Dermatology Flashcards

1
Q

Describing an individual skin lesion

A

SCAM

S- size, shape
C- colour
A- associated secondary change
M- Morphology, Margin

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2
Q

Signs of melanoma within a skin lesion

A
ABCD
A- asymmetry- lack of mirror image in any of the 4 quadrants)
B- irregular Border
C- two + colours within the lesion 
D- Diameter >6mm
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3
Q

Comedone

A

A plug in a sebaceous follicle containing altered sebum, bacteria and cellular debris

  • can present as open (blackhead)
  • closed - whitehead
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4
Q

Functions of the skin

A
  1. Protective barrier against environmental insults
  2. Temperature regulation
  3. Sensation
  4. Vitamin D synthesis
  5. Immunosurveillace
  6. Appearance/Cosmesis
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5
Q

4 Major cell types of the epidermis

A

Keratinocytes- produce keratin
Langherhan’s cells - present antigens adn activate T-lymphocytes
Melanocytes- produce melanin
Merkel Cells - contain specialised nerve endings for sensation

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6
Q

4 layers of the epidermis

A

Stratum basale - actively dividing cells, deepest layer

Stratum spinosum (prickle cell layer)- differentiating cells

Stratum granulosum (granular cell layer) cells lose their nuclei and contain granules of keratohyaline- secrete lipid into the intercellular spaces

Stratum corneum - layers of keratin, most superficial layer (horny layer)

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7
Q

Pathology of the epidermis

A
  • changes in epidermal change over time (psoriasis)
  • changes in the surface of the skin or loss of the epidermis (scales, crusting, exudate, ulcers)
  • changes in pigmentation of the skin
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8
Q

What makes up the dermis

A

collagen, elastin and glycoaminoglycans (synthesised by fibroblasts) - provide strength and elasticity
Also contains immune cells, nerves, skin appendages and lymphatic and blood vessels

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9
Q

Pathology of the dermis

A

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

  • disorders of skin appendages e.g. disorders of hair, acne
  • Changes related to lymphatic and blood vessels e.g. erythema/urticaria
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10
Q

stages of wound healing

A

Haemostasis
Inflammation
Proliferation
Remodelling

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11
Q

Causes of urticaria, angioedema and anaphylaxis

A

idiopathic, food, drugs, morphine, ACE-i, insect bites, contact, viral or parasitic infections, autoimmune or herediatary

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12
Q

Description of urticaria

A

local increase in permeability of capilllaries and small veules
prostoglandins, leukotrienes and chemotactic release
main mediator = histamine released by skin mast cells

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13
Q

Presentation of urticaria

A

welling involving the superficial dermis, raising the epidermis
itchy wheals

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14
Q

Presentation of angioedema

A

deeper swelling involving the dermis and subcutaneous tissues
swelling of tounge and lips

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15
Q

Presentation of anaphylaxis

A

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

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16
Q

Managment of urticaria, angioedmea and anaphylaxis

A

antihistamines for urticaria
corticosteroids for severe urticaria and angioedema
adrenaline, corticosteroids and antihistamines for anaphylaxis

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17
Q

Erythema nodosum

description

A

hypersensitivity reaction

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18
Q

Causes of erythema nodosum

A
Group A B-haemolytic streptococcus
Primary TB 
Pregnancy
Malignancy 
Sarcoidosis
IBD
Chlamydia
Leprosy
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19
Q

Presentation of erythema nodosum

A

Discrete tender nodules which may become confluent
Lesions appear for 1-2 weeks and leave bruise like discolouration as they resolve
do not ulcerate and resolve without atrophy or scarring
Shins are the most common site

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20
Q

Description of Erythema multiforme

A

Acute self-limiting condition
Mainly precipitated by herpes simplex virus
Infections and drugs are other causes
Mucosal involvement absent or limited to only one mucosal surface

Discrete red annular lesions, with a paler ring and a red inner ring.

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21
Q

Description of Steven-Johnson syndrome

A

mucocutaneous necrosis with at least 2 mucosal sites involved
drugs/infections main associations
epithelial necrosis with few inflammatory cells involved on histopathology

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22
Q

Description of Toxic Epidermal Necrolysis

A

usually drug induced
acute severe disease characterised by extensive skin and mucosal necrosis accompanied by systemic toxicity
full thickness epidermal necrosis with subepidermal detachment

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23
Q

Management of Erythema Multiforme, Steven-Johnson syndrome and Toxic Epidermal necrolysis

A

Early recognition and call for help

Full supportive care to maintain haemodynamic equilibrium

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24
Q

Complications of Erythema Multiforme, Steven-Johnson syndrome and Toxic Epidermal necrolysis

A

Sepsis
electrolyte imbalance
multisystem organ failure

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25
Description of acute meningococcaemia
Serious communicable infection transmitted by respiratory secretions bacterial in circulating blood
26
Causes of acute meningococcaemia
gram negative diplococcus Neisseria meningitides
27
Presentation of acute meningococcaemia
meningitis- headache, fever, neck stiffness septicaemia - hypotension, fever, myalgia non-blanching purpuric rash on the trunk and extremities (may be preceded by a blanching maculopapular rash ) may progress to ecchymoses, haemorrhagic bullae and tissue necrosis
28
Ecchymoses
a discolouration of the skin resulting from bleeding underneath, typically caused by bruising
29
Management of acute meningococcaemia
Antibiotics | prophylactic abx for close contacts
30
Complications of acute meningococcaemia
septic shock DIC multi-organ failure death
31
Erythryoderma | Description
exfoliative dermatitis involving at least 90% of the skin surface
32
Causes of Erythryoderma
previous skin disease (eczema, psoriasis) lymphoma drugs (sulphonamides, gold, sulphonylureas, penicillin, allopurinol) idiopathic
33
Presentation of Erythryoderma
Skin appears inflamed, oedematous and scaly | Systemically unwell with lymphadenopathy and malaise
34
Management of Erythryoderma
treat underlying cause where known emollients and wet wraps to maintain skin moisture topical steroids to help relieve inflammation
35
Complications of Erythryoderma
``` Secondary infection fluid loss and electrolyte imbalance hypothermia high out-put cardiac failure and capillary leak syndrome (most severe) overall mortality 20-40% ```
36
Eczema herpeticum (Kaposi's varicelliform eruption) Description
widespread eruption | serious complication of atopic eczema or other skin conditions
37
Causes of Eczema herpeticum (Kaposi's varicelliform eruption)
herpes simplex virus
38
Presentation of Eczema herpeticum (Kaposi's varicelliform eruption)
extensive crusted papules, blisters and erosions | systemically unwell with fever and malaise
39
Management of Eczema herpeticum (Kaposi's varicelliform eruption)
anti-virals e.g. aciclovir | antibiotics for secondary bacterial infection
40
Complications of Eczema herpeticum (Kaposi's varicelliform eruption)
Herpes hepatitis encephalitis disseminated intravascular coagulation rarely - death
41
Necrotising fasciitis Description
rapidly spreading infection of the deep fascia with secondary tissue necrosis
42
Causes of Necrotising fasciitis
Group A haemolytic streptococcus or Mixtures of aerobic and anaerobic bacteria
43
Risk factors for necrotising fasciitis
abdominal surgery medical co-morbidities - DM, malignancy 50% of cases in previously healthy individuals
44
Presentation of necrotising fasciitis
severe pain erythematous, blistering and necrotic skin systemically unwell with fever and tachycardia prescence of crepitus (subcutaneous emphysema) XR may show soft tissue gas
45
Management of necrotising fasciitis
urgent referral for extensive surgical debridement IV abx mortality up to 70%
46
Erysipelas and cellulitis description
spreading bacterial infection of the skin erysipelas- acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue cellulitis - involves deep subcutaneous tissue
47
Causes of Erysipelas and cellulitis
staphylococcus aureus and streptococcus pyrogenes RF- immunosuppression, wounds, leg ulcers, toeweb intertrigo and minor skin injury
48
Presentation of Erysipelas and cellulitis
most common in the lower limbs local signs of inflammation - tumour, rubor, calor and dolor may be associated with lymphangitis systemically unwell with fever, malaise or rigors esp. erysipelas Erysipelas differentiated from cellulitis by well-defined, red raised border
49
Management of Erysipelas and cellulitis
Abx- flucloxacillin or benzylpenicillin | supportive care- rest, leg elevation, sterile dressings and analgesia
50
Complications of Erysipelas and cellulitis
local necrosis, abscess and septicaemia
51
Staphylococcal scalded skin syndrome description
commonly seen in infancy and early childhood
52
Causes of Staphylococcal scalded skin syndrome
production of circulating epidermolytic toxin from phage group II, benzylpenicillin resistant (coagulase positive) staphylococci
53
Presentation of Staphylococcal scalded skin syndrome
``` develops over hours to days worse over face, neck, axillae or groin scald like skin appearance followed by large flaccid bulla typical perioral crusting intraepidermal blistering lesions are painful recovery usually 5-7 days ```
54
Management of Staphylococcal scalded skin syndrome
antibiotics - systemic penicillinase-resistant penicillin, fusidic acid, erythromycin or appropriate cephalosporin analgesia
55
Causes of superficial fungal infections
- dermatophytes (tinea/ringworm) - yeasts (candidiasis, malassezia) - moulds (aspergillus)
56
Presentation of fungal infections
usually unilateral and itchy
57
Management of fungal infections
establish diagnosis from skin scrapings/ hair/ nail clippings (dermatophytes) skin swabs for yeasts general measures- treat known precipitating factors (underlying immunosuppression, moist environment) - topical antifungals (terbinafine cream) - oral anti-fungal agents - itracpnaozole - avoid topical steroids
58
Description of BCC
slow growing, locally invasive malignant tumour of the epidermal keratinocytes rarely metastasises most common malignant skin tumour
59
Causes of BCC
``` UV exposure history of frequent or severe sunburn in childhood skin type I (frequently burns, never tans) increasing age male immunosuppression previous history of skin cancer genetic predisposition ```
60
Presentation of BCC
various morphological types - nodular (most common) - superficial (plaque like) - cystic - morphoeic (sclerosing) - keratotic - pigmented Nodular BCC = small skin coloured papule or nodule with surface telangiectasia and pearly rolled edge may have a necrotic or ulcerated centre (rodent ulcer)
61
Management of BCC
surgical excision mohs micrographic surgery for high risk recurrent tumours radiotherapy where surgery isn't appropriate cryotherapy, curettage and cautery, topical photodynamic therapy and topical treatment (imiquimod cream)
62
Complications of BCC
local tissue invasion and destruction
63
Description of SCC
locally invasive malignant tumour of the epidermal keratinocytes or it's appendages potential to metastatise
64
Causes of SCC
UV exposure pre-malignant skin conditions (actinic keratoses) chronic inflammation (leg ulcers, wound scars) immunosuppression genetic predisposition
65
Presentation of SCC
keratotic (scaly/crusty) ill defined nodule which may ulcerate
66
Management of SCC
surgical excision moh's micrographic surgery radiotherapy for non-resectable tumours
67
Description of malignant melanoma
invasive malignant tumour of the epidermal melanocytes | potential to metastatise
68
Causes of malignant melanoma
``` excessive UV exposure skin type I history of multiple moles/atypical moles family history previous history of melanoma ```
69
Presentation of malignant melanoma
``` ABCDE symptoms A- asymmetry B- border irregularity C- colour irregularity D- Diameter >6mm E- Evolution of lesion (changes in size/shape) Symptoms- bleeding/itching ``` - more common on the legs in women and the trunk in men
70
Types of malignant melanoma
superficial/ nodular --> common on the lower limbs/trunk in young and middle aged adults, related to intermittent high intensity UV lentigo --> common on the face in the elderly acral lentiginous melanoma - common on palms, soles and nail beds in the elderly
71
management of malignant melanoma
surgical excision radiotherapy chemotherapy for malignant disease
72
Description of eczema
papules and vesicles on an erythematous base | most commonly atopic - develops early childhood and resolves during teenage years
73
Causes of eczema
primary genetic defect in skin barrier function (filaggrin) | exacerbated by infections, allergens, sweating, heat, severe stress
74
Presentation of eczema
itchy erythematous dry, scaly pathces more common on the face and extensor aspects of limbs in infants flexor aspects in children and adults acute lesions are erythematous, vesicular and weepy chronic scratching/ rubbing can lead to excoriations and lichenification may show nail pitting and ridging
75
Management of eczema
- avoid exacerbating features - frequent emoillients ± bandages and bath/ soap substitutes - topical steroids for flare ups - topical immunmdulators (tacrolimus) - oral therapies - antihistamines, antibiotics and antivirals - phototherapies - immunosuppression - oral prednisolone, azathioprine, ciclosporin
76
Complications of eczema
secondary bacterial infection | secondary viral infection - molluscum contagiosum, viral warts and eczema herpeticum
77
Acne vulgaris description
inflammatory disease of pilosebaceous follicle
78
Causes of acne vulgaris
``` hormonal (androgens) increased sebum production abnormal follicular keratinisation bacterial colonisation (propionibacterium acnes) inflammation ```
79
Presentation of acne
non-inflammatory lesions - open and closed comedones | inflammatory lesions - papules, pustules, nodules and cysts
80
management of acne vulgaris
topical therapies - benzoyl peroxide and topical antibiotics, topical retinoids oral therapies - oral antibiotics, antiandrogens (females) oral retinoids for severe acne
81
Complications of acne vulgaris
post-inflammatory hyperpigmentation/scarring/deformity | psychological and social effects
82
Description of psoriasis
chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration
83
Types of psoriasis
``` chronic plaque psoriasis guttate (raindrop lesions) seborrhoeic (nasolabial and retroauricular) flexural pustular (palmar-plantar) erythrodermic (total body redness) ```
84
Causes of psoriasis
complex interaction between genetic, immunological and environmental factors precipitating factors include trauma, infection, drugs, stress and alcohol
85
Presentation of psoriasis
well demarcated erythematous scaly plaques lesions can be itchy, burning or painful common on extensor surfaces and scalp auspitz sign (scratch and gentle removal of scales causes capillary bleeding 50% associated nail changes arthropathy
86
Management of psoriasis
avoid precipitating factors emollients topical therapies - vit D analogues, topical corticosteroids, coal tar preparations, topical retinoids, keratolytics phototherapy oral therapies - methotrexate, retinoids, ciclosporin, mycophenolate mofetil, fumaric acid esters biologics- infliximab, etanercept, efalizumab
87
Bullus pemphigoid description
blistering skin disorder that usually affects the elderly
88
Causes of bullus pemphigoid
autoantibodies against antigens between the epidermis and dermis causes a sub-dermal split in the skin
89
Presentation of bullus pemphigoid
tense, fluid filled blisters on an erythematous base lesions are often itchy may be preceeded by a non-specific itchy rash - usually affects trunk and limbs (mucosal involvement less common)
90
Management of bullus pemphigiod
wound dressings, monitor for infection topical steroids oral steroids, tetracyline with nicotinamide, immunosuppression (azathioprine, mycophenolate mofetil and methotrexate)
91
Description of pemphigus vulgaris
blistering skin disorder which usually affects the middle-aged
92
Causes of pemphigus vulgaris
autoantibodies against antigens in the epidermis | cause an intra-epidermal split in the skin
93
Presentation of pemphigus vulgaris
flaccid easily ruptured blisters forming erosions and crusts lesions are often painful usually effects mucosal areas
94
Management of pemphigus vulgaris
wound dressings, monitor for infection, good oral hygiene oral therapies- high dose steroids, immunosuppressive agents- methotrexate, azathioprine, cyclophosphamide, mycophenolate mofetil
95
History of venous ulcers
often painful, worse on standing | history of venous disease
96
Common sites of venous ulcers
malleolar area | more commonly medial than lateral
97
Lesion of venous ulcers
large, shallow, irregular ulcer | exudative and granulating base
98
Features associated with venous ulcers
warm skin normal peripheral pulses leg oedma, haemosiderin and melanin deposition lipodermatosclerosis atrophie blanche (white scarring with dilated capillaries)
99
Possible investigations in venous ulcers
normal ABPI
100
Management of venous ulcers
compression bandaging (After excluding arterial insufficiency)
101
History in arterial ulcers
painful esp at night worse when legs are elevated history of arterial disease
102
common sites of arterial ulcers
pressure and trauma sites (pretibial, lateral supramalleolar, distal points (toes) )
103
Lesion of arterial ulcers
small, sharply defined deep ulcer | necrotic base
104
Associated features of arterial ulcers
cold skin weak or absent peripheral pulses shiny, pale skin loss of hair
105
Possible investigations of arterial ulcers
ABPI <0.8 = prescence of arterial insufficiency | - Doppler studies and angiography
106
Management of arterial ulcers
vascular reconstruction | compression bandaging is contraindicated
107
History of neuropathic ulcers
often painless abnormal sensation history of diabetes or neurological disease
108
Common sites of neuropathic ulcers
pressure sites - soles, heels, toes, metatarsal heads
109
Lesion in neuropathic ulcers
variable size and depth granulating base maybe surrounded by or underneath a hyperkeratotic lesion
110
Associated features of neuropathic ulcers
warm skin normal peripheral pulsese (cold, weak or absent pulses in neuroischaemic ulcers) peripheral neuropathy
111
Possible investigations in neuropathic ulcers
ABPI <0.8 implies neuroischaemia | XRay to exclude osteomyelitis
112
Management of neuropathic ulcers
wound debridement | regular repositioning, appropriate footwear and good nutrition
113
History of lichen planus
family history | may be drug induced
114
Common sites of lichen planus
forearms, wrists and legs | always examine oral mucosa
115
lesion in lichen planus
violaceous (lilac) flat-topped papules | symmetrical distribution
116
Associated features | lichen planus
nail changes and hair loss | lacy white streacks on the oral mucosa and skin lesions (Wickham's striae)
117
Possible investigations lichen planus
skin biopsy
118
Management of lichen planus
corticosteroids | anti-histamines
119
Actinic keratoses
pre-malignant crumbly yellow-white scaly crusts on sun-exposed skin fro dysplastic intra-epidermal proliferation may regress/recur treat with - diclofenac gel, fluorouracil, imiqimod, cryotherapy, surgical excision
120
Bowen's disease
SCC in situ well defined, slowly enlarging red scaly plaque with a flat edge full thickness dysplasia/carcinoma in situ treat with cryotherapy, fluorouracil or imiquimod, photodynamic therapy or surgical excision
121
Paget's disease of the nipple
itchy red scaly or crusted nupple | from direct extension of intraductal adenocarcinoma
122
non-scarring alopecia
alopecia areata - smooth well defined round patches of hair loss on scalp. spontaneous regrowth in 3/12 consider sterpods
123
scarring alopecia
inflammatory diseases damage follicular stem cells or follicles are damaged by trauma or tumour
124
Pressure ulcers | pathology
uninterrupted pressure on the skin leads to ulcers and extensive painful subcutaneous dectruction shearing forces, friction and moisture and implicating factors
125
risk factors for pressure ulcers
extremes of age | reduced mobility and sensation, vascular disease, chronic or terminal illness
126
Staging of pressure ulcers
1. non-blanching erythema over intact skin 2. partial thickness skin loss 3. full thickness skin loss extending into fat 4. destruction of muscle, bone or tendons
127
Scabies
mites burrow and lay eggs which hatch as larvae very itchy papules, vesicles, pustules and nodules affecting finfger webs, wrist flexure, axillae, abdomen, buttocks and groin Treat with permethrin