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Year 5 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Atopic eczema epidemiology

A

Commonest inflammatory skin condition in UK
Prev 15-20%
Onset usually 2 to y months
50-70% clear by age10
70% positive family history
50% associated atopy

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2
Q

Clinical features of atopic eczema (acute)

A

on flexural surfaces . Cheek or extensor if <10 months
Pruritus, ill defined erythema, scaling, papules, vesicles, exudate

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3
Q

Clinical fearures of chronic atopic asthma

A

flexural areas
Pruritus
Ill defined erythema and scaling
lichenifications
Pigmentary changes
Fissures

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4
Q

Pathophysiol of atopic eczema

A

combo of generic (fillagrin null mutations in maybe 30% of severe disease), immune and microbiome (overgrowth of staph aureus). Environmental factors eg hygiene hypothesis

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5
Q

Diagnosis of atopic eczema

A

clinical diagnosis ith child with itchy skin condition plus visual dermatitis or history of
Plus some other things
Define impact on quality of life
Normally not associated with food allergy
Consider allergy testing if reaction immediately post food
Consider allergic contact if reacting to emollients etc

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6
Q

Treatment of atopic eczema

A

emollient
Prevent and treat infection (bleach bath)
Identify and avoid triggers
Topical steroids
2nd line: Topical tacrolimus, oral immunosuppressants, biologic (dupilumab)

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7
Q

Consider severity of eczema

A

using scoring tools, eg clear, mild (areas dry skin, infrequent itching), moderate (areas od dry, frequent itch, redness), and severe.
And step up approach according to this

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8
Q

Steps of steroid creams

A

mild: Hydrocortisone (eg dactocort)
moderate: Eumovate (eg clobetasone)
Potent: Betnovate (eg elocon, betnovate)
Super potent: Dermovate

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9
Q

Calcineurin inhibitors

A

used in patients with eczema using large amounts of steroids to avoid skin thinning
Eg tacrolimus topically
50% local skin inflammation and itching on initial use

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10
Q

Complications of ectopic eczema

A

Secondary infection (partic s aureus)
Psychosocial
Erythyrodermix
Growth retardation
Eye involvement

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11
Q

S aureus secondary infection for eczema

A

crusting, weeping, pustulation and or surrounding cellulitis
Toical antibiotics and cellulitis for two weeks

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12
Q

Eczema herpeticum

A

areas of rapidly worsening painful eczema
Clustered blisters and maybe punched out rosions
Possible fever lethargy or distress
Treatment: Start systemic acyclovir as soon as suspected and topics, steroids
Ophthalmology input if any suspicion of eye involvement

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13
Q

Seborrhoeic dermatitis

A

form of eczema with yeast, much more common in middle aged men
Greasy scaling erythema affecting scalp, eyebrows, crease of nose, ears, chest, umbilicus
Treatment: Ketroconazole shampoo, topical miconazole, topical corticosteroids

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14
Q

discoid eczema

A

multiple coin shaped vesicular crusted,highly pruritic plaques often on limbs
Typically middle aged males
Differentials: Tinea, Bowens, psoriasis
Poss role of s aureus and irritants
Need regular emollients and potent corticosteroids

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15
Q

pomphylox eczema

A

recurrent itchy vesicles and blisters on hands and feet
More common in Young adults and atopics
TX regular emolients and corricosteroids

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16
Q

Stasis eczema

A

associated with venous insufficiency
Chronic eczema of lower legs often with varicose veins, oedema, haemosiderin deposition
Diffeffengials are contact dermatitis to topical treatments for leg ulcers

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17
Q

Asteatotoc eczema

A

elderly. Typically on legs
Often background of dry skin
Lacy network of fine red superficial fissures
Crazy paving
Treat background dry skin and toppicql corticosteroidss

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18
Q

Irritant contact dermatitis

A

due to irritant exposure eg detergent, some individuals more susceptible than others
Eg nursing, catering
Typically prolonged exposure on hands
Emollients and soap substitutes.
If chronic lichenified eczema may need really potent corticosteroids

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19
Q

features of classic plaque psoriasis

A

Well defined erythematous plaques (salmon)
Tricky overlying scale
Quite symmetrical
Preference for extensor surfaces

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20
Q

Psoriasis epidemiology

A

chronic inflammatory skin disease
75%onset before age 40, bur not commonly in children
Nail involvement frequently
Associated arthropathy
Equal gender distribution 2-3% of worlds population affected

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21
Q

pathogenesis of psoriasis

A

epidermal hyperproliferation and aberrant differentiation
Papillomatosis
Acanthosis (generalized thickening)
parakeratosis
Angiogenesis
Predominantly T cell mediated
Genetic susceptibility partic if early onset

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22
Q

External triggers of psoriasis

A

Injury, friction and inflammation
Infection eg strep
Drugs (beta blockers, ace inhib, anti malarials. Lithiim, systemic steroid withdrawal)
Alcohol
Stress

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23
Q

Issues of psoriasis for patients

A

Itching
Sorenss
Excess flaking of skin
Cosmetic appearance
Inconvenience of treatments
Signif impact on quality of life

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24
Q

psoriasis affecting face

A

Significant overlap w seborrhaeic dermatitis
Manage in the same way so no real need for distinction
Not really plaques unlike elsewhere in body
If psoriasis elsewhere more likely to make that diagnosis

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25
Q

Flexural/inverese psoriasis

A

Well defined erythema, but scale lost due to apposition of surfaces.

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26
Q

Nails in psoriasis

A

pitting
Onycholysis (lifts up from underlying nail bed)
Affecting multiple widespread nails

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27
Q

Guttate psoriasis

A

Young adults develop teardrop size psoriatic plaques
Typically widespread eg over trunk
Possibly after bacterial trigger eg strep
Treat with phototherapy otherwise unlikely to resolve.

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28
Q

Pityriasis rosea

A

reactive rash probs triggered by HHV 6 or 7
Develop large primary patch called the Herald patch, then develops outwards
Oval erythematous patches with overlying scale eg Christmas tree distribution over back.
No treatment needed

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29
Q

Pustular psoriasis

A

localized to hands and feet =;- palmar-plantar pustulosis
Or generalized pustular psoriasis \potentially life threatening)
Indicates sterile collection of neutrophils
Along with erythema and brown spots (sites of resolving pustules)
Very itchy and painful
Smoking particularly associated

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30
Q

Erythrodermic psoriasis

A

> 97% of body surface area
Marked changes,
At risk of developing skin failure and be very unwell.

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31
Q

Psoriatic arthritis presence

A

5-7% patients with psoriasis but under diagnosed
Particular patterns of involvement
But just be aware of probability and multiple joints

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32
Q

Comorbidities in psoriasis

A

Metbaolic syndrome
Alcohol use
Smoking
Mental health problems

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33
Q

Broad treatment options for psoriasis

A

topical treatments
UV light
Systemic medications

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34
Q

Topical treatments for psoriasis

A

emollients (not that important)
Topical vitamin D analogues, typically with topical steroid
Tar eg exorex lotion

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35
Q

Chronic venous changes legs

A

haemosoderine deposits
Varicose veins
Venous flare
Red scaly eczematous patch

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36
Q

what is venous eczema

A

eczema caused by chronic venousninsufficiency
Excess fluid in legs irritates skin causing eczema

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37
Q

Management venous eczema

A

treat eczema: Emollients, yopical steroid, soap substitute
Treat underlying cause: Elevate legs and compress

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38
Q

Cellulitis appearance

A

shiny appearance
Erythema
Area of trauma
Swelling

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39
Q

What is celljlitks

A

acute infection of deep dermis and ssubcuticular tissue
Commonly strep pyogenes and Staph aureus
Incr risk if diabetic or immunosuppressed
Typically painful spreading erythema and swelling AND systemically unwell
Look between toes as tinea pedis can lead to port of entry

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40
Q

Treatment of cellulitis

A

treat with antibiotics
Wash with dermol 500

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41
Q

lipodermatosclerosus

A

not cellulitis but looks like it
Often bilateral
Normal or near normal CRP. No tempersture
Evidence of chronic venous changes

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42
Q

Management of lipodermatosclerosus

A

ABPIs and compression stockings
Initially topical steroids to reduce inflammation
Emollient and soap substitute

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43
Q

erythema nodosum features

A

septal panniculitus
More commone in women age 20-30
Commonly associated with prodromal symptoms
Tender erythematous ‘bruise like’ nodules
Bilateral and symnetrical
Lower legs and occ arms
Fade over 2-6 weeks
Don’t scar

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44
Q

Causes of erythema nodosum

A

1/3 no chase identified
Infection
Infection
Drugs: OCP, Penicillins
Sarcoidosis
IBD partic Crohns
Pregnancy
Rheumatological disease
Malignancy: AML, Hodgkin Lymphoma

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45
Q

Erythema nodosum management

A

FBC, ESR, urinalysis, CXR
full history
Treat underlying cause
NSAIDs
Elevation and support stockings
Rarely need oral corticosteroids

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46
Q

Differential diagnoses red legs

A

cellulitis
Acute lipodermatosclerosis
Venous stasis eczema
Other eczema (contact, allergic, asteatotic)
DVT
Drug eruption
Others: Vasculitis, erythema nodosum

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47
Q

Skin organ failure

A

acute onset blistering or erosive rash
Rash with mucosal involvement
Rash in context of recent new meds
Acute rash with systemic symptoms
Extensive skin involvement

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48
Q

erythroderma appearajde

A

Inflammatory skin disease affecting >90% surface of skin
Erythematous
Inflamed
Extensive
Confluent on buttocks and legs and more patchy on arms and upper back

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49
Q

Consequences of erythroderma

A

fluid and electrolyte loss
hypothermia
Haemodynamic compromised, high output cardiac failure esp in elderly
Barrier dysfunction so risk of infection
Protein loss and so hypoalbuminaemia
Oedema

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50
Q

Treatment of erythroderma

A

bed rest
BP, pulse temp
Fluid balance chart
Correct fluid or electrolyte abnormalities
Withdraw suspect drive ug
Treat any infection, reverse barrier nursing
Smother in emolloents
Treat underlying cause, may possibly need systemic steroids

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51
Q

Stevens Johnson synfrome features

A

Patchy bright red eroded area of skin
Scaling, peeking skin around edge
Darker mottled pur0le red patches
Background linen looks blood stained

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52
Q

Course of Steven’s Johnson syndrome/toxic epidermal necrolysis

A

occur after ingestion of drug
Prodrome of 1-14 days, flu like syndrome, skin tenderness pain, conjunctival burning
Skin lesions with diffuse erythema then become dusky. Late then flaccid blisters, regrowth of epidermis
Steven Johnson syndrome is less tha 10% of skin, TEN >30%
Mucosal membrane involvement

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53
Q

Causes of SJS or TEN

A

drugs: Sulfur based, NSAIDS, anticonvulsNts, penicillins, quinolones, vancomycin, allopurinol
Infections (partic in children): Mycoplasma, EBV, histoplasmosis, adenovirus

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54
Q

Management of SJS and TEN

A

withdraw causative medication
Refer to specialist centre
Correct fluid and electrolytes
Treat sepsis
Analgesia
Ophthal, gynae, ENT
Evidence for IVIg etc limited

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55
Q

Erythema multiforme

A

target lesions, bilateral and symmetrical
Minor: Just on skin
Majro: Mucposal involvement
Typically caused by HSV or mycoplasma
Treat underlying cause and support

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56
Q

Staphylococcal scalded skin syndrome

A

peeling eroded skin, red and blistered
Looks like burn
More common in children
Often flexural
Painful
Staphylococcal exotoxins
Treat with antibiotics

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57
Q

Urticaria description

A

hives ‘nettle’ rash
Sudden onset pruritic, pink oedematous raised lesion of the superficial dermis
Individual lesions usually last under 24h
Fluctuating
Alone or with associated angioedema or anaphylaxis?

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58
Q

Treatment of urticaria

A

if any anaphylaxis treat that
Non sedating antihistamines eg cetirizine, loratidine, fexofenadine
If persistent add H2 antihistamine eg ranitidine and montelukast 10mg
Try to avoid oral steroids but may reduce duration of acute reaction

59
Q

necrotising fasciitis

A

life threatening soft tissue infection
Progresses rapidly
Painful out of proportion to what can be seen
Often doesn’t respond to abx
Freqyently preceded by trauma eg surgery, ulcer, IVDU, insect bite
Risk FACTORS. DM, immune deficiency, obesity, malignNcy, surgery, malnutrition, alcohol abuse

60
Q

Appearance of necrotising fasciitis

A

rapidly spreading
Poorly demarcated
Purple/brown/black erythema

61
Q

Management of NEC fasc

A

urgent surgicalnreview
Theatre for debridement
Broad spec abx

62
Q

causes of itch (groups)

A

Dermatological
Systemic
Drugs
Neurological
Psychogenic
Mixed

63
Q

dermatological causes of peuritus

A

dermatitis eg atopic, contact, seborrhoeic
Urticaria
Lichen planus
Skin infections, scabies, lice, fungal
Psoriasis
Cutaneous T cell lymphoma
Immunobullous disease
Xerosis

64
Q

Scabies appearance

A

mite where female mite burrows in and lays egg in burrow
After period of 4-6 weeks, hypersensitivity to mite faeces develops and then get itching and excoriations
Very infectious on close physical contact
Burrows primarily hands and feet
Can get rash of inflammatory pustules, eg in axillary folds, umbilicus, thighs, genitalia

65
Q

Diagnosis of scabies and treatment

A

pathognomonic sign is burrow
Treat patient and close physical contacts simultaneously (even if they are asymptomatic)
Scabicide, eg permethrin is 1st line. 2 topical treatments one week apart
Wash clothes and bed linen at high temp day after treatment

66
Q

systemic diseases causing pruritus

A

renal disease
Cholestasis partic PBC
haematological -Fe deficiency, polycythaemia vera
Malignancy
Endocrine disorders, esp thyroid disease
HIV
Connective tissue disease
Post herpetic neuralgia

67
Q

Management of pruritus

A

avoid soaps and detergents
Treat underlying conditions
Topical emollients and maybe with menthol and steroids if active inflammation
Anti histamines
If neurological, think about other things eg TCAs

68
Q

Vitiligo

A

acquired skin depigmentation (loss of epidermal melanocytes)
1/3 family history
Assoc w other autoimmune conditions
Consider cosmetic impact
Treat with potent topical steroids and poss UV light treatment

69
Q

Alopecia

A

areata= well defined areas of hair removal
Totalis = entire scalp is involved
Universalis = all of body hair is involved

70
Q

Cutaneous vasculotis

A

palpable purpura (non blanching)
Usually lower legs
Lesions can become ischaemic and necrose forming ulcers
Causes according to range of vasculitic causes
Investigate for systemic involvement (urine dip)
Treat cause, reduce stasis and topical steroids

71
Q

Erythema nodosum

A

Erythematous, indurated plaques and nodules on lower legs (esp shins)
Painful, lasts 2-3wka
Doesn’t scar
Common prodromal and systemic symptoms

72
Q

dermatomyositis clinical featuresf

A

cutaneous lesions: Periorbital reddish/purple erythema (heliotrope rash), flat topped papules over dorsal aspect of IP joints of hands, photosensitivity, nail fold telangectasia and ragged pupils
MusCle inflammation

73
Q

derm management of dermatomyositis

A

sun avoidance and protection
Rest
Topical sterols or tacrolimus
Often systemic steroids with rheumatology input

74
Q

systemic lupus erythematosus skin features

A

malar rash sparing nasolabial fold. Erythema znd oedema
Fine scale
Non scarring (unlike discoid lupus)
No pustules (unlike rosacea)
Photosensotivity
Oral ulcers

75
Q

management of SLE

A

shared care w rheumatology and rena’
Photoprotection, topical steroids, hydroxychloroquinw, stop smoking

76
Q

Sarcoidosis

A

red brown plaques annular or nodules
Enlargement of scars with infiltrated plaques
Variety of appearances (great imitator)
Derm involvement with 25% of those w sarcoid

77
Q

dermatology management of sarcoidosis

A

very potent topical steroids
Intralesional steroids
Other drugs eg hydroxychloroquine, methotrexate, tetracyclines, May need systemic steroids

78
Q

Systemic sclerosis symeptoms

A

Skin tightness
Raynaud’s
Joint pain/swelling
Dyspnoea
Muscle pain and weakness
Dysphagia/dyspepsia
Anorexia, fatigue, weight loss

79
Q

What’s happening in systemic sclerosis

A

Collagen accumulation and then vascular damage
Limited cutaneous or diffuse cutaneous
consider internal organs involvement

80
Q

Ix for systemic sclerosis

A

anti centromere antibodies in limited SS
Anti scl70 antibodies in diffuse SS
CXR, echo, check all other sympt

81
Q

Management of Raynauds

A

stop smoking
Gloves and socks
Calcium antagonists, AGII receptor blocker,
GTN patvhes, sildenafil, antoplatelets

82
Q

Dermatitis herpetiformis

A

typically beginning in early adult life
Symmetrically distributed papules and vesicles, often excoriated
Elbows, knees, buttocks, extensor forearms, scalp, occ face
Intensely pruritic
Associated with coeliac disease
;manage w gluten free diet

83
Q

Acanthosis nigricans

A

hyperpigmented and velvety texture skin
Symmetrically distributed most in intertriginous area eg sxillae, groin neck
Skin tags common
Marker of insulin resistance

84
Q

Viral warts appearance

A

filiform finger like projections
Particularly common in children, but any age
Spread by direct contact or autoinnoculation
Frequently painful plus social embarassment
Can be hyperkeratotic veruccA patches
Very common in immunosuppression and be very hard to clear

85
Q

Management of viral warts

A

often disappear on own in childhood
Salicylic acid/wart paint
Also cryotherapy and maybe surgery if large
Zinc supplements can help?

86
Q

Epidermoid cyst

A

Cystic enclosure of epithelium within dermis
Punctum visible
Keratin and lipid rich debris (foul smelling and cheesy)
Solitary or, multiple dermal subcutaneous nodules
0.5-5cm
Most common central trunk and face
Incorrectly referred to as sebaceous cysts

87
Q

Pilar cyst appearance

A

smooth mobile, firm found nodule
No punctum visible
Autodomsl dominant pattern of inheritance
Largely asymptomatic
F>M
Middle aged
Over 90% on scalp
In 2/3 cases multiple
Can be q large

88
Q

seborrhaeic kerratosis appearance

A

Tan brown
Stuck on appearance
Greasy surface
Rough/warty surface
Comedo like openings with dead keratin
“chocolate chip muffin’
Very very common in old people
Are v variable

89
Q

Dermatofibroma appearance

A

common button like dermal nodule
Lower limbs and upper arms
Can occur after insect bites
Can be itchy

90
Q

Lipoma fearures

A

dome shaped or egg shaped lump
2-10cm diameter
Feels smooth and soft
Easily moved by the skin
May have a rubbery or doughy consistency
Most common on shoulders, neck, trunk and arms, but fan be anywhere where there is fat under the skin
Grow slowly
Occasionally if multiple and vasfularised then can be quite painful (angiolipoma)
Very difficult to manage lors

91
Q

Cherry angioma

A

also known as campbell de Morgan spots
Collection of blood vessels
Commonly mistaken by patients as a red mole
Tend to appear in older people

92
Q

Telangectasia

A

Visible small linear broken capillaries
Usually related to sunlight exposure
Or venous insufficiency on legs
Or maybe prolonged use super potent topical steroids

93
Q

Haemangioma

A

rubbery bright red lesions comprising collection of blood vessrls
Can be present at birth

94
Q

Pyogenic granuloma

A

presents as shiny red ulcerated nodule reactively
Rapidly developing haemangioma (but this is a misnomer) following trauma
Usually first appears as a painless red, brownish red or blue-black spot
Grows rapidly over a period of days to weeks to final size 1-3cm
Typically bleeds easily and may ulcerate to form a crusts sore
Discomfort and profuse bleeding possible - mat need tight plaster

95
Q

Keratinic carcinoma prevalence

A

commonest human cancer 3-8% annual increase in incidence
>100000 cases s year, maybe 500 deaths
25% SCC 75% BCC

96
Q

Risks for BCC

A

Intermittent sun exposure
Childhood sun exposure
Fair skin /inability to tsn
Blue eyes
Red/blonde hair
Hunan papillomaviruses’ 36-60%
Some impact immunosuppression
Photosensitising drugs eg fluoroquinolone, chemo
Phototherapy
Ionizing radiation

97
Q

Risks for SCC

A

cumulative lifetime UV exposure
Fair skin/inability to tan
Blue eyes
Blonde or red hair
>90% HPV
ImmunosuPpression v v much
Photosensitizing drugs eg chemo and fluoroquinolones
Tobacco smoking (mucosal)

98
Q

Fitzpatrick skin I and II

A

always burns, never tans
Usually burns, sometimes tans
At much more risk of SCC and BCC

99
Q

Spectrum of keratinocyte dyspasia

A

normal
Solar keratosis (partial thickness of dysplasia)
Bowens disease (full thickness dysplasia)
Squamous cell carcinoma

100
Q

Solar keratosis appearance

A

scaly rough patches on an erythematous backgound
Ill defined and often feel like sandpaper
Variable keratotic aspect

101
Q

Bowens disease appearance

A

scaly erythematous patch
Often asymptomatic, predominant concern for symptoms
Don’t respond to treatments for eczema, fungal infections or psoriasis
Risk of progression to SCC 3-5%

102
Q

Causes of cutaneous horn

A

Viral wart
Actinic keratosis
SCC

103
Q

SCC appearance

A

Cutaneous horn w “meaty base”
Normally dome shaped which grow quickly and with central keratin plaque
If poorly differentiated, tend to erode and form an ulcer
tend to occur on head and neck

104
Q

Risks of SCC

A

Immunosuppression
Chronic ulceration
Chronic inflammation eg lichen sclerosis (vulval and penile)
Arsenic or industrial chemicals
HPV

105
Q

BCC appearance

A

pearly
Translucent papule
Rolled edge
Telangectasia
Ulcerarion
Very likely head and necka d temple
Metastasis extremely rare

106
Q

Variants of BCC

A

Nodular
Superficial (stretch skin and see pearly edge?)
Pigmented (more common darker skin types)

107
Q

Malignant melanoma prevalence

A

5-10% of skin cancers
But 75% of cancer deaths

108
Q

Differential diagnosis of pigmented lesions

A

melanocytic lesiosn:
Naevi (moles)
Dysplastic naevi (melanoma in situ)
Melanoma

Non melanocytic lesion:
Vascular eg haemangioma
Sebhorrhoeic keratis

109
Q

ABCDE assessment for melanoma

A

asymmetry
Border
Colour
Diameter (>6mm)
Evolution

Quite low threshold for referral

110
Q

Subtypes of melanoma

A

superficial spreading
Nodulsr
Acral

111
Q

Superficial spreading melanoma assedsment

A

assess breslow thickness once entirely excised
30-50% arise from existing melanocytic naevi
Rapid vertical growth
Poor prognosis as become invasive quite quickly

112
Q

Acral lentiginous melanoma

A

moost common in dark skinned individuals
Peripheries egg soles of feet
Late presentation often misdiagnosed as fungal

113
Q

Prognosis factors for melanoma

A

Breslow thickness - early detection crucial
Mitotic rate
Ulceration
Nodal status

114
Q

Management of melanoma

A

full skin and node exam
Excision w 2mm margin for histol
WLE depending on Breslow thickness
Sentinel node biopsy if breslow thickness >0.8mm
Adjuvant immunotherapy
Completion lymphadenectomy

115
Q

Melanoma survival

A

overall 5 year around 80%
If thickness greater than 1mm can be signif less good

116
Q

Vulval eczema appearance

A

pink erythema quite diffusely on outer oarts
Not much scale
Possible lichenification and thickened skin if chronic
Chronic = lichen simplex chronicus

117
Q

Irritation in the vulva

A

moisture: Heat, sweat, vaginal discharge, occlusive liners
Incontinence
Cleaning: toilet tossue, wet wipes, soaps, antiseptics
Friction: Tight clothing, exercise

118
Q

Common allergies in vulval contact dermatitis

A

clothing dyes
Fragrances (many sanitary towels are fragranced)
Lanolins
Preservatives
Steroids
Rubber chemicals
Medications eg anti fungals

119
Q

Genital skin care

A

avoid potential irritants: Soap, doiches, bodywash, bouble bath, wipes, powder, sprays, dyed toilet paper, panty liners
Unscented bland emollients: Cetraben, hydromol, zeroderm, epimax
Pat rather than rub dry
Loose clothing from natural fibres

120
Q

Management of vulval eczema

A

topical steroids (high potency if severe, usually moderate eg eumovate. Daily 2-4weeks, then 2x weekly as maintenance)
Avoid irritants, consider patch testing
Check iron levels

121
Q

Genital psoriasis appearance

A

Much brighter redness, possibly salmon pink
Well defined edges
Glazed appearance
Tends to affect hair bearing places and labia majors
No scale
Can also be under breasts etc
Specifically aske parients! 60% have genital involvement at some stage and huge impact on QOL

122
Q

Genital psoriasis treatment

A

Tricky
Many psoriasis meds are irritants
Risk of atrophy with long term use of steroids (and more potent in flexural sites)
Combination products: Trimovate (clobetasone, oxytetracycline, nystatin)
may need systemics eg methotrexate

123
Q

thrush symptoms

A

Candida vulvovaginitis
Itchy red swollen introitus and labia with cottage cheese like exudate
Rare in children and postmenopausal women without HRT as needs oestrogen. Swab these people

124
Q

Risks for vulvovaginal candidiasis )(thrush)

A

diabetes mellitus, partic poor control
Antibiotic use esp broad spec
Incr oestrogens eg in pregnancy and HRT
Immunosuppression - local or systemic, HIV

125
Q

Treatment of thrush

A

clotrimaxole pessaries or creams
Stat oral dose 150mg fluconazole (not in pregnancy)
Repeat in 3 days if severe

126
Q

Impetigo appearance

A

Gooden crusting
Maybe flaccid blisters if bullous
Erytehrmatous and crusted (dried sebum, blood, bacterial debris)
Swab skin
Treat w antibiotics

127
Q

What is a pustule

A

collection of neutriohils

128
Q

Diff fungal infections

A

Body: Ringworm, or tinea corporis
Feet: Tinea pedis
Nails: Tinea unguium
Scalp: Tinea capitis

129
Q

Pitriasis versicolor

A

common fungal infection
Three colors
Often back if people hot and sweaty

130
Q

Different pustular rashes

A

acne vulgaris
Acne rosacea
Other non acne: Folliculitis, furunculosis, pustular psoriasis etc

131
Q

Acne vulgaris prevalence

A

almost every teenager to some degree
Androgens play a role
More prevalent and severe in male teenagers’
More frequent and persistent in adult females
Less in less developed countries?

132
Q

Pathophys of acne

A

chronic inflammatory disease of pilosebaceous unit
Mainly affect areas if skin w highest density of units, eg face, neck, upper chest, shoulders, back
Related to incr sebum and clogging of hair pores, then secondarily bacterial infection and inflammation

133
Q

Aetiology of acne

A

normal physiological reaction to high androgen in puberty
Genetics
Maybe smoking (neutrophilic conditions?)
Possibly diet but not def
rrarely secondary to underlying endocrine or drugs: PCOS, hormone producing tumours

134
Q

Drugs related to acne

A

phenytoim
Isoniazide
Moisturiser
Phenobarbitone
Lithium
Lithium
Estrogen (OCP)
Steroids

And some new cancer drugs

135
Q

Acne presentations

A

Variable but in sebjorraeic areas
Non inflammatory: Open comedones (blackheads), closed comedones (whiteheads)
Inflammatory lesions: Papules (small red bumps), pustules (white or yellow squeezable spots), inflamed nodules (large red lumps)
Secondary lesions: Scars, pigmentation (hypo and hyper)

136
Q

Investigations for acne?

A

majority foes not need investigation
In children only if signs of virilisation
Refractory severe acne consider secondary cause eg PCOS, anabolic steroids, tumour

137
Q

Management of acne

A

life style: Sunshine may help some patients, but reassure patients
Conservative: Face washing important, non alkaline. Non oil based/occlusive. Removr make up at end of day. Try not to scratch squeeze or pick (but acne can scar if not touched)
Medical treatemnts: More preventing future spots not scarring or inflammation already happened.

138
Q

Drugs for mild acne

A

all treatments take 3-4 months to have an effect. And norm prevent rather than treat, may initially be a little worse before getting Better
Topical prep: Retinoids
If also papules etc: Combo of benzoyl perkxide, retinoid and antibiotic.
need to put on all spot prone skin

139
Q

Drugs moderate acne

A

ofal anti inflammatory antibiotics 3-6 month course, eg lymecycline or erythromycin
If hormonal pattern, consider oral contraceptive
Combine topical retinoid alongside.

140
Q

Management of severe resistant acne

A

refer to dermatology
They can give isotretinoin (Roaccutane) = vitamin A derivative
Contraception ESSENTIAL for females
Baseline bloods
Don’t take with tetracycline
Impact on drry skin, suns sensitivity, teratogenic and LFTs, arthralgia and mood (controversial, but should be avoided if high risk mental health issues)
69% long term cure

141
Q

Maintenance therapy for acne

A

encourage continued appropriate skdin care
High risk eg remake female pattern
Consider combination topical adapelene, benzoyl peroxide 1-2 nights per seek
If spot free 3-4 months can reduce of stop

142
Q

Acne conglobata

A

very severe form of nodulo cystic acne

143
Q

Acne fulminans

A

ijnfammatory form of acne can start qhite suddenly then needs prednisolone

144
Q

Acne rosacea

A

Lots of redness with papules and pustules
Affects photosensitive areas
Typically begins after age 30 as redness on cheeks, nose chin ot forehead that may come and go
Partic common in fair skinned people wkfh history of flush/blush
Irritated by topical products, and alcohol, spicy food, temp change and hot drinks
Avoid irritation, and topical metronidazole or ivermectin
Next step would be oral tetracycline

Year 5 (11 decks)

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