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
2
Q
What are the 3 layers to the skin ? superficial to deep
A
- epidermis
- dermis
- hypodermis (subcutis)
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)
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
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
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)
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
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
9
Q
What is the hypodermis ?
A
major body store of adipose tissue (Varies in size)
- contains blood and lymph vessels, sweat glands
10
Q
list some non-melanoma skin cancers ?
A
- Basal cell carcinoma
- Squamous cell carcinoma
11
Q
what is a BCC ?
A
non-melanoma form of skin cancer that rarely metastasises
- most common type of cancer in the world
12
Q
What cell layer does BCC affect ?
A
affects the stratum basale of the epidermis
13
Q
what causes BCC development ?
A
develop from mutations (usually PTCH, TP53 genes)
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
15
Q
describe BCC vs SCC UV RF ?
A
- SCC (chronic cumulative)
- BCC (intermittent intense)
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
17
Q
where on body are BCCs usually located ?
A
SLOW GROWING
face, nose, forehead, cheeks, nasolabial folds
18
Q
BCC Ix ?
A
- History + exam + dermoscopy
- Definitive Dx requires biopsy + histopathological examination
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)
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
21
Q
What is SCC ?
A
form of non-melanoma skin cancer
- 2nd most common skin can following bcc
- risk of malignancy
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
23
Q
SCC RF ?
A
- UV radiation (esp UVB)
- immunosuppresion
- Fitzpatrick types I+II
- increasing age
- male
- smoking
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
25
SCC Ix + Mx ?
2WW for potential SCC
- Biopsy (WLE), CT, MRI, sentinel lymph node biopsy
- If lymph node spread, radiotherapy
26
name some pre-malignant skin conditions ? why are these concerning ?
pre malignant keratinocyte tumours: actinic keratosis, bowens disease
- can progress to become SCCs
27
What is actinic keratosis ? describe ?
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
28
actinic keratosis Hx ?
developed over yrs in sun exposed sites, no rapid growth, no pain, no bleeding
(no ability to metastasise but can become SCC)
29
what is Bowens disease ? another name for this ? describe it ?
SCC in situ: full thickness displays of epidermal keratinocytes (when the cancerous cells are confined to the epidermis)
- no ability to metastasise
30
Bowens disease Mx ?
- Mx: topical (5-flurouracil), cryotherapy, C+C, PDT
31
What is melanoma ? arises where ?
it is a malignant cancer that arises from melanocyte layer (epidermal basal layer)
32
melanoma aetiology ?
melon occurs when melanocytes time cells undergo genetic transformation and proliferate uncontrollably
33
what is melanoma in situ ? invasive ? metastatic ?
- in situ ( confined to epidermis
- invasive (spread to dermis)
- metastatic (tumour spread to other issues)
34
what are the subtypes of melanoma ? most common ? most aggressive ? most common in POC ?
- Superficial spreading melanoma (most common)
- Nodular melanoma (most aggressive)
- lentigo maligno melanoma
- Acral lentigenous melanoma (most common in POC)
35
what is sacral lentigenous melanoma ?
no connection to UV exposure
- worse prognosis
- located on soles of feet, nails
36
melanom RF ?
- personal/FHx of melanoma
- Pale skin (Fitzpatrick I/II)
high freckle density
- Hx of sunburn
- tanning bed exposure
- increasing age
- outdoor occupation
- UV exposure
37
describe melanoma lesion ?
A: asymmetrical
B: borders: irregular, jagged, poorly defined
C: colour: variation, change
D: diameter: most melanom >6mm
E: elevation, everything else
38
What is the most important prognostic factor in melanoma ?
breslow thickness (the depth that the melanoma extends to)
39
describe the stages to melanoma ? depends on what ?
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
40
Melanoma Mx ?
2ww
- side local excision +/- sentinel lymph node biopsy
- radiotherapy, immunothepry
41
What is psoriasis ?
chronic autoimmune inflam condition characterised by clearly demarcated red, scaly patches
42
psoriasis aetiology ? explain
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
what is the relationship between FHx and psoriasis ?
1/3 patients have a FHx (genetic component bt no clear genetic link - multifactorial)
44
psoriasis precipitating factors ?
- precipitating: infections (esp strep for guttate), hormonal changes (post partum), initiation/withdrawal of drugs (BB, lithium, ACEI, NSAIDs)
45
psoriasis exacerbating macros ?
- trauma (abrasions, sunburn)
- alcohol
- stress
(sun exposure) (though for most patients this has positive impacts)
46
psoriasis presentaiton ? most common type ?
- 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
psoriasis associated sx ?
- psoriatic arthritis (10-20% patients)
- Nail psoriasis (pitting, thickening, discolouration, onycoloysis)
- IBD
48
What screening tool is used to determine if there is joint involvement in psoriasis ?
PEST score
49
psoriasis Ix ?
clinical dx, if dx unclear then skin biopsy
- PASI (scoring system (psoriasis area + severity index)
50
psoriases Mx ? (4 levels)
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
What is eczema ?
chronic atopic condition caused by defects in normal continuity of skin barrier => inflam of skin (sx can really vary)
52
eczema px ? distribution ?
- 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
eczema pathophys ?
defects in barrier that skin provides => tiny gaps => entrance for irritants/microbes (infection)/ allergens => immune response => inflam
54
what coring system is used to assess severity of dermatology conditions ?
DLQI (dermatology life quailed index)
55
what is the overall approach to eczema Mx ?
maintenance therapy and mx of flares
56
what is eczema maintenance therapy ?
create artificial barrier over skin to compensate with defective one (emollients)
- avoid scratching/scrubbing skin
- avoid harsh soaps/irritants/allergens
57
describe the step-wise approach to eczema flares up mx ?
- emolliants
- topical steroids
- systemic tx
- phototherapy (marrow band UVB)
58
59
describe topical steroid use in eczema mx ?
use weakest steroid for shortest period
- mild (hydrocortisone), v potent (derogate)
60
describe systemic tx in eczema mx ?
- course of prednisolone
- methotrexate
- ciclosporin
- azathioprine
61
what are eczema pts more prone to infections ?
skin barrier breakdown => entry point for infective organisms
62
what is eczema herpeticum ? px ? causative organism ?
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
eczema herpeticum mx ?
viral swab of vesicles
- treat with acyclovir
64
eczema herpeticum complications ?
children can be v unwell
- bacterial super infection => more serious illness
65
what is the most common causative organism of bacterial eczema infection ? mx ?
s.aureus
- mx: oral Abx (flucloxacillin)
66
What is acne vulgaris ? characterised by ? (what morphology)
disorder of the pilosebaceous unit
- characterised by pustules, papule + comedones
67
describe the pathophysiology of acne - what are the 4 contributing factors ?
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
what are some acne RF ?
- hormonal shifts (PCOS, CAH, exogenous (steroids, testosterone))
medications
high glycaemia index foods
69
acne Px ?
- closed comedome (withhead)
- open someone (blackhead)
- papules
- pustelues
- nodules
- cysts
70
Acne Mx ?
- topical therapies: salicylic acid, benzoyl peroxide, topical retinoids
- systemic therapies: OCP, Abx, isotretinoin
71
list some isotreinion SE ?
- dry skin/lips
- photosensitivity
- depression/suicidal ideation
- TEN
72
What is rosacea ?
centrofacial distribution of inflam lesions
- papular pustular roasiae (dome shaped erythematous papule)
73
What is phymatous rosacea ?
sebaceous gland hypertrophy + fibrosis (can make nose big)
74
What is ocular rosacea ?
can occur with or without cutaneous manifestations
- dry, gritty/itchy eyes, blepharitis
75
how does UV exposure affect rosacea ?
makes it worse
76
What is molluscs contagiosum ? how spread ? mx ?
benign lesion caused by MCV
- normal in childhood (reassure)
- spread by direct contact
- Mx: none (self limiting and will resolve in months), cryotherapy
77
difference between between seborrhoea keratosis and solar lentigo ?
solar lentigo tends to be macular
78
What are leg ulcers ? name 4 common types
wounds or breaks in skin that do not heal due to underlying pathology
- venous ulcers
- arterial ulcers
- diabetic foot ulcers
- pressure ulcers
79
describe arterial ulcers ? what causes them ? describe the actual ulcer
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
describe venous ulcers ? what causes them ? describe the actual ulcer
Due to pooling of blood + waste products secondary to venous insufficiency 9hyperpigmentation, venous eczema, lipodermatosclerosis)
- occur in gaiter area (between top of foot and bottom of the calf muscle)
- bigger and more superficial
- irregular sloping border
- more likely to bleed
- pain relieved by elevation
81
what ix would you do for suspected leg ulcer ? (3)
- ABPI (used to assess for arterial disease)
- blood tests (assess for infection and comorbididitesi - HbA1c)
- charcoal swab (if infection suspected)
82
arterial ulcer mx ? what is NOT done ?
- mx same as PAD: urgent referral to vascular to consider surgical revascularisation
- debridement and compression are NOT used
83
venous ulcer mx ? (3)
- Cleaning, debridement and dressing (need good district nurse input)
- compression therapy is used to treat venous ulcers (after arterial disease is excluded with ABPI)
- analgesia (avoid NSAIDs)
84
What is impetigo ?
superficial bacterial infection of the skin
- v contagious nd spread through direct contact (+towels)
85
Most common causative organism of impetigo ? name 2
- s. aureus
- s. pyogenes
86
what are the 2 different types of impetigo ? describe ? which one is more common
- Non-bullous (most common): crusted honey-coloured lesions
- bullous: invade intact skin, systemically unwell
87
Impetigo RF ?
- atopic eczema
- trauma to skin
- immune suppression
- burns
- usually children
88
impetigo Mx ? Dx ?
- clinical Dx
- if localised: hydrogen peroxide
- if more widespread: topical Abx
89
What is Erysipelas ? which skin layers does it affect ?
(type of cellulitis): superficial form of cellulitis: affects upper dermis + superficial cutaneous lymphatics
90
Erysipelas causative organism ?
almost always group A strep (s. pyogenes)
91
Erysipelas px ? where on body ?
face, lower legs
- well demarcated, oedema, swollen, tender, fever/malaise/lymphadenopathy
92
Erysipelas Dx ? Mx ?
- clinical dx, consider blood tests
- Mx: analgesia (as is v painful), elevation/compression (if lower leg), abx (always systemic so oral/IV)
93
What is cellulitis ? causative organisms ?
common bacterial infection of lower dermis + submit tissue
- strep pyogenes, s. aureus
94
cellulitis px ?
- unilateral, erythamtous rash (diffuse or well-demarcated), hot, tender, oedematous, blisters, ulcers
- fever/ malaise/ lymphadenopathy
95
cellulitis mx ?
- similar to erysipelas
- clinical dx, analgesia, Abx (systemic)
96
difference between cellulitis and erysipelas ?
if it spreads to lower dermis then it is cellulitis
- depends on the depth that is infected
97
What is Herpes simplex ? where 2 the 2 most common strands affect ? how transmitted ?
can affect any area of skin or mucous membrane
- HSV1: oral/facial infections
- HSV2: genital/rectal infections
transmission: sexual, childbirth, direct contact, minor injury
98
herpes Px ? over time ?
- primary episode: localised burning/tingling, painful clustered vesicles/pustules/erosions
- recurrent eps: usually milder, at same primary site, when relative immune suppression
99
what is eczema herpiticum ? px ?
HSV1 infection in pt with pre-existing skin condition (atopic eczema)
- px: widespread, erythematous, painful with vesicles + pus
100
eczema herpeticum Mx ? complications ?
Mx: viral swab, with acyclovir
complications: can be life threatening with immunosuppressed (bacterial superinfection => more severe infection (needs Abx))
101
What is tines capitis ? affects who ?
fungal infection, contagious
- epi: pro-adolescent children, immune compromised adults
102
tinea capitus Px ?
well demarcated hair loss, itching, dryness + erythema of the scalp, scaly
103
tines capitus dx ? mx ?
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)
104
what different types of burns are there ? (4) causes
- thermal
- contact
- chemical
- electrical
105
what counts as a major burn ?
>15% TBSA (>10% children) of partial or full thickness burns
106
in what two ways is burn severity determined ? why important
- TBSA
- burn depth
guides therapy
107
what fluids and how much should be given for a burn ? over what time frame ?
hartmanns crystalloid
- 4ml x Weight x %TBSA
- 50% given with first 8 hours and the remaining 50% given in the remaining 16
