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Phase II > Derm > Flashcards

Derm Flashcards

1
Q

Symptoms of exzema

A

x

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2
Q

What is atopy

A

Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema)

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3
Q

Papule vs nodule

A

Papule - A circumscribed, elevated, solid lesion, less than 1 cm.

Nodule - A palpable, solid lesion, greater than 1 cm in diameter. These are usually found in the dermal or subcutaneous tissue, and the lesion may be above, level with, or below the skin surface.

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4
Q

What is a macule

A

Macule - A circumscribed flat area less than 1 cm of discoloration without elevation or depression of surface relative to surrounding skin.

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5
Q

What is a patch

A

Patch - A circumscribed area of discoloration, greater than 1 cm, which is neither elevated or depressed relative to the surrounding skin.

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6
Q

What is a plaque

A

Plaque - A well-circumscribed, elevated, superficial, solid lesion, greater than 1 cm in diameter.

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7
Q

What is a vesicle

A
  • A small, superficial, circumscribed elevation of the skin, less than 0.5 cm, that contains serous fluid.
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8
Q

What is a bulla

A
  • A raised, circumscribed lesion greater than 0.5 cm that contains serous fluid.
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9
Q

What is a tumour

A

Tumor - Solid, firm lesions typically > 2 cm that can be above, level with, or beneath the skin surface. Also known as a mass

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10
Q

What is a pustule?

A

Pustule - A small (< 1 cm in diameter), circumscribed superficial elevation of the skin that is filled with purulent material. Can also be described as a vesicle filled with pus.

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11
Q

Examination findings in atopic eczema

A

O/E: Lichenification around, hyperpigmented possible, extensor in Asian and black, hypopigmentation (reversible with treatment), follicular in black people – around follicles. Papular or nodular.

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12
Q

Complications of atopic eczema

A

Immune response impaired – lymphatics ect as dry so impetigo, sleep deprivation, erythroderma, infection. Eczema herpeticum. Stap Aureus normally with crusting, weeping. Can group A strep, post strep glomerular nephritis.

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13
Q

Treatment of eczema herpeticum

A

Multiple lesions, systemically unwell, can get anywhere but also on face. (Eczema Herpeticum) Aciclovir, punch out lesions
Treat quickly- emergency

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14
Q

Treatment of atopic eczema

A

1) Emollient, corticosteroid (topical),
topical calcineurin, antiseptics

Cream vs ointment e.g epaderm, hydromol, emollin
Aim to use 250-500g a week
Massage with directions of hairs
Wet wraps/ bandage
Bath oils
Soap substitute
Antiseptic moisturisor

Antihistamine not useful but may help sleep

Topical tacrolium or pimecolimus

2) Systemics: Abx, antihistamine, pred, photo

nasal carriage eradication

3) Systemics: Aza, MMF, Ciclosporin, MTX

Ciclo monitor BP and renal function

Aza monitor TMPT, LFT and FBC

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15
Q

Dangers of steroids on body

A

2 tier for steroids so 2 options for exacerbation. Thinner on face, groins and armpits, don’t suddenly stop severe. Thinning is reversible at first. Steroids can mask tinea infection – tinea incognito.

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16
Q

What is Seborrhoeic eczema

A

Young males, red flakey, sides of nose, foreheads, scalp (scaling and dandruff), groin, axillae, genital
Anti fungal with steroid

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17
Q

What is asteatotic eczema

A

Pruritic, dry, cracked, lack of oil. Elderly and 20s

Emollients only needed

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18
Q

What is contact dermatitis/ eczema?

A

Can be irritant, allergic or photocontact
Red, itchy burning rash
Allergic more widespread, irritant just in area of contact
Allergic:
Often Nickel, develops later in life. Strange distribution, chromate in liver and in builders in cement. Possible on neck from perfume or nail varnish, rubber, hair dye (PPD) (can be sudden in later life),
P: Patch testing – 12 circles, red eczematous (not skin prick which is type 1 whereas eczema is type 4 and T cell related (48 hour)). Acutely antiseptic soak.
Irritant: Constantly washing hands
P: Pain nail varnish over

Treatment

  • Cold moist compress
  • Antihistamine for itch
  • Avoid scratching
  • Wash with soap and cool water to get rid of substance
  • Corticosteroids
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19
Q

What is stasis dermatitis/ venous eczema?

A

Vericose veins, venous hypertension, red eczematous response in lower legs, white area = atophy blonche, hemosiderin leads to brown tissue can get leg ulcers from it. Irritation and thickening, itching. May lead to cellulitis
P: Compression bandages, intermitten pneumatic compression pumps, raise legs, avoid injury, keep active, emollients, steroid, vascular surgery

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20
Q

psoriasis epidemiology

A

Demographics: 2% of pop, M=F (chronic plaque), <40years, incidence is stable, genetic association. 2 types. 1<40. 2>40. Different genetics for each.

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21
Q

Signs of psoriasis

A

Nails-pitting, Onycholysis (lifting of distal nail plate), Hyper-keratotic, brittle, may occur atypical e.g. natal cleft (top of bum crack).

Red, scaling, symmetrical plaque, extensor, scalp, lower back. Pitting of nails, Onycholysis, oil spots (orange/yellow), nail dystrophy. 50% have nail involvement.

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22
Q

DDX psoriasis

A

Fungal – symettrical scaley, cutaneous T cell lymphoma, guttate can be pityriasis rosea, discoid or sebhorraic eczema

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23
Q

Psoriasis investigation

A

Scraping and histology

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24
Q

Triggers psoriasis

A

. Also environmental triggers e.g. strep, HIV, trauma – Koebner phenomenon- e.g. bites. Also drug triggers e.g. NSAIDS, BB, stress, lithium, anti-malarials.

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25
Q

Symptoms psorisis

A

Same as signs but poor QoL worse than DM

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26
Q

Types psoriasis

A

Plaque, guttate, inverse pustular and erythrodermic

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27
Q

Treatment psoriasis

A

Explain treatments are suppressive and no cure.
1) Vitamin D, Dovobet (Steroid and calcipotiol (Vit D) ointment) – Vit D normalises differentiation and antiinflam – can cause irritation in skin- large areas= hypercalcaemia
2) Keratolytics, e.g. urea and lactic acid
3) Vitamin A , dithrinol (purple stain skin and shower) – anthrolin- affects keratinocyte prolif- causes skin itch/burning- can stain skin- in patients only, tar? Issues with cosmetic acceptability- cruder the tar the better it works.
4) Emolliants
5) Coal tar –exorex
6) Topical steroids, Cling film with ointment can maximise absorption, strong steroids cause remission when stopped so need to titrate downwards (see steroids) (also can cause pustular)- striae ulceration. Rarely used. Side effects if over 10% of body surface. potent only 8 weeks, very potent only 4
7) Acitretin (retinoid) or DMARDS e.g MTX, Cyclosporin
8) Light treatment, PUVA, sunbed or paint psorylin (photophorin), less used as cancer risk.
UVB – don’t need psorylin, safer. Need to go to hospital 3x a week for both.
9) Biologics Infliximab 75% improvement in 80% severe cases

Steps:

1) Topical first line Vit D, Topical corticosteroids, Tar.
2) Day treatment: Dithranol/ tar, phototherapy – lengthy, needs washing off, time commitment
3) Systemic and biological >10% of body

NICE - not severe (topical)

  • Start with Vit D and steroid OD each
  • Double dose
  • Add Coal tar or Potent cortico
  • Go to very potent
  • Treatment resistant add short-contact dithranol (cream/ ointment)
  • On scalp, consider karyolytics to remove scale. Dont escalate to dithranol
  • On flexures, face, genitals, more likely to get steroid side effects, consdider calcineurin inhibitors via specialist

NICE - severe (extensive 10% or not controlled or guttate (phototherapy) or major impact of wellbeing. Go to PHoto first then systemic or straight to systemic

  • Phototherapy. Narrowband UVB for plaque or guttate 3x a week. PUVA (oral or topical) (Psoralen with local UVA irradiation) for Palmoplantar pustulosis - risk of cancer with PUVA.
  • Resistnat to phototherapy - systemic, broad, narrow UVB or PUVA.
  • Rsistant to everything? TNF antag e,g, infliximab
  • Systemic therapy, agent based on patient with adjunct topical therapy. MTX first line, then ciclo (fast response). third - acitretic (retinoid). forth line - dimethyl fumerate or apremilast. fifth line biologics
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28
Q

How to assess psoriasis

A 
Comorbidities
Arthritis (15%)
Psycho social effects
Validated tool e.g. PEST (psoriasis epidemiology screening tool)
Assess CV riski
-Lipid modification
- RFs for CVD
Risk of VTE in hospital

Severity:
Physicians Global asssessment (PGA), the body surfact affected, nails and hair (difficult to treat sites), systemic upset e.g. erythroderma or generalised pustular psoriasis
Psoriasis area and severity index (PASI)

Dermatology QoL Index (DLQI)

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29
Q

Monitoring with MTX

A

LFTs and serum procollagen III (cirrosis but low PPV, high NPV)

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30
Q

What is guttate psoriasis

A

After strep or bacterial UTRI. Good UV therapy evidence. Guttate= drop. Small lesions over upper trunk and proximal extremities.
Centropedal/ truncal distribution
Self limiting in 60% (children). Looks like raindrops, rapid growth over weeks.

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31
Q

What is generalised pustular psoriasis?

A

Dermatological emergency. Withdrawral of steroids causes.

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32
Q

What is palmopustular psoriasis

A

What it says on the tin, feet too. Not psoriasis immunologically. Not always both.
Most women >40. 25% have chronic plaque psoriasis.
Smoking is associated and thyroid disease.
DDX: Pustular eczema

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33
Q

What is guttate psoriasis

A

After strep or bacterial UTRI. Good UV therapy evidence. Guttate= drop. Small lesions over upper trunk and proximal extremities.
Centropedal/ truncal distribution
Self limiting in 60% (children). Looks like raindrops, rapid growth over weeks.

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34
Q

Types of strep

A

a haemolytic e.g. viridans, strep pneumoniae
b haemolytic, Group A = pyogenese
Group

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35
Q

Skin manifestations of DM

A

Yeast candida infections – corners and inside mouth, genitalia, groin, breast
Setellite lesions away from main bodies
Candida balanitis in males
Can cause granuloma annulare – small dermal papules- asymptomatic
Necrobiosis lipoidica – legs, yellow centre, active red edge, damages small and large blood vessels. Often in shins
Crotenemia
Diabetic dermopathy (shin spots) – dull red papules, progress to well-circumscribed small round atrophic hyperpigmented skin lesions. Peripheral nephropathy/ vasc comp association. Very common.
Acral (toes and fingers) dry gangrene
Diabetic bulla – spontaneous painless blister often in acral locations
Diabetic cheiroarthropathy - Prayer sign – stiff (glycosylation of collage) cant put palms flat. Waxy skin thickening over dorsum of hand with restricted mobility particularly extension of MCP, PIP. Up to 30% with longstanding disease
Waxy skin
Malum perforans – painless long lasting ulcer

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36
Q

Causes of erythema nodosum

A

Sarcoidosis, TB, OCP, IBD

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37
Q

What is pyoderma gangrenosum and what causes this?

A

Acute inflame, break down and ulcerate, dusky blue red edge (yet to ulcerate). Exudate in centre. Can lead to chronic wound. Biopsy shows lots of dermal inflam. Sterile lesions. Topical or systemic steroids. Assoc cond e.g. IBD and RA, haematological disease. Immune mediated

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38
Q

Acne vulgaris symptoms

A

Comedones (spots) either open (blackhead) or closed (white head), increased secretion of oily sebum, microcomedones (precursor only seen with microscope), papules, nodules, pustules. Anxiety, low self-esteem, depression

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39
Q

Pathophysiology and cause of acne vulgaris

A

Hair follicles clogged with dead skin cells and oil from the skin and possible scarring – primarily affects oily skin. In the dermal layer. 1 -Excessive deposition of keratin leads to comedo formation, 2 - colnoisation by specific bacteria propionbacterium acnes, 3- local cytokine release. 4- Increased oil secretionGenetic cause and androgens. No effect of cleanliness or sunlight, unclear role of diet and cigarette smoking.

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40
Q

Which medications may worsen acne

A

lithium, hydantoin, isoniazid, glucocorticoids, iodides, bromides, and testosterone

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41
Q

Categories of acne according to NICE

A

NICE – mild moderate or severe
Mild = Non-inflam comedones, limited extent
Moderat = mix of inflam and non inflam, papules and pustules, may extend to shoulders and back
Sever acne = nodules and cysts (nodulocystic acne). Many papules or pustules, extensive.

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42
Q

Treatment of acne

A
  • Reassurance but not trivialize. Dispel myths. Educate on faty food, hygiene, infection, don’t pick.
  • Self care: Don’t wash more than twice a day, use mild soap or warm water, water based emollients only. Benzyl peroxide only useful over the counter drug
  • If mild:
  • Topical treatment
  • Topical retinoid (tretinoin, isotretinoin, or adapalene) (edapeline)
  • Benzoyl peroxidase (especially if pustules)
  • Azelaic acid if others poorly tolerated
  • COCP in woman consider
  • Review
  • If no response of moderate based on risk of scarring (widespread) or psychosocial morbidity combines with topical antibiotic or benzoyl peroxidase with retinoid (often poor tolerated)
  • Consider oral abx with topical if on back or shoulders. Discontinue if no improvement.
  • If severe
  • Refer (oral isotretinoin (roaccutane))
  • Treat as if moderate while waiting
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43
Q

Roaccutane ADRs

A
  • Transient worsening (1-4months)
  • Chelitis/ dry fragile skin/ photosensitivity
  • Myalgia, headache
  • Tetatorogenic – 2 forms of birth control
  • Depression and suicide
44
Q

Benzoyl peroxidase ADRs

A

• Skin irritation

45
Q

Topical retinoid ADRs

A
  • Photosensitivity
  • Odemea/puritis/stinging
  • Blistering
46
Q

What is neurofibromatosis? Findings, symptoms and treatment

A

Autodom- numerous tumours >5 café au lait macules. Non cancerous tumours. No prevention or cure. Surgery can remove problemative or cancerous tumours. Hearing loss, cataracts, muscle wasting with certain types. Tumours may compress nerves
Can get pheocromocytomas

47
Q

What is erysipelas? Symptoms,

A

(strep group A/ beta haemo pyogenes), good boarder. Spreading rapidly. More superficial than cellulitis. Fever, headache, vomiting.
Can change to necrotising fasciitis, septic arthritis, glomerulonephritis, recurrence
Abx

48
Q

Signs of systemic sclerosis

A

Arthritis and disfigurement of hands - Sclerodactyly - atrophy of soft tissues and ulceration
Tendency of finger tips to infarct (digital ulcers)
Calcinosis cutis (deposits in skin)
Microstomia (small mouth)
Telangiectasia

49
Q

Dermatomyositis signs

A

Macular rash (shawl sign)
Nailfold erythema (dilated capillary loops)
Gottron’s papules (red papules over knuckles)
Heliotrope sign – lilac purple and swelling around eyes

50
Q

What is erythema multiform and what can cause it?

A

Discoid inflamed plaques with blister in the middle. Tends to be peripheral. No cause in 50% or 2-3 weeks after penicillin, HSV infection, Orf

51
Q

Four topical steroids and their relative strengths

A

Hydrocort 1% Weakest
Eumovate Middle
Dermovate Really strong, only licenced for hands and arms
Betnovate Really strong – psoriasis flares

52
Q

What is erythroderma? Causes and RF? Symptoms

A

Skin failure – fluid loss, infection, heat loss and catabolic
H: 90% of body is erythematous, caused by eczema, drugs, lymphoma or psoriasis. Male, fever, shivering, malaise, 2-6 days then scaling, acute medical emergency. Significant mortality.

53
Q

Erythroderma management

A

P: Admit, supportive care e.g. fluid balance and temp, nutrition support. Bed rest, bland topicals. Later then steroids or anti psoriatic.

54
Q

What is staph scalded skin syndrome or localised bullous impetigo? Management/

A

Infant and adults. Exotoxin destroys desmosomes
H: superficial split in epidermis, renal patients more at risk due to failure to excrete toxin. Widespread formation of fluid filled blisters, thin walled and easily ruptured. Children under 6 or immunocompromised/ renal failure adults.
I: Characteristic histology
P: Supportive care, Abx

55
Q

What is toxic epidermal necrolysis

A

Toxic epidermal necrolysis
Serious – full thickness epidermal loss e.g. keratinocyte loss from drugs.
H: Rapid, Chloramphenicol, sulphonamide, amoxicillin, anticonvulsants, NSAIDS
P: High mortality – score TEN predicts. ITU, Dermatologists, Opthalmology, Gyeunocology, Remove cause. Pain relief. Dressings – silicon and absorbant dressings. Corticosteroids controversial, so is ciclosporin. IV IGs – anti apoptotic, no increased infection risk unlike other approaches

56
Q

What is miliaria

A

H: Sweat retention (sweat rash) – often misses people. Back buttocks, legs, immobile from pyrexia in ITU, ‘cant breath skin’, itchy, only on occluded surface, resolves spontaneously.

57
Q

What is molluscum contagiosum? treatment?

A

Viral (MCVirus), common in children
H: +/- itch, atypical in immunosuppressed
O/E: Pearly, ‘water warts’, dome shaped, 1-5mm, umbilicated, last 18months, contagious, self limiting, rare to treat, anywhere but hands and feet
C: eczema
P: most resolve, can do cryotherapy or topical podophylin, squeezing

58
Q

Causes of alopecia?

A
  • Age: Male pattern (most common)
  • Autoimmune: Alopecia areata (second most common)
  • Scarring causes: Lichenplaneness, psoriasis
  • Non Scarring causes: SLE (Discoid lupus which only effects epidermis and is more common than SLE), androgen insufficiency
  • Metabolic: Anaemia and Hypothyroid
59
Q

Cause, demographic and treatment of male pattern baldness

A

Hair follicles less sensitive to DHT
H: Late 20s-30s
P: Partially reversible with finasteroid in 2/3 men (not NHS), Minoxid 50% effective

60
Q

Describe lipoma and treatment

A 
Slow growing
sub cut
FX
Soft – rubbery or doughy
2-10cm in diameter
Shoulders neck trunk and arms
Can be surgically removed
61
Q

Describe sebacous adenoma

A

Slow growing, pink or yellow papule, associated with Muir Torre and predispose to cancer (HNPCC).

62
Q

Describe seborrheic keratosis

A

Basal cell papilloma or seborrheic wart are other names
Proliferation of epidermis
Senile wart, benign skin tumour, can get caught.
O/E: Barnacle appearance (no hanging over), pigment network (changes in this indicate melanoma), on dermascopy looks like brain with gyri and sulci. Can itch. Multiple on trunk >40 years. Variable appearance, stuck on appearance.

63
Q

Managment of seborrheic keratosis

A

P: Leave alone or cryo, curettage, shave excision (literally scracape it of so you don’t cut the epidermis, done with a scapel.

64
Q

Complications of seborrheic keratosis, how to tell if its cancer?

A

C: Precursor to Bowen’s keratosis which is a precursor to SCC
DDX: For moles look at ABCD – asymmetry, boarder, colour (more varity= worse), Differences e.g. lobules and skin changes.

65
Q

What a melanocytic naevi? Red flags?

A 
Moles, often at puberty
Junctional naevus = flat (junction)
Compound (dermis and epidermis)
Intradermal (just dermis) varying colour
Blue naevus
Halo Naevus (loss of pigment around in young adults
Congential naevs – no risk of malignancy, may grow hair
If varying colour and shape think melanoma
Asymetrical
Boarder
Colour
Difference
Extra features (bleeding)
66
Q

What is a trichilemmal cyst

A

(pilar cyst)
From hair follicle.
Used to be called sebaceous cyst but not actually from there.
Bottom of hair follicle, filled with kerratin.
Slowly get bigger over years
Middle aged women
Scalp
Benign but can be removed (can get infected)
Cyst lining from cells in route of hair
more firm, mobile, subcutaneous nodules measuring 0.5 to 5 cm in diameter

67
Q

What is an epidermoid cyst

A 
From hair follicle (on body not really head)
Young and middle aged adults
Face and Neck
Punctum
Normally asymptomatic – can be infected
Easy to remove
Pedunculated
Cyst lining from epidermis cells
Benign but can be removed (can get infected)
68
Q

BCC epidemiology, RFs and prognosis

A 
Best prognosis
Very common 30% of whites
Red hair- blue eyes, freckles
FX as heridetary factors
Immunosuppression
Arsenic
Early sun exposure
UV
69
Q

SCC epidemiology and prognosis

A

Less common
UV, same RF as solar keratosis
Immunosuppression/ chronic inflame
Uncommon mets but more if larger or lip tongue ear or areas of inflam

70
Q

Melanoma epidemiology

A 
Rare
White skin – fair skin and environment.
Increasing prevalence.
More common in women.
Incidence increasing.
71
Q

BCC appearence

A 
Purley colours – shiny
Irregular BVs
Non keratotic (Translucent)
Rolled edge
Whipcord boarder (well demarcated)
Macular or raised
Present as scar or red patch (need to stretch the skin)
Locally destructive
Rare mets (if large)
Often multiple cancers – risk of melanoma and SCC.
72
Q

SCC appearence

A 
Scab
Rapid growth
Not shiny, pearly, scaly, hyperkeratosis (produces keratin horns), fleshy base.
Fragile surrounding
Vermillion (light red) lip = lips
Fleshy base = malignant
Follow up 3-5 years for lymphadenopathy, 50% develop mets
More prog = less keratin
Pain= mets
73
Q

Melanoma appearence

A 
Aggressive
Life threatening.
Present as mole, lump bump or macular.
Prognosis linked to depth – thicker the depth then the worse.
Asymetry, boarder, colour, diameter >6mm is old now use Different (from other moles), ABCD
Typical notched boarder.
2 colours acceptable.
Often presents as ‘new and changing’.
Itching and bleeding can be normal
74
Q

What is a Keratoacanthoma?

A 
Keratoacanthoma
Hard keratin plug
Rapidly grows
Self limiting
Same distribution as normal SCC
Managed the same due to difficulty diffentiating.
75
Q

Treatment BCC

A

Identify risk tumours – face as you can damage organs – nasolabial folds risk – large tumours as hard to excise completely. Stretch skin and look for edges. Can overlap with SCC. >2cm diameter.
Exicise to clear surgical plane and 4mm margin or 6mm if >2.
Mohs used (constant biopsy) if high risk/ tissue preservative needed
Radiotherapy in old and palliative (long term cosmetic affects and risk of cancer)
Curettage and cautery for small.
Avoid cryo unless small nodular.
Topical only for superficial.

76
Q

Treatment SCC

A

identify high risk – non sun exposed, differentiation, size, immunosuppression, depth, face.
Exision 4mm, >2 then 6
Cautery only palliative or <1cm
Radiotherapy if tissue conservation is needed (fractuated) also if wont tolerate surgery or as adjunct.
Cryo if <1cm

Follow up regularly
Small chance of recurrence in low risk cancers
Look in lymph and scar for 2 years (will find most)
Immunodeficient for longer

77
Q

Treatment of melanoma

A

Excision of the primary and may need a graft. Needed to go down to fascia so can look ugly. 2 week wait rule.
20% relapse. Normally regional lymph.

78
Q

Bowens history and examination

A

Precursor to SCC, Full thickness but shows less squamous phenotypic differentiation (so still has a visible outer layer of skin). SCC in situ, can laterally spread before invasion. Dysplasia just in epidermis.
H: Old ladies legs, contact with oils or HPV. Fixed non itchy erythematous patches, multiple, scaly, non tendor, no response to steroids or moisturiser.
O/E: More cobbled than solar keratosis, scale easy to pull off, well defined

79
Q

Management of Bowen’s

A

Efudix (5 flurouracin) (if widespread, only affects damaged skin – highly metabolic areas), Cryo, imiquimod (another cream – immune response to abnormal antigens), curettage and cautery, excision, photodynamic therapy – skin is sensitised with porphrins. Spf50 avoid sunlight, hat.)

80
Q

Describe the benign tumours of the skin

A 
Slower growing, multiple makes them more likely.
Inspection and papaltion – 
•	solid- 
o	smooth
	Skin coloured – lipoma
	Red – angioma
	Brown – Melanocytic naevus
	Yellow- sebaceous gland adenoma/ hyperplasia
o	rough 
	brown = Seborrhoeic keratosis, 
	skin coloured = wart).
•	Fluctuant (moveable and compressible) – cyst or abscess
•	Fluid filled – blisterine disorders
81
Q

Warts symptoms and treatment

A

Viral, resembles bluster/ cauliflower. HPV. Often painless. Often self resolve in months to years. Salicylic acid and cryo help

82
Q

Describe Cherry angioma

A

(Campell de Morgan)
Dilated capillaries, 50% of adults
Asymptomatic, more with age
No treatment needed

83
Q

What is a pyogenic granuloma?

A 
Lobular proliferation of blood vessels
Head neck and peripheries
Young people
Curettage and quartery
Can grow and look unsightly
Mimics melanoma (Amelanotic melanoma)
84
Q

Describe telangiectasia causes

A

Spider naevus – center arteriole with surrounding network – pregnancy, most have1, liver disease, hereditary, Cushings, Venous hypertension (preggers, age, occupation), smoking resolve spontaneous
COCP

85
Q

What is a capillary haemangioma

A

H: Collection of raised capillaries, seen in neonates, 6-12 months = normal life spam.
P: Propanolol can shrink, laser, steroids

86
Q

What is a dermatofibroma?

A 
(Fibrous Histiocytoma)
Firm nodule in the dermis – prolif of histiocytes and fibroblasts.
Variable pigment
located particularly on legs
Most commonly due to an insect bite.
No treatment but biopsy
All have central scar
87
Q

What is mycosis funoides?

A

T cell lymphoma Staged based on degree of skin, lymph and haem. Non-Hodgkin
H: Patch or plaque on skin, Can overlap like autum leaves. Abnormal colour, slightly scaly, dotted pigmentation (destroyed hair follicles)
O/E: Scaly, red, atrophic, mottled, loses hair
DDX: Normally diagnosed as eczema or psoriasis
P: Moist, steroids, Phototherapy (extremely sensitive)
If extensive then radio or chemo
Prognosis: Normal lifespan unless advanced.

88
Q

Causes of blisters. associations of genetic disease

A

Causes: Taruma, infection (Bullous impetigo in newborn), drugs, autoantibodies (bullous pemphigoid, mucous membrane pemphigoid, Pemphigus Vulgaris), genetic disease (junctional emidermolysis bullosa).
Pathophysiology: dermal-epidermal junction:
Trauma = Weak spot = lamina lucida ‘clear zone’ in EM. Most blisters occur here after trauma = ‘subepidermal blister.
Adhesion proteins e.g. hemidesmosomes. May get congential or acquired autoimmune loss of these e.g. Junctional epidermolysis bullosa = mutation in Type 1 collage. Bullous pemphigoid – Autoantibodies against Type 17 collagen – also oedema due to inflame cells.
Loads on hereditary blisters with varying presentations. Most hereditary = EB type (Dystrophic, simplex of junctional) may occur with muscular dystrophy or pyloric agenesis.
Most acquired are like bullous pemphigoid or mucous membrane pemphigoid (autoimmune).

H: Not always fluid filled as very superficial – widening of spaces between cells. Present as erosional due to this and breaking easily. E.g. Pemphigus Vulgaris (AI). Look scar like can be Pemphigus foliaceus as blisters are event more superficial.
Bullous impetigo also involves theses desmosomes as Stap toxins cleave to form blisters.

89
Q

Treatment of blisters

A

Genetic – gene, protein cell and drug therapy. Prenatal diagnosis for those at risk
Acquired – immunosuppression e.g. corticosteroids or DMARDs

90
Q

What do you call an in situ melanoma?

A

Lentigo maligna

In situ melanoma, irregular outline

91
Q

Pityriasis rosea history

A

Most often young adults but anyone. UTRI may occur first. Discomfort, starts with herald patch lesion (red, flakey oval patch) followed in ½ weeks by a rash lasting <12 weeks, christmas tree distribution. Numberous 5-10mm patches (macules) of pink or red, flakey oval shaped rashs – may get inverse distribution mostly on extremities. May get mild to severe itching, may get low grade fever, headache and fitgue. Most no symtoms

92
Q

Pityriasis rosea treatment

A

Spontaneously resolves. Antihistamines or topical steroid for itch. Reassurance. Sunlight can help

93
Q

What is pityriasis versicolor?

A

(tinea versicolour) (dermatomycosis furfuracea)

Yeast infection. Versicolor = to turn colour

94
Q

Solar keratosis history and examination

A

Scales/ rough patches on red backgroun in regions that get sun. Normally asymptomatic, check it’s not SCC (10-15% chance it becomes one). Bald scalp, back of hands. Being fair and working outdoors.
O/E: Picture below = field change sun damage. Crust =keratin buildup, can also get on warts. Palpate – will be rough. Can be tender ‘pinprick’. Can be nodules on back of ear – check this.

95
Q

Solar keratosis plan

A

Efudix (5 flurouracin) (if widespread, only affects damaged skin – highly metabolic areas), topical diclofenac, podophyllin, Cryo, imiquimod (another cream – immune response to abnormal antigens), curettage and cautery, excision, photodynamic therapy – skin is sensitised with porephoryn. Spf50 avoid sunlight, hat.

96
Q

Solar lentigo what is it?

A

Liver spot, age, UV, normal

97
Q

Describe tinea? trreatmennnt

A

H: Toes, goin, clear in centre, circular, itchy, scraping.
P: Topical antifungal e.g. timidine, and steroid

98
Q

Rosacea history, examination, comps

A

H: Old alcoholics, male (stopped steroids- soborrheic eczema)
O/E: Red cheeks, BVs in cheeks, acne,
C: Rhinophyma (big bulbous nose)

99
Q

Rosacea treatment

A

Topical metronidazole, systemic then doxy

100
Q

Types of urticaria

A

xMultiple types

  • Physical, ask extends to hot and cold, demographism (exaggerated wealing when skin is stroked)
  • Intermediate hypersesnsitivity (linked with angioedema (dermis) although can occur in others)
  • Immune complex – infection
  • Idiopathic, stress, viral

ITCHY

101
Q

Treatment urticaria

A

P: Cetirizine, Montelukast (LTRA), Faxafenidine (antihistamine)

102
Q

Dermatitis herpetiformis history ddx

A

Rare
H: Skin type 1 common, linked to celiac, autoimmune, excoriations, itchy, extensor surfaces, symmetrical. Versicular skin rashes. (almost like purpura)
DDX: Scabies, eczema, linear IgA disease

103
Q

Dermatitis herpetiformis treatment

A

No gluten (1year), dermatology

104
Q

Lichen planus History and comps

A

Unknown cause, viral trigger? Thought to be autoimmune
H: Itchy, Can be kerbener – scar site
O/E: Erythematous, follows linear lines with scratches (Koebner phenomenon), symmetrical, flexor surfaces, papules flatter and can pigment/ become hypertrophic. Wickams striae in mouth and lips – white lines. Often on genitals.
C: Self-limiting, may lead to malignant change, involve mouth or nails, alopecia. Last 10-12 months

105
Q

Scabies history

A 
Contagious infestation by mite
Sever itchiness
Pimple-like rash
2-6 weeks to get symptoms
Everywhere or just wrist, between fintgers, waisline
Comp with bacterial infection
Crowded conditions
Long period of direct skin contact needed
106
Q

Lichen planus treatment

A

Topical steroid moderate potency. Hard to treat! Also retinoids, sulfasalazine, phototherapy

107
Q

Scabies treatment

A

P: Permethryn cream – all people in house at same time. Wash all clothes and bed. Scabies doesn’t go above head (unless kids). 7 days. Malathion another one. Remain alove for 2 days on clothing. Pruitis from poo so can linger. More itchy at night. Eumovate for itch.

Phase II (18 decks)

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