is cellulitis
- depends on the depth that is infected

94
Q

What is Herpes simplex ? where 2 the 2 most common strands affect ? how transmitted ?

A

can affect any area of skin or mucous membrane
- HSV1: oral/facial infections
- HSV2: genital/rectal infections
transmission: sexual, childbirth, direct contact, minor injury

95
Q

herpes Px ? over time ?

A
  • primary episode: localised burning/tingling, painful clustered vesicles/pustules/erosions
  • recurrent eps: usually milder, at same primary site, when relative immune suppression
96
Q

what is eczema herpiticum ? px ?

A

HSV1 infection in pt with pre-existing skin condition (atopic eczema)
- px: widespread, erythematous, painful with vesicles + pus

97
Q

eczema herpeticum Mx ? complications ?

A

Mx: viral swab, with acyclovir
complications: can be life threatening with immunosuppressed (bacterial superinfection => more severe infection (needs Abx))

98
Q

What is tines capitis ? affects who ?

A

fungal infection, contagious
- epi: pro-adolescent children, immune compromised adults

99
Q

tinea capitus Px ?

A

well demarcated hair loss, itching, dryness + erythema of the scalp, scaly

100
Q

tines capitus dx ? mx ?

A

dx: clinical Dx, microscopy + culture (hair plucking and skin scraping - so that you pick up ectothrix (cover surface of hair) and endothrix (retained inside hair)
- Mx: oral terbinafine (anti-fungal) plus ketoconazole shampoo (reduces infectivity)

4 - Med (12 decks)

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