DERM Flashcards

1
Q

what should you do when performing an examination of the skin?

A

There are four important principles in performing a good examination of the skin: INSPECT, DESCRIBE, PALPATE and SYSTEMATIC CHECK

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2
Q

when you are inspecting the skin what should you note?

A

General observation
Site and number of lesion(s)
If multiple, pattern of distribution and configuration

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3
Q

when describing and examining a lesion on the skin what should you note?

A

SCAM
Size (the widest diameter), Shape Colour
Associated secondary change Morphology, Margin (border)

palpate the individual lesion and note the surface, consistency, mobility, tenderness and temperature

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4
Q

what features of a lesion would increase the likelihood of it being a melanoma?

A

*If the lesion is pigmented, remember ABCD
(the presence of any of these features increase the likelihood of melanoma):

Asymmetry (lack of mirror image in any of the four quadrants)
Irregular Border
Two or more Colours within the lesion Diameter > 6mm

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5
Q

what is a naevus?

A

A localised malformation of tissue structures

e.g. Pigmented melanocytic naevus is a mole

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6
Q

what are comedones?

A

A plug in a sebaceous follicle containing altered sebum, bacteria and cellular debris; can present as either open (blackheads) or closed (whiteheads)

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7
Q

what words are used describe the distribution of a lesion?

A

Generalised - All over the body
Widespread - Extensive
Localised - Restricted to one area of skin only
Flexural - Body folds i.e. groin, neck, behind ears, popliteal and antecubital fossa
Extensor - Knees, elbows, shins
Pressure areas - Sacrum, buttocks, ankles, heels
Dermatome - An area of skin supplied by a single spinal nerve
Photosensitive - Affects sun-exposed areas such as face, neck and back of hands
Koebner phenomenon - a linear eruption arising at the site of trauma

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8
Q

what words are used to describe the configuration of a lesion?

A

Discrete - Individual lesions separated from each other
Confluent - Lesions merging together
Linear - in a line
Target - concentric rigs (like a dartboard)
annular - like a circle or ring (e.g. ringworm)
Discoid/Nummular - a coin-shaped/round lesions (e.g. discoid eczema)

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9
Q

what is the different terminology used to describe the colour of lesions?

A

Erythema - Redness (due to inflammation and vasodilation) which blanches of pressure e.g. palmar erythema
Purpura - red or purple colour (due to bleeding into the skin or mucous membrane) which does not blanch on pressure. It can be petechiae (small pinion macules) or ecchymoses (larger bruises-like patches)
Hypo pigmentation - areas of paler skin
Depigmentation - white skin due to absence of melanin
Hyperpigmentation - darker skin which may be due to various causes

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10
Q

what is the different terminology to describe morphology of lesions?

A

macule - a flat area of altered colour (freckles are macular)
patch - larger flat area of altered colour or texture -(port wine stain is a patch)
Papule - solid raised lesion less than 0.5cm in diameter
Nodule - solid raised lesion greater than 0.5cm in diameter with a deeper component
Plaque - palpable scaling raised lesion >0.5cm in diameter
vesicle (small blister) - raised, clear fluid-filled lesion <0.5cm in diameter
Bulla (larger blister) - raised, clear fluid filled lesion greater than 0.5cm in diameter
Pustule - pus containing lesion less than 0.5 cm in diameter
Abscess - localised accumulation of pus in the dermis or subcutaneous tissue
Weal - transient raised lesion due to dermal oedema - e.g. in urticaria
boil/furuncle - staph infection around or within a hair follicle
carbuncle - staph infection of adjacent hair follicles (multiple boils/furuncles)

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11
Q

what is the terminology used to describe secondary lesions??

A

a secondary lesion is a lesion that evolves from a primary lesion

Excoriation - loss of epidermis following trauma Lichenification - well defined roughening of the skin with accentuation of skin markings
Scales - flakes of stratum corneum - happens in psoriasis
Crust - Rough surface consisting of dried serum, blood, bacteria and cellular debris that has exuded through an eroded epidermis (e.g. from a burst blister) - happens in impetigo
Scar - New fibrous tissue which occurs post-wound healing, and may be atrophic (thinning), hypertrophic (hyperproliferation within wound boundary), or keloidal (hyperproliferation beyond wound boundary)
Ulcer - loss of epidermis and dermis
fissure - an epidermal crack often due to excess dryness
Striae - Linear areas which progress from purple to pink to white, with the histopathological appearance of a scar (associated with excessive steroid usage and glucocorticoid production, growth spurts and pregnancy)

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12
Q

what does alopecia, hirsutism and hypertrichosis mean?

A

alopecia - loss of hair
Hirsutism - androgen-dependent hair growth in a female
Hypertrichosis - non-androgen dependent pattern of excessive hair growth

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13
Q

what is the terminology used to describe nails?

A

Clubbing - loss of angle between the posterior nail fold and nail plate - associations include suppurative lung disease, cyanotic heart disease, inflammatory bowel disease and sometimes can be idiopathic)
Koilonychia - spoon shaped depression of the nail plate - associated with iron deficiency anaemia, congenital and idiopathic)
Onycholysis - separation of the distal end of the nail plate from the nail bed - associated with trauma, psoriasis, fungal nail infection and hyperthyroidism
Pitting - punctate depressions of the nail plate

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14
Q

what are the functions of normal skin?

A
protective barrier against environmental insults 
temperature regulation
sensation 
vitamin D synthesis 
immunosurveillance 
apprearance
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15
Q

what is the structure of the normal skin?

A

The skin is the largest organ in the human body. It is composed of the epidermis and dermis overlying subcutaneous tissue. The skin appendages (structures formed by skin-derived cells) are hair, nails, sebaceous glands and sweat glands.

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16
Q

what are the four cell types in the epidermis?

A

Keratinocytes - produce keratin as a protective barrier
Langerhans’ cells - present antigens and activate T-lymphocytes for immune protection
Melanocytes - produce melanin, which gives pigment to the skin and protects the cell nuclei from UV radiation induced DNA damage
Merkel cells - contain specialised nerve endings for sensation

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17
Q

what are the layers of the epidermis?

A

There are 4 layers in the epidermis, each representing a different stage of maturation of the keratinocytes. The average epidermal turnover time (migration of cells from the basal cell layer to the horny layer) is about 30 days.

Stratum Basale - basal cell layer - actively deciding cells (deepest layer)
Stratum spinous - prickle cell layer - differentiating cells
Stratum granulosum - granular cell layer - So-called because cells lose their nuclei and contain granules of keratohyaline. They secrete lipid into the intercellular spaces.
Stratum corneum (horny layer) - layer of keratin, most superficial layer

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18
Q

what pathology can occur n the epidermis?

A

a) changes in epidermal turnover time - e.g. psoriasis (reduced epidermal
turnover time)
b) changes in the surface of the skin or loss of epidermis - e.g. scales,
crusting, exudate, ulcer
c) changes in pigmentation of the skin - e.g. hypo- or hyper-pigmented skin

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19
Q

what is the dermis made up from?

A

The dermis is made up of collagen (mainly), elastin and glycosaminoglycans, which are synthesised by fibroblasts. Collectively, they provide the dermis with strength and elasticity.

The dermis also contains immune cells, nerves, skin appendages as well as lymphatic and blood vessels.

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20
Q

what pathology can occur in the dermis?

A

changes in the contour of the skin or loss of dermis e.g. formation of
papules, nodules, skin atrophy and ulcers

disorders of skin appendages e.g. disorders of hair, acne (disorder of
sebaceous glands)

changes related to lymphatic and blood vessels e.g. erythema
(vasodilatation), urticaria (increased permeability of capillaries and small venules), purpura (capillary leakage)

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21
Q

what are the different types of hair?

A

a) lanugo hair (fine long hair in fetus)
b) vellus hair (fine short hair on all body surfaces)
c) terminal hair (coarse long hair on the scalp, eyebrows, eyelashes and
pubic areas)

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22
Q

what is a sebaceous gland?

A

sebaceous glands produce sebum via hair follicles - they secrete sebum onto the skin surface which lubricates and waterproofs the skin
the sebaceous glands are stimulated by the conversion of androgens to dihydrotestosterone and therefore become active at puberty.
pathology of sebaceous glands may involve increased sebum production and bacterial colonisation e.g. acne. Also may involve sebaceous gland hyperplasia

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23
Q

what are sweat glands?

A

sweat glands regulate body temperature and are innervated by the sympathetic nervous system
they can be eccrine and apocrine sweat glands
Eccrine sweat glands are universally distributed in the skin
Apocrine sweat glands are found in the axillae, areolae, genitalia and anus and modified glands are found in the external auditory canal. They only function from puberty onwards and action of bacteria on the sweat produces odour.

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24
Q

what are the stages of wound healing?

A

Wound healing occurs in 4 phases: haemostasis, inflammation, proliferation and remodelling

Haemostasis - vasoconstriction and platelet aggregation and clot formation

Inflammation - vasodilation, migration of neutrophils and macrophages, phagocytosis of cellular debris and invading bacteria

proliferation - granulation tissue formation and angiogenesis , re-epithelialisation

Remodelling - collagen fibre re-organisation, scar maturation

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25
Q

how should you manage an emergency in dermatology?

A

full supportive care - ABC of resuscitation
withdrawal of precipitating agents
management of associated complications
specific treatments for specific conditions

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26
Q

what are some causes of urticaria, angiooedema and anaphylaxis ?

A
can be idiopathic 
food (nuts, sesame seeds, shellfish, dairy products)
drugs (penicillin, contrast media, NSAIDs, morphine, ACEi)
insect bites 
contact - e.g. latex
viral or parasitic infections 
hereditary 
autoimmune
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27
Q

what is urticaria?

A

Urticaria is due to a local increase in permeability of capillaries and small venules. A large number of inflammatory mediators (including prostaglandins, leukotrienes, and chemotactic factors) play a role but histamine derived from skin mast cells appears to be the major mediator. Local mediator release from mast cells can be induced by immunological or non-immunological mechanisms.

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28
Q

how does urticaria present?

A

swelling involving the superficial dermis, raising the epidermis
itchy wheals

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29
Q

how does angioedema present?

A

deeper swelling involving the dermis and subcutaneous tissues

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30
Q

how does anaphylaxis present?

A

bronchospasm, facial and laryngeal oedema, hypotension; can present initially with urticaria and angioedema

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31
Q

how is urticaria managed?

A

antihistamines

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32
Q

how is severe acute urticaria and angioedema managed?

A

corticosteroids

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33
Q

how is anaphylaxis managed?

A

adrenaline

hydrocortisone and chlorphenamine

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34
Q

what is erythema nodosum and what causes it?

A

a hypersensitivity response to a variety of stimuli

causes by group A beta-haemolytic streptococcus, primary TB, pregnancy, malignancy, sarcoidosis, IBD< chlamydia and leprosy

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35
Q

how does erythema nodosum present?

A

discrete tender nodules which may become confluent
lesions continue to appear for 1-2 weeks and leave bruise like discolouration as the resolve
lesions not ulcerate and resolve without atrophy or scaring
the shins are the most common site

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36
Q

what is erythema multiforme?

how does it present?

A

it is often of unknown cause, it is an acute self-limiting inflammatory condition with HSV being the main precipitating factor

other infections and drugs are also cause

there are target lessons
initially seen on the back of the hands/feet before spreading to the torso, upper limbs are more commonly affected than lower limbs, pruritus is occasionally seen and s usually mild

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37
Q

what is Stevens-Johnson syndrome and toxic epidermal necrosis?

A

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are a spectrum of the same pathology, where a disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of skin. Generally, SJS affects less that 10% of body surface area whereas TEN affects more than 10% of body surface area.

Certain HLA genetic types are at higher risk of SJS and TEN.

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38
Q

what are the causes of SES and TEN?

A
Medications
Anti-epileptics
Antibiotics
Allopurinol
NSAIDs
Infections
Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV
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39
Q

how does SJS and TEN usually present?

A

the condition has a spectrum of severity - some are mild cases and some can be fatal

patients usually start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin. They then develop a purple or red rash that spreads across the skin and starts to blister.

A few days after blistering starts, the skin starts to break away and shed leaving the raw tissue underneath. Pain erythema, blistering and shedding can also happen to the lips and mucous membranes. Eyes can become inflamed and ulcerated. It can also affect the urinary tract, lungs and internal organs

40
Q

how do you manage SJS and TEN?

A

they are medical emergencies and patient should be admitted to a suitable dermatology or burns unit for treatment.
Good supportive care is essential - including nutritional care, antiseptics, analgesia and ophthalmology input.

Treatment options include steroids, immunoglobulins and immunosuppressant medications guided by a specialist

41
Q

what are the complications of SJS and NES?

A

Secondary infection: The breaks in the skin can lead to secondary bacterial infection, cellulitis and sepsis.

Permanent skin damage: Skin involvement can lead to scarring and damage to skin, hair, nails, lungs and genitals.

Visual complications: Depending on the severity, eye involvement can range from sore eyes to severe scarring and blindness.

42
Q

what is acute meningococcaemia?

A

a serious communicable infection transmitted via respiratory secretions; bacteria get into the circulating blood

caused by gram negative diplococcus neisseria meningitides

they will have features of meningitis and a non-blanching purpuric rash on the trunk and extremities, which may be preceded by a blanching maculopapular rash and can rapidly progress to ecchymoses, haemorrhage bullae and tissue necrosis

Complications - septic shock, DIC, organ failure and death

43
Q

what is erythroderma?

A

it is exfoliative dermatitis involving at least 90% of the skin surface
the skin appears inflamed, oedematous and sclay
often the will be systemically unwell with lymphadenopathy and malaise

44
Q

what are the causes of erythroderma?

A

previous skin disease - e.g. eczema, psoriasis
lymphoma
drugs - e.g. sulphonamides, gold, sulphonylureas, penicillin,allopurinol, captopril
idiopathic

45
Q

what is eczema herpeticum ?

A

aka kapok’s varicelliform

it is widespread eruption - a serious complication of atopic eczema caused by HSV.

There will be excessive crusted papules, blisters and erosions and they will be systemically unwell with fever and malaise

manage with antivirals and antibiotics for secondary infection

can lead to herpes hepatitis, encephalitis, DIC

46
Q

what is necrotising fasciitis ?

A

it is a medical emergency which is difficult to recognise in the early stages
a rapidly spreading infection of the deep fascia with secondary tissue necrosis

type 1 is caused by mixed anaerobes and aerobes (often occurs post surgery in diabetics

type 2 is caused by streptococcus pyogenes

47
Q

what are the features of necrotising fasciitis ?

A

acute onset
painful erythematous lesions develop
often presents as rapidly worsening cellulitis with pain out of keeping with physical features
extremely tender over infected tissue

48
Q

how do you manage necrotising fasciitis?

A

urgent surgical referral debridement

IV Abx

49
Q

what is cellulitis?

A

spreading bacterial infection in the skin which involved the deep SC tissue

50
Q

what is erysipelas ?

A

spreading bacteria infection of the skin which is an acute superficial form of cellulitis and involves the dermis and upper SC tissue

51
Q

what causes cellulitis and what are the risk factors?

A

typically due to infection by Streptococcus pyogenes or Staphylcoccus aureus

risk factors include immunosuppression, wounds, leg ulcers, toeweb intertrigo and minor skin injury

52
Q

how does cellulitis present?

A

local signs of inflammation - swelling (tumor), erythema (rubor), warmth (calor), pain (dolor); may be associated with lymphangitis

They may have systemic upset such as fever

commonly occurs in lower body e.g. shins

53
Q

what classification is used to guide how patients with cellulitis are managed?

A

Eron classification

class 1 - There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities

class 2 - The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection

class 3 - The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize

class 4 - The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis

54
Q

wean is it recommended that patients with cellulitis are admitted for IV ABx?

A

Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromized.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.

55
Q

how is cellulitis managed?

A

The BNF recommends flucloxacillin as first-line treatment for mild/moderate cellulitis. Clarithromycin, erythromycin (in pregnancy) or doxycyline is recommended in patients allergic to penicillin.

NICE recommend that patients severe cellulitis should be offered co-amoxiclav, cefuroxime, clindamycin or ceftriaxone.

56
Q

what are the complications of cellulitis?

A

Local necrosis, abscess and septicaemia

57
Q

what is staphylococcal scalded skin syndrome?

A

it is caused by a production of circulating epidermolytic toxin from staphylococci

58
Q

how does staphylococcal scalded skin syndrome present ?

A

Develops within a few hours to a few days, and may be worse over
the face, neck, axillae or groins
A scald-like skin appearance is followed by large flaccid bulla
Perioral crusting is typical
There is intraepidermal blistering in this condition
Lesions are very painful
Sometimes the eruption is more localised
Recovery is usually within 5-7 days

59
Q

how do you manage to staphylococcal scalded skin syndrome?

A

antibiotics - e.g. a systemic penicillinase-resistant penicillin, fusidic acid, erythromycin or appropriate cephalosporin)
analgesia

60
Q

what are the most common causes of superficial fungal infections

A

three main groups:

  • dermatophytes (tinea/ringworm)
  • yeasts (e.g. candidiasis, malassezia)
  • moulds (e.g. aspergillus)
61
Q

how does tinea present?

A
Tinea corporis (tinea!infection of the trunk and limbs) - Itchy,
circular or annular lesions with a clearly defined, raised 
and scaly edge is typical

Tinea cruris (tinea infection of the groin and natal cleft)– very itchy, similar to tinea corporis

Tinea pedis (athlete’s foot) – moist scaling and fissuring in toewebs, spreading to the sole and dorsal aspect of the foot

Tinea manuum (tinea infection of the hand)– scaling and dryness in the palmar creases

Tinea capitis (scalp!ringworm) – patches of broken hair, scaling and inflammation

Tinea unguium (tinea infection of the nail)– yellow discolouration, thickened and crumbly nail

Tinea incognito (inappropriate treatment of tinea infection with topical or systemic corticosteroids)–defined and less scaly lesions

62
Q

how does candidiasis skin infection present?

A

white plaques on mucosal areas, erythema with satellite lesions in flexures

63
Q

how does Pityriasis/Tinea versicolor present?

A

it is an infection with malassezia furfur
scaly pale brown patches on upper trunk that fail to tan on sun exposure
usually asymptomatic

64
Q

what does tinea refer too?

A

a specific type of fungal infection caused by dermatophyte fungus.

65
Q

how is tinea investigated?

A

Skin scrapings, hair or nail clippings - typical features can be seen of microscopy (hyphae (branching, rod-shaped filaments of uniform width with septa) - therfore often cultures often not needed and not done as they can take months to come back

Wood lamp examination - fluorescence of skin under UV light

66
Q

how is tinea managed?

A

General measures - treat any known precipitating factors (e.g. underlying immunosuppressive condition, moist environment)

Tinea capitis - scalp ringworm - treat with oral anti-fungals - terbinafine or griseofulvin, topical antifungal shampoos can be added (selenium sulfide topical)

Tinea corporis, cruris or pedis - treat with topical allylamine antifungal therapy - terbinafine topical

Tinea unguium (nail) - systemic terbnafine

** make sure to avoid the use of topical steroid as it can lead to tinea incognito

67
Q

how is pityriasis veriscolor managed?

A

ketoconazole shampoo

if this doesn’t work then oral itraconazole

68
Q

what are the main types of skin cancer?

A

basal cell carcinoma
squamous cell carcinoma
malignant melanoma (most life threatening)

69
Q

what is a basal cell carcinoma?

A

it is a common, slow goring locally invasive (but rarley metastasis) malignant tumour of the epidermal keratinocytes that is often related to exposure to sunlight

70
Q

what are risk factors for basal cell carcinoma?

A
  • UV radiation
  • sun exposure
  • history of severe sun burn
  • skin type 1 - always burns never tans
  • X-ray exposure
  • arsenic exposure
71
Q

how does a basal cell carcinoma present ?

A

papules with associated telangiectasis (nodular BCC) - the centre may have a necrotic or ulcerated centre
plaques, nodules and tumours with rolled borders
small crusts and non-healing wounds
non healing scabs

72
Q

what investigations would you perform for BCC?

A

biopsy

73
Q

how are SCC managed?

A
surgical  removal 
curettage 
Mohs micrographic surgery 
cryotherapy 
topical cream: imiquimod, fluorouracil 
radiotherapy
74
Q

what is a squamous cell carcinoma?

A

a locally invasive malignant tumour of the epidermal keratinocytes or its appendages, which has potential to metastasise (although rare - 2-5% )

75
Q

what are risk factors for SCC?

A
exposure to sunlight 
psoralen UVA therapy 
actinic keratoses and bowen's disease 
immunosuppression
smoking 
long standing leg ulcers
76
Q

how do SCC present?

A

Solitary papule / nodule, often eroded at the centre, or crusty, purulent or bleeding
Usually a ‘fleshy’ lesion
May resemble giant warts, but, unlike warts, may be painful
Usually in a sun-exposed area
Often hard, scaly, dome-like structures
Can bleed or itch
Also related to smoking, and may be present on the lower lip

77
Q

what are indicators of poor and good prognosis in SCC?

A

Good: well differentiated, <20mm diameter, <2mm deep, no associated disease

Poor: poorly differentiated, >20mm in diameter, > 4mm deep, immunosuppression for whatever reason.

78
Q

what investigations for SCC?

A

biopsy

also consider CT/MRI/PET to see for mets

79
Q

how is SCC managed?

A

surgical excision with 4mm margins if lesion is <20mm
If tumour greater than 20mm margins should be 6mm
Mohs micrographic surgery may be used in high risk patients and in cosmetically important sites

80
Q

what is a malignant melanoma?

A

an invasive malignant tumour of the epidermal melanocytes which has the potential to metastasise

81
Q

what are risk factors for malignant melanoma?

A
Fam history 
history of atypical naevi 
skin type 1 or 2 
red or blonde hair 
high freckly density 
sun exposure 
sun bed use 
light eye colour
xeroderma pigmentosum
82
Q

how does malignant melanoma present?

A

the ABCDE symptoms

  • asymmetrical shape
  • border irregularity
  • colour irregularity
  • diameter >6mm
  • evolution of the lesion (change in size or shape)
  • symptoms - bleeding, itching

MAJOR CRITERIA - change in size, shape or colour
MINOR CRITERIA - diameter >6mm, inflammation, oozing or bleeding, altered sensation

83
Q

what are the different types of malignant melanoma?

A

Superficial spreasing melanoma - a growing mold with the typical diagnostic features, usually on lower limbs, young and middle aged adults, related to intermittent high intensity UV exposure

Nodular melanoma - common the the trunk in young and middle aged adults, relate to ntermittent high intensity UV exposure, red or black lump which bleeds or oozes

Lentigo maligna - common on the dace, in the elderly population, related to long term skin exposure. Usually a growing mole with diagnostic features

Acral lentiginous melanoma - common on the palms, soles and nail bed, in elderly population, no clear relation to UV exposure

84
Q

how is malignant melanoma treated

A

surgical excision
radiotherapy
chemo - if there are mets

85
Q

what is Eczema?

A

it is an inflammatory skin condition characterised by dry, pruritic skin which a chronic relapsing course

It can affect all age groups but is commonly diagnosed before 5 years of age.

it is charactarised by papules and vesicles on an erythematous base

86
Q

how does eczema present?

A

commonly presents as itchy, erythematous dry scaly patches
more common on the face and extensor aspects of limbs in children and flexor aspects of limbs in adults
Acute lesions are erythematous, vesicular and weepy
chronic scratching/rubbing can lead to excoriations and lichenification
may show nail pitting and ridging of the nails

87
Q

how is eczema managed?

A

Emollients - help to improve the barrier
Steroids - help to reduce inflammation

Emollients is first line 
topical steroids (hydrocortisone topical) is second line 
In severe cases wet wraps and oral ciclosproin may be used 

EMOLLIENTS:

  • creams - water based, least potent
  • lotions - water and oil components - moderately potent
  • Ointments - oil based - most potent
88
Q

what is acne?

A

acne is an inflammatory skin disease affecting the pilosebaceous unit (oil glans)

89
Q

what are the main pathogenetic factors which contribute to acne?

A

Sebaceous gland hyperplasia and excess sebum production
Abnormal follicular differentiation
Cutibacterium acnes colonisation
Inflammation and immune response

Often hormones (androgen) have an impact

90
Q

how does acne present?

A
Non-inflammatory lesions (mild acne) - open and closed comedones (black heads and whiteheads) 
Inflammatory lesions (moderate and severe acne) - papules, pustules, nodules and cysts 

commonly affects the face, chest and upper back

91
Q

how is acne managed?

A

mild acne with no inflammation - topical retinoid or salicylic acid
mild acne with inflammation: topical retinoid and topical antibiotic (clindamycin topical or erythromycin topical). A topical benzoyl peroxide can be added

for severe acne - oral antibiotics, oral retinoids (isotretanoin)
if hormonal - oral anti-androgens

92
Q

what is psoriasis?

A

it is a chronic inflammatory skin disease due to hyper proliferation of keratinocytes and inflammatory cell infiltration.
It is multifactorial and not fully understood yet
There are some genetic associated
Immunological - abnormal T cell activity stimulates keratinocyte proliferation
Environment - it is recognised that psoriasis may be worsened (skin trauma, stress), triggered (e.g. streptococcal infection) or improve (e.g. sunlight) by environmental factors

93
Q

what are the subtypes of psoriasis?

A

plaque psoriasis - the most common sub type resulting in the typical well demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp
Flexural psoriasis - in contrast to plaque psoriasis the skin is smooth
Guttate psoriasis - transient psoriatic rash frequently triggered by a streptococcal infection. Multiple red, teardrop lesions appear on the body
Pustular psoriasis - commonly occurs on the palms and soles

94
Q

how does psoriasis present?

A

well-demarcated erythematous scaly plaques
lesions can sometime be itchy, burning or painful
common on the extensor surfaces of the body and over the scalp
50% have associated nail changes (pitting, onycholysis))
5-8% suffer from associated psoriatic arthropathy

95
Q

how is psoriasis managed?

A

avoid precipitating factors
use emollients to reduce scales

Mild:
topical corticosteroid
topical vitamin D analogue

Moderate to severe: 
phototherapy 
methotrexate
biological agent - infliximab
oral retinoid - acitrtin